The Keto Diet: A Genetic Perspective on Low-Carb, High-Fat Eating
The ketogenic (keto) diet has gained significant popularity over the past decade, praised for its potential to aid in weight loss and improve certain health conditions. It’s a low-carbohydrate, high-fat eating plan that shifts the body’s metabolism into a state called ketosis, where fat becomes the primary energy source. For those exploring the keto diet, especially within a personalised wellness framework, it’s essential to weigh the pros and cons based on scientific evidence.
What is the Keto Diet?
The keto diet drastically reduces carbohydrate intake—typically to less than 50 grams per day—and increases fat consumption to make up about 70-75% of daily calories, with protein comprising the remainder1. By limiting carbohydrates, the body depletes its glycogen stores and begins to burn fat for energy, producing ketones in the process—a metabolic state known as ketosis2.
Pros of the Keto Diet
1. Effective Weight Loss
- Satiety and Caloric Intake: High-fat and moderate-protein diets are known to promote satiety, potentially leading to reduced caloric intake3. A systematic review and meta-analysis found that individuals following a ketogenic diet experienced greater weight loss compared to those on low-fat diets over the short term4.
2. Improved Blood Sugar Control
- Stabilising Blood Glucose: By minimising carbohydrate intake, the keto diet can help stabilise blood sugar levels, which is particularly beneficial for individuals with type 2 diabetes or insulin resistance5. A study showed that patients on a ketogenic diet had improved glycaemic control and reduced dependency on diabetes medications6.
3. Neurological Benefits
- Epilepsy Management: The keto diet was originally developed for the management of epilepsy. Studies have demonstrated its effectiveness in reducing seizure frequency in both children and adults with drug-resistant epilepsy7.
- Potential Cognitive Enhancements: Emerging research suggests that ketones may provide neuroprotective effects, potentially benefiting neurodegenerative diseases like Alzheimer's8. Some studies report improvements in cognitive function and memory9, although these studies are based on animal models and further research is required.
4. Cardiovascular Health Improvements
- Lipid Profile Changes: Some individuals on the keto diet experience increases in HDL (good cholesterol) and decreases in triglycerides, which are positive markers for heart health10.
Cons of the Keto Diet
1. Nutrient Deficiencies
- Lack of Essential Nutrients: Excluding or severely limiting fruits, whole grains, and certain vegetables can lead to deficiencies in vitamins, minerals, and fibre. Nutrients like potassium, magnesium, and vitamins B and C may be lacking, which are vital for various bodily functions.
2. Digestive Issues
- Fibre Deficiency: The low intake of fibre-rich foods can lead to constipation and negatively impact gut health11. A healthy gut microbiome relies on dietary fibre, and its absence may disrupt gut flora balance12.
3. Potential Cardiovascular Risks
- High Saturated Fat Intake: Consuming high amounts of saturated fats may increase LDL (bad cholesterol) levels, potentially raising the risk of heart disease13. This effect can vary based on individual genetics and fat sources in the diet14.
4. "Keto Flu" and Other Side Effects
- Adaptation Symptoms: During the initial transition to ketosis, some people experience symptoms like fatigue, headache, nausea, and irritability, commonly referred to as the "keto flu"15.
- Long-Term Sustainability: The restrictive nature of the diet can make it difficult to adhere to over the long term, leading to potential weight regain and metabolic disturbances when normal eating patterns are resumed16.
Genetic Considerations: How Your Genes May Influence Your Response to the Keto Diet
Understanding genetic variations can provide insights into how individuals might respond to the keto diet. Here are some key genetic factors to consider:
1. Fat Metabolism Genes (e.g., APOE)
- Cholesterol Levels: Variants of the APOE gene, particularly the APOE4 allele, are associated with higher LDL cholesterol levels when consuming a high-fat diet17. Individuals with this genetic variant may need to monitor their lipid profiles closely on the keto diet.
2. Carbohydrate Metabolism Genes (e.g., AMY1)
- Amylase Production: The AMY1 gene affects salivary amylase production, influencing carbohydrate digestion18. Individuals with fewer copies of the AMY1 gene may tolerate low-carb diets like keto better than those with more copies.
3. Lipid Transport Genes (e.g., FABP2)
- Fat Absorption: Variants in the FABP2 gene can influence how efficiently dietary fats are absorbed19. This may affect individual responses to high-fat diets in terms of weight loss and lipid levels.
4. Inflammation-Related Genes (e.g., IL6, TNF)
- Inflammatory Responses: Genetic predispositions to inflammation can impact how the body responds to dietary changes. For some, the keto diet may reduce inflammatory markers, while others may not experience the same benefit20.
Evidence-Based Insights: What the Research Says
- Weight Loss and Metabolic Health
- Short-term studies consistently show that the keto diet can lead to significant weight loss and improvements in metabolic health markers21. However, long-term data is limited, and some studies suggest that these benefits may diminish over time22.
- Cardiovascular Effects
- Research on the keto diet's impact on heart health is mixed. While some studies report improvements in HDL cholesterol and triglycerides, others note increases in LDL cholesterol, especially in individuals with certain genetic backgrounds23.
- Gut Health
- The keto diet's low fibre content can negatively affect gut microbiota diversity24. A diverse microbiome is associated with numerous health benefits, including immune function and mental health25.
- Sustainability
- Adherence to the keto diet can be challenging due to its restrictive nature26. Dietary compliance is crucial for long-term success, and individuals may find it difficult to maintain the diet over extended periods.
Balancing Genetics and Diet: Personalised Nutrition for Optimal Health
- Genetic Testing and Analysis
- Utilising genetic testing can help identify how your body may respond to the keto diet, allowing for personalised dietary recommendations27.
- Monitoring Health Markers
- Regular monitoring of lipid profiles, blood glucose, and other health indicators is essential when following the keto diet, especially for those with genetic predispositions to certain conditions28.
- Tailoring the Diet
- Adjusting the keto diet to include healthy fat sources (e.g., avocados, nuts, olive oil) and incorporating low-carb, high-fibre vegetables can help mitigate some of the potential risks29.
- Professional Guidance
- Consulting with healthcare professionals, such as dietitians or nutritionists, can provide personalised advice and help address any concerns related to genetics and the keto diet.
Conclusion: Is the Keto Diet Right for You?
The keto diet offers potential benefits, including weight loss, improved blood sugar control, and neurological advantages. However, it also presents challenges like nutrient deficiencies, digestive issues, and potential cardiovascular risks. Understanding your genetic makeup can provide valuable insights into how you might respond to the keto diet, allowing for a more personalised and effective approach.
By integrating genetic insights with nutritional guidance, you can make informed decisions about whether the keto diet aligns with your health goals and biological needs.
Disclaimer: This article is intended for informational purposes only and does not constitute medical advice. Always consult with a healthcare professional before making significant changes to your diet or lifestyle.
References
- Paoli, A., Rubini, A., Volek, J. S., & Grimaldi, K. A. (2013). Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. European Journal of Clinical Nutrition, 67(8), 789–796.
- Volek, J. S., & Phinney, S. D. (2012). The Art and Science of Low Carbohydrate Performance. Beyond Obesity LLC.
- Gibson, A. A., Seimon, R. V., Lee, C. M., et al. (2015). Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Obesity Reviews, 16(1), 64–76.
- Bueno, N. B., de Melo, I. S. V., de Oliveira, S. L., & da Rocha Ataide, T. (2013). Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. British Journal of Nutrition, 110(7), 1178–1187.
- Westman, E. C., Tondt, J., Maguire, E., & Yancy, W. S. (2018). Implementing a low-carbohydrate, ketogenic diet to manage type 2 diabetes mellitus. Expert Review of Endocrinology & Metabolism, 13(5), 263–272.
- Hallberg, S. J., Gershuni, V. M., Hazbun, T. L., & Athinarayanan, S. J. (2019). Reversing Type 2 Diabetes: A Narrative Review of the Evidence. Nutrients, 11(4), 766.
- Neal, E. G., Chaffe, H., Schwartz, R. H., et al. (2008). The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. The Lancet Neurology, 7(6), 500–506.
- Kashiwaya, Y., Bergman, C., Lee, J. H., et al. (2013). A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer's disease. Neurobiology of Aging, 34(6), 1530–1539.
- Taylor, M. K., Sullivan, D. K., Swerdlow, R. H., et al. (2018). A High-Fat Ketogenic Diet Induces a Unique Metabolic State in Mice. American Journal of Physiology-Endocrinology and Metabolism, 314(6), E446–E452.
- Forsythe, C. E., Phinney, S. D., Fernandez, M. L., et al. (2008). Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids, 43(1), 65–77.
- McDonald, T. J. W., & Cervenka, M. C. (2019). The expanding role of ketogenic diets in adult neurological disorders. Brain Sciences, 8(8), 148.
- Zinöcker, M. K., & Lindseth, I. A. (2018). The Western Diet–Microbiome-Host Interaction and Its Role in Metabolic Disease. Nutrients, 10(3), 365.
- Sniderman, A., Lamarche, B., & Tilley, J. (2019). Apolipoprotein B, low-density lipoprotein particle number, and risk of cardiovascular disease: why we can’t forget about LDL particle number. Cardiovascular Drugs and Therapy, 33(3), 473–479.
- Ferguson, J. F., Phillips, C. M., & McMonagle, J. (2017). Nutrigenetics of cholesterol metabolism: observational and dietary intervention studies in the postgenomic era. Nutrition Reviews, 75(6), 442–457.
- Salminen, A., & Kaarniranta, K. (2010). Genetics vs. entropy: longevity factors suppress the NF-κB-driven entropic aging process. Ageing Research Reviews, 9(3), 298–314.
- Johnston, B. C., Kanters, S., Bandayrel, K., et al. (2014). Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis. JAMA, 312(9), 923–933.
- Corella, D., & Ordovás, J. M. (2014). How does the APOE genotype influence dietary effects on cardiovascular disease risk? Journal of Internal Medicine, 275(2), 97–108.
- Perry, G. H., Dominy, N. J., Claw, K. G., et al. (2007). Diet and the evolution of human amylase gene copy number variation. Nature Genetics, 39(10), 1256–1260.
- Baier, L. J., Sacchettini, J. C., Knowler, W. C., et al. (1995). An amino acid substitution in the human intestinal fatty acid binding protein is associated with increased fatty acid binding, increased fat oxidation, and insulin resistance. The Journal of Clinical Investigation, 95(3), 1281–1287.
- Phillips, C. M. (2013). Nutrigenetics and metabolic disease: current status and implications for personalised nutrition. Nutrients, 5(1), 32–57.
- Brehm, B. J., Seeley, R. J., Daniels, S. R., & D'Alessio, D. A. (2003). A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of Clinical Endocrinology & Metabolism, 88(4), 1617–1623.
- Noto, H., Goto, A., Tsujimoto, T., & Noda, M. (2013). Low-carbohydrate diets and all-cause mortality: a systematic review and meta-analysis of observational studies. PLoS One, 8(1), e55030.
- Rosenbaum, M., & Leibel, R. L. (2010). Adaptive thermogenesis in humans. International Journal of Obesity, 34(S1), S47–S55.
- Włodarska, M., & Krajmalnik-Brown, R. (2018). Diet, gut microbiota, and type 2 diabetes: what are the links? Current Opinion in Clinical Nutrition and Metabolic Care, 21(5), 364–369.
- DeGruttola, A. K., Low, D., Mizoguchi, A., & Mizoguchi, E. (2016). Current understanding of dysbiosis in disease in human and animal models. Inflammation and Regeneration, 36(1), 13.
- Gardner, C. D., Trepanowski, J. F., Del Gobbo, L. C., et al. (2018). Effect of low-fat vs low-carbohydrate diet on 12-month weight loss in overweight adults and the association with genotype pattern or insulin secretion. JAMA, 319(7), 667–679.
- Ordovás, J. M., & Mooser, V. (2004). Nutrigenomics and nutrigenetics. Current Opinion in Lipidology, 15(2), 101–108.
- Samaha, F. F., Iqbal, N., Seshadri, P., et al. (2003). A low-carbohydrate as compared with a low-fat diet in severe obesity. The New England Journal of Medicine, 348(21), 2074–2081.
- Brinkworth, G. D., Noakes, M., Buckley, J. D., Keogh, J. B., & Clifton, P. M. (2009). Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. Archives of Internal Medicine, 169(20), 1873–1880.