The ‘Cliff Notes’ on Ketogenic Diets
Ketogenic diets are becoming one of, if not, the, most popular diet in the mainstream right now. A Google search for “Ketogenic Diet” now returns over 21,000,000 results and many of the top-selling health books and most-read articles are focussed on the diet.
Despite this popularity, the ketogenic diet is misunderstood and there are many myths and misunderstandings. Not to mention that a lot of people overcomplicate it!
Why keto?
Ketogenic diets have been used to successfully treat childhood epilepsy since the 1920s. (1-4) Since that time, ketogenic and other low carbohydrate, high-fat diets have demonstrated a host of benefits for many health conditions, weight and fat-loss, (5-10) and for improving some aspects of sports (especially endurance) performance for some. They are also being studied for use as part of the treatment and prevention strategy for neurodegenerative disorders like Parkinson’s and Alzheimer’s disease, (11, 12) diabetes, (13, 14) cancer, (15-18) and autism (19) among other conditions.
What IS keto?
Ketosis refers to the metabolic state that typically occurs during fasting or carbohydrate restriction. In this state ‘ketone bodies’ are created from fats and some amino acids. Restricting carbohydrate results in reduced insulin levels, which in turn reduces lipogenesis (the creation of fat) and the accumulation and retention of fat stores.
The body continues to use considerable amounts of carbohydrates initially when you restrict or avoid carbs in the diet. This is provided by liver glycogen, which is broken down into glucose but when these glycogen reserves begin to become depleted, an alternative fuel source is needed. The Central Nervous System (CNS), including the cells of the brain and spinal cord, cannot effectively use fat for fuel and so, they typically rely on glucose, but the brain can effectively run on ‘ketone bodies’ when there are fewer carbohydrates available.
What are ‘ketone bodies’?
Ketone bodies are fuels that can be used by the brain and most tissue throughout the body. They are created fatty acids (from fat) and some amino acids from protein. The ketone bodies are Acetoacetate, beta-hydroxybutyric acid (BOHB) and Acetone. These ketone bodies are produced through a process called ‘ketogenesis’ in the liver. Acetoacetate is the primary ketone body, and this is converted to BOHB, which functions as the main fuel in ketosis. The body always produces ketones, but when you drastically restrict carbs in the diet it has to produce more to supply the fuel shortfall for the brain and nervous system.
What are ketogenic diets?
Ketogenic diets are quite simply diets that are low enough in carbohydrate to encourage the creation of ketone bodies in much higher than normal amounts. This ketonaemia (the presence of ketones in the blood) is called ‘Nutritional Ketosis’ (often shortened to NK).
Nerd alert!
Very low carbohydrate ketogenic diets (VLCKDs) typically result in BOHB levels of ≥ 0.5 mmol.L-1 (20) and this level is used as a ‘cut off’ point for achieving ketosis by nutrition researchers. (21) The ten-fold range of BOHB from 0.5 to 5.0 mmol.L-1 has been suggested by low-carb gurus Stephen Phinney and Jeff Volek as the functional definition for NK. (22, 23) I had the opportunity of asking Dr Phinney how they originally determined this range, and the lower cut-off and he said that they arrived at these figures based on the point at which participants symptoms of keto-induction were mitigated in their studies on ketogenic diets.[1]
So, in simple terms, a ‘good’ keto diet is very low in carbohydrate, moderate to high in protein and high in fat.
In simple terms, a keto diet is very low in carbohydrate, moderate to high in protein and high in fat.
Note:
Many people think that a keto diet has to be really low in protein and extremely high in fat but this isn’t the case. Check out my article on protein and keto to find out more.
How to Do Keto
The simple man’s guide to keto
Simply avoid ‘obligate’ carbs…
This means that you create high-quality meals, based on whole foods, and simply avoid grains, tubers, legumes, and fruit. Easy as that!
So, a meal would contain:
1-2 palm-sized portions of protein
I.e. meat, fish, chicken, eggs
Green, yellow, red, and orange – non-starchy veggies like lettuces, cabbages, cauli, broccoli, spinach, etc.
2-3+ fist-sized portions of vegetables
1-2 thumb-sized portions of healthy fats
Cook with olive oil or butter or ghee. Coconut oil is also great. Use hemp or flax oils only as dressings (don’t cook with them) and use olive oil for anything. Also: nuts, seeds, avocado.
If desired add a few nuts, seeds, or berries
Use herbs and spices liberally
A bit more in-depth…
So, you want to actually know how much to eat! Honestly, the simple guide above will work for almost everybody who wants to try keto, but if you want/need to nerd out a bit more, here are some ratios that can help you to determine your optimal keto macronutrient intake.
- Protein: 1.4 g – 2.5 g per kg body weight per day
- Fat: 60-80% of calories
- Carbs: Whatever is left
Note: there is some large variability in the ratios above! That is because everybody is different and some people can tolerate much higher amounts of carbs and still achieve ketosis. Some rough ‘rules of thumb’ that might help you to determine whether you should start on more or less are:
If you are more insulin sensitive, you can probably tolerate slightly more carbs. If you are more insulin resistant (i.e. closer to pre-diabetic) then you should have less.
If you are more active, or you’re trying to put on muscle, you can probably tolerate (and benefit from!) more carbs too.
Conclusion
There you have it! Keto need not be so complicated. If you simply stick to a diet based on 80%+ natural, unprocessed foods, eat meals when hungry (don’t snack), and avoid added sugars, grains, tubers, legumes, and fruit, you’ll likely achieve ketosis and get the benefits, without the stress.
Study the science behind ketogenic diets and how to apply them to a range of outcomes for performance or health conditions with the Keto-Mastery course, taught by ketogenic nutrition researcher Dr Cliff Harvey
References
1. Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in children: a systematic review of efficacy. Pediatrics. 2000;105(4):e46.
2. Keene DL. A systematic review of the use of the ketogenic diet in childhood epilepsy. Pediatr Neurol. 2006;35(1):1-5.
3. Neal EG, Chaffe H, Schwartz RH, Lawson MS, Edwards N, Fitzsimmons G, et al. The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. Lancet Neurol. 2008;7(6):500-6.
4. Levy RG, Cooper PN, Giri P, Pulman J. Ketogenic diet and other dietary treatments for epilepsy. The Cochrane Library. 2012.
5. Yancy WS, Jr., Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med. 2004;140(10):769-77.
6. Bueno NB, de Melo ISV, de Oliveira SL, da Rocha Ataide T. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. Br J Nutr. 2013;110(07):1178-87.
7. Volek JS, Quann EE, Forsythe CE. Low-Carbohydrate Diets Promote a More Favorable Body Composition Than Low-Fat Diets. Strength and Conditioning Journal. 2010;32(1):42-7.
8. Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. The Journal of pediatrics. 2003;142(3):253-8.
9. Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS, Jr., Brehm BJ, et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials. Arch Intern Med. 2006;166(3):285-93.
10. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I, et al. Weight loss with a low-carbohydrate, mediterranean, or low-fat diet. N Engl J Med. 2008;359(3):229-41.
11. Henderson ST. High carbohydrate diets and Alzheimer’s disease. Med Hypotheses. 2004;62:689-700.
12. Vanitallie TB, Nonas C, Di Rocco A, Boyar K, Hyams K, Heymsfield SB. Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility study. Neurology. 2005;64:728-30.
13. Hussain TA, Mathew TC, Dashti AA, Asfar S, Al-Zaid N, Dashti HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition. 2012;28(10):1016-21.
14. Nielsen JV, Joensson EA. Low-carbohydrate diet in type 2 diabetes: stable improvement of bodyweight and glycemic control during 44 months follow-up. Nutr Metab (Lond). 2008;5:14.
15. Warburg O. On the origin of cancer cells. Science. 1956;123(3191):309-14.
16. Seyfried TN, Flores R, Poff AM, D’Agostino DP, Mukherjee P. Metabolic therapy: A new paradigm for managing malignant brain cancer. Cancer Letters. 2015;356(2, Part A):289-300.
17. Bozzetti F, Zupec-Kania B. Toward a cancer-specific diet. Clinical Nutrition. 2015(0).
18. Vidali S, Aminzadeh S, Lambert B, Rutherford T, Sperl W, Kofler B, et al. Mitochondria: The ketogenic diet—A metabolism-based therapy. The International Journal of Biochemistry & Cell Biology. 2015(0).
19. Evangeliou A, Vlachonikolis I, Mihailidou H, Spilioti M, Skarpalezou A, Makaronas N, et al. Application of a ketogenic diet in children with autistic behavior: pilot study. Journal of child neurology. 2003;18(2):113-8.
20. Gibson A, Seimon R, Lee C, Ayre J, Franklin J, Markovic T, et al. Do ketogenic diets really suppress appetite? A systematic review and meta‐analysis. Obes Rev. 2015;16(1):64-76.
21. Guerci B, Benichou M, Floriot M, Bohme P, Fougnot S, Franck P, et al. Accuracy of an electrochemical sensor for measuring capillary blood ketones by fingerstick samples during metabolic deterioration after continuous subcutaneous insulin infusion interruption in type 1 diabetic patients. Diabetes Care. 2003;26(4):1137-41.
22. Volek JS, Phinney SD. The Art and Science of Low Carbohydrate Living: Beyond Obesity. New York, USA: Beyond Obesity; 2013.
23. Volek JS, Phinney SD. LOW CARBOHYDRATE LIVING. New York,
USA: Beyond Obesity; 2011.
[1] Oral communication, August 28th, 2014
