So far in this series, I’ve discussed the origins of the ketogenic diet and the biological role of ketone bodies (Part 1), whether living in a state of ketosis is normal and natural (Part 2), and whether ketogenic diets are effective for weight loss (Part 3). In this post, I’m going to explore one of the major health claims made for ketogenic diets, that they reverse insulin resistance and effectively treat diabetes.

Ketogenic Diets and Diabetes

Claims that ketogenic diets effectively treat diabetes are rife on the Internet and in popular books. Keto enthusiasts claim that carbohydrate consumption is the cause of the insulin resistance that drives type 2 diabetes^[1].

Insulin resistance is known to be an important risk factor for the development of the complications of diabetes^[2], both microvascular – diabetic eye (retinopathy), nerve damage (neuropathy) and kidney disease (nephropathy) – and macrovascular – coronary artery disease, peripheral artery disease, and stroke. Ketogenic diet advocates argue^[3], removing carbohydrates from the diet effectively treats the cause of diabetes and its complications: “insulin resistance functionally manifests itself as ‘carbohydrate intolerance’. When dietary carbohydrate is restricted to a level below which it is not significantly converted to fat (a threshold that varies from person to person), signs and symptoms of insulin resistance improve or often disappear completely”.

Children and young adults put on ketogenic diets to manage epilepsy were found to have higher arterial stiffness parameters, an early marker of vascular damage.

There are certainly studies which demonstrate the effectiveness of ketogenic diets for reducing various markers of diabetic control. For example, one study^[4] compared a ketogenic diet with “unlimited amounts of animal foods (i.e., meat, chicken, turkey, other fowl, fish, shellfish) and eggs, limited amounts of hard cheese (e.g., cheddar or swiss, 4 ounces per day), fresh cheese (e.g., cottage or ricotta, 2 ounces per day), salad vegetables (2 cups per day), and non-starchy vegetables (1 cup per day)” to a low-glycemic, reduced-calorie diet and found the ketogenic diet superior in reducing blood glucose, hemoglobin A1C, and fasting insulin levels along with reductions in injected insulin and oral diabetes medications.

But there are multiple lines of evidence contradicting the ‘carbs cause diabetes, so low-carb cures diabetes’ belief.

What Does the Science Say?

First, most intervention studies on ketogenic diets are short-term, but the limited evidence available from studies with longer follow-up periods indicates that the beneficial effects of ketogenic diets on biomarkers dissipate over time, long-term adherence is difficult, and there are higher rates of kidney stones, osteoporosis and hyperlipidemia^[5].

Then there are epidemiological, or population-based studies, which consistently demonstrate that reducing carbohydrate intake increases the risk of diabetes:

• The rate of type 2 diabetes in China rose from 2.6% in 2000 to 9.7% in 2010, with the most dramatic rise occurring in urban areas^[6]. But rice and other grain intake has dropped dramatically in China over that time, while oil and animal product intake rose – as did obesity rates^[7].
• Likewise, indigenous Mexican communities such as the Tepehuano, Huichol and Mexicanero were found to have zero diabetes just before the turn of the 20th century, while eating an extremely high carbohydrate diet consisting mostly of unrefined corn, beans, rice and squashes^[8]. Pima Indians living in Mexico on high in complex carbohydrate diets deriving on average 25% of energy from fat and 11% from protein, have less than one-fifth the prevalence of diabetes^[9] compared to Pima living in the US on a higher fat and protein diet.
• The Health Professionals Follow-Up Study tracked over 40,000 US men who were free of type 2 diabetes at baseline for up to 20 years, and found that those who ate a low-carbohydrate diet rich in animal fat and protein were 37% more likely to develop diabetes^10].
• Vegans – who naturally eat a high-carbohydrate diet – were found to have half the risk of developing type 2 diabetes as meat-eaters, even after adjusting for physical activity and body mass index^[11]; in other words, even overweight, and sedentary vegans had a reduced risk of diabetes due to eating carbohydrate-rich plants!

In intervention studies, low-fat plant-based diets have been found to be superior to conventional diabetes diets which restrict carbohydrate intake.

• Diabetic men on insulin therapy were confined to a metabolic ward and were fed a restricted carbohydrate diet typically recommended to diabetics (20% protein, 43% carbohydrate, 37% fat), followed by a very low fat, high carbohydrate and high in plant fiber diet (21% protein, 70% carbohydrate, 9% fat) for the remainder of the study^[12]. Participants were instructed to eat more if they lost weight on the high carbohydrate diet to factor out the effect of weight loss on insulin sensitivity. As a result, every single patient reduced his daily dose of insulin while on the high carbohydrate diet, from an average of 26 units per day to 11 units per day, and several were able to discontinue insulin altogether. Despite the reduction in insulin, fasting and postprandial plasma glucose values were lower in most patients on the high carbohydrate diet than on the standard diabetes diet.
• In a 74-week clinical trial comparing a low-fat whole food, plant-based diet to a diet conforming to American Diabetes Association guidelines, the plant-based diet improved blood sugar and lipid levels more than conventional diabetes dietary recommendations^[13].
• A systematic review of studies using plant-based diets for diabetes^[14] found that they significantly improved glycemic control, despite (or perhaps because of) increases in carbohydrate intake by, on average, 14% of energy, while decreasing fat by 12%.

What Drives Insulin Resistance – Carbohydrates or Fat?

It’s been known since the 1930s that dietary fat decreases insulin sensitivity^[15] – or to put it another way, causes insulin resistance. Among the various types of dietary fat, the saturated type found mostly in animal products but also in coconut and palm oils has the worst effect on insulin sensitivity. Epidemiological studies indicate that “subjects with higher intakes of fat are more prone to develop disturbances in glucose metabolism, type 2 diabetes or impaired glucose tolerance, than subjects with lower intakes of fat.” Additionally, experimental studies clearly demonstrated that diets high in fat impaired insulin sensitivity, while diets low in fat but high in carbohydrates improved it^[16].

The underlying mechanism in insulin resistance is characterized by accumulation of lipids (fats) in muscles, the liver and eventually the pancreas:

• Muscles take up free fatty acids from the bloodstream to use as fuel, and will take up more when fat is the primary macronutrient in the diet. However, when dietary fat intake is persistently high, they begin to accumulate more fat than they can oxidize (burn as fuel), and this intramyocellular lipid accumulation results in the muscle cells becoming insulin resistant^[17].
• Insulin resistance in muscular tissue increases fat deposition in the liver, causing the liver to become insulin resistant too^[18]. This hepatic insulin resistance drives the liver to continually release glucose and raises triglycerides (fats) levels in the bloodstream, worsening the fatty liver.
• Because of the insulin resistance in the muscles and the liver, the pancreas is initially forced to produce and secrete more insulin. But then the higher levels of circulating triglycerides begin to also cause fat accumulation in and around the pancreas, killing off the insulin-secreting beta cells (“lipotoxicity”) and eventually resulting in inadequate insulin production. At this point, blood glucose levels rise and the symptoms of type 2 diabetes occur.

These 3 pathological manifestations of insulin resistance are driven by ‘positive energy imbalance’^[19] – that is, consuming more energy than we use in our daily activities. A whole food, plant-based diet – high in unrefined, complex carbohydrates and low in fat – is, as mentioned in Part 3 of this series, the most effective dietary intervention for long-term weight loss published in a peer-reviewed journal^[20]. Even when instructed to eat ad libitum (that is, until they were full, with no portion control) and without being asked to increase their exercise level, overweight and obese participants in the BROAD Study were able to achieve average weight losses of 12 kg in 1 year.

Which Diet Is Best for the Long-Term Health of Diabetics?

Finally, it’s important to note that diabetics don’t die of diabetes per se; they die from its complications. The major cause of death in diabetics is cardiovascular disease, and a low-fat, whole food, plant-based diet is the only diet shown to reverse coronary artery disease^[21].

On the other hand, children and young adults put on ketogenic diets to manage epilepsy were found to have higher arterial stiffness parameters^[22], an early marker of vascular damage. This fact alone should be enough warning about the long-term risks of ketogenic diets, and encourage the use of low-fat, plant-based diets as the gold standard for diabetes management.

In summary, human populations living on high in complex carbohydrate, low-fat diets comprised primarily of minimally processed plant foods have historically enjoyed extremely low rates of diabetes. When they make the ‘epidemiological transition’ to a Western-style diet, which inevitably means a reduction in complex carbohydrates and an increase of animal and refined plant foods (including fats, oils, flour and sugar), their diabetes rates soar.

While ketogenic diets may lead to temporary improvements in glycemic control, they lose their effectiveness over time, are fundamentally unnatural to humans, and are unable to prevent the life-threatening complications of diabetes.

Why take the risk of a ketogenic diet, when a whole food, plant-based diet is a delicious, sustainable and proven method of preventing, managing, and even reversing diabetes?

Learn more about the ketogenic diet from the previous articles in this series:

Part 1 – What Is the Ketogenic Diet?

Part 2 – Is the Ketogenic Diet Natural for Humans?

Part 3 – Does the Ketogenic Diet Really Work for Weight Loss?

References

1. Taylor, R. (2012), Insulin Resistance and Type 2 Diabetes. Diabetes 61(4) 778-779. http://diabetes.diabetesjournals.org/content/61/4/778
2. Donga, E., Dekkers, O.M., Corssmit, E.P.M. & Romijn, J.A. (2015), Insulin resistance in patients with type 1 diabetes assessed by glucose clamp studies: systematic review and meta-analysis. Eur J Endocr
3. 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. Eur J Clin Nutr.;67(8):789-96. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/
4. Westman, E.C., Yancy, W.S., Mavropoulos, J.C., Marquart, M. & McDuffie, J.R., (2008), The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab.;5:36. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633336/
5. Kosinski, C. & Jornayvaz, F.R., (2017), Effects of Ketogenic Diets on Cardiovascular Risk Factors: Evidence from Animal and Human Studies. Nutrients.;9(5):517. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452247/
6. Li, H., Oldenburg, B., Chamberlain, C., O’Neil, A., Xue, B., Jolley, D., Hall, R., Dong, Z. & Guo, Y., (2012), Diabetes prevalence and determinants in adults in China mainland from 2000 to 2010: a systematic review. Diabetes Res Clin Pract.;98(2):226-35. https://www.ncbi.nlm.nih.gov/pubmed/22658670
7. Wang, H. & Zhai, F., (2013). Programme and policy options for preventing obesity in China. Obes Rev.;14 Suppl 2(0 2):134-40. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048452/
8. Guerrero-Romero, F., Rodríguez-Morán, M. & Sandoval-Herrera, F., (1997), Low prevalence of non-insulin-dependent diabetes mellitus in indigenous communities of Durango, Mexico. Arch Med Res.;28(1):137-40. https://www.ncbi.nlm.nih.gov/pubmed/9078601
9. Schulz, L.O., Bennett, P.H., Ravussin, E., Kidd, J.R., Kidd, K.K., Esparza, J. & Valencia, M.E., (2006), Effects of traditional and western environments on prevalence of type 2 diabetes in Pima Indians in Mexico and the U.S. Diab Care;29(8):1866-71. https://www.ncbi.nlm.nih.gov/pubmed/16873794
10. de Koning, L., Fung, T.T., Liao, X., Chiuve, S.E., Rimm, E.B., Willett, W.C., Spiegelman, D., & Hu, F.B., (2011), Low-carbohydrate diet scores and risk of type 2 diabetes in men. Am J Clin Nutr.;93(4):844-50. https://www.ncbi.nlm.nih.gov/pubmed/21310828
11. Tonstad, S., Butler, T., Yan, R. & Fraser, G.E., (2009), Type of vegetarian diet, body weight, and prevalence of type 2 diabetes. Diab Care.;32(5):791-6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671114/
12. Anderson, J.W. & Ward, K., (1979), High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. Am J Clin Nutr.;32(11):2312-21. https://www.ncbi.nlm.nih.gov/pubmed/495550
13. Barnard, N.D., Cohen, J., Jenkins DJ, et al. (2009), A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. Am J Clin Nutr. 2009;89(5):1588S-1596S. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677007/
14. Yokoyama, Y., Barnard, N.D., Levin, S.M. & Watanabe, M. (2014), Vegetarian diets and glycemic control in diabetes: a systematic review and meta-analysis. Cardiovasc Diagn Ther.;4(5):373-82. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221319/
15. Lichtenstein, A.H. & Schwab, U.S. (2000), Relationship of dietary fat to glucose metabolism. Atherosclerosis;150(2):227-43. https://www.ncbi.nlm.nih.gov/pubmed/10856515
16. Himsworth, H.P., (1934), Dietetic factors influencing the glucose tolerance and the activity of insulin. J Physiol.;81(1):29-48. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1394223/
17. Kraegen, E.W. & Cooney, G.J., (2008), Free fatty acids and skeletal muscle insulin resistance. Curr Opin Lipidol.;19(3):235-41. https://www.ncbi.nlm.nih.gov/pubmed/18460913
18. Taylor, R. (2008), Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetolog.;51(10):1781-9. https://www.ncbi.nlm.nih.gov/pubmed/18726585
19. Ibid.
20. Wright, N., Wilson, L., Smith, M., Duncan, B. & McHugh, P., (2017), The BROAD study: A randomised controlled trial using a whole food plant-based diet in the community for obesity, ischaemic heart disease or diabetes. Nutr Diabetes. 7(3):e256. https://www.ncbi.nlm.nih.gov/pubmed/28319109
21. Ornish, D., Scherwitz, L.W., Billings, J.H., Brown, S.E. et al (1998), Intensive lifestyle changes for reversal of coronary heart disease. JAMA;280(23):2001-7. https://www.ncbi.nlm.nih.gov/pubmed/9863851
22. Kossof, E., (2014), Danger in the pipeline for the ketogenic diet? Epilepsy Curr.;14(6):343-4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325592/