“The ketogenic diet is a powerful tool to treat T2D. For many patients, it is absolutely life-changing. It needs specialized training to use it effectively and safely. It is not uncommon to see the need of hundreds of units of insulin evaporate in days or weeks.”  (Michael Mindrum, MD 4/19/2019)

Interest in the ketogenic diet is expanding among the general public and medical professionals alike, and for good reason. A large and rapidly expanding body of scientific literature supports the use of this very low carbohydrate, high fat dietary approach for numerous health concerns,  including type 2 diabetes, metabolic syndrome and associated comorbidities, diverse neurological and neurodegenerative disorders, and difficult-to-treat issues, such as migraine and lymphatic disorders (lymphedema, lipedema). In previous articles, we’ve covered the basics of nutritional ketosis and various potential therapeutic applications of ketogenic diets. This time, we’ll take a closer look at select mechanisms of the ketogenic diet that underlie its efficacy in some of these situations.

There are few interventions more effective for improving glycemic control in type 2 diabetes and metabolic syndrome than carbohydrate restriction. It’s so powerful, in fact, that a team of researchers active in this field have said it should be the first approach in diabetes management, and presented twelve lines of evidence to support their case. Since type 2 diabetes (T2D) is a condition defined by high blood sugar, it’s nearly self-evident that reducing consumption of foods that raise blood sugar the most ought to be a foundational aspect of disease management:

“At the end of our clinic day, we go home thinking, ‘The clinical improvements are so large and obvious, why don't other doctors understand?’ Carbohydrate restriction is easily grasped by patients: Because carbohydrates in the diet raise the blood glucose, and as diabetes is defined by high blood glucose, it makes sense to lower the carbohydrate in the diet.”  (Eric Westman, MD)

This was understood as far back as 1877:

“There are few diseases which present to the practitioner so clear an indication of what is to be done [...] a Diabetic should exclude all saccharine [sugary] and farinaceous [starchy] materials from his diet.” (William Morgan, MD, Diabetes Mellitus: Its History, Chemistry, Anatomy, Pathology, Physiology and Treatment)

Dramatic reduction in dietary carbohydrate intake has a rapid and powerful effect on lowering blood glucose, to the point that individuals with T2D may need to decrease or even altogether discontinue insulin injections on the first day of adopting a ketogenic diet:

“With the ketogenic diet, there may be as much as a 50–100 mg/dL reduction in blood glucose on the first day of eliminating foods containing starch or sugar. We have seen individuals on very high doses of insulin (hundreds of units of insulin) no longer need insulin on the first day of eliminating carbohydrates from the diet.” (Westman et al., 2018)

This observation echoes results from a 2017 study looking at the feasibility and effects of a ketogenic diet for T2D. Along with impressive reductions in HbA1c, diabetes medications—including insulin injections—were discontinued or reduced in a substantial proportion of subjects. (As always, patients should work with their physician to make any adjustments to their medications and not do so on their own.)

Ketogenic diets don’t only lower blood glucose; they also lower insulin levels, which is a critical point. Because T2D is diagnosed solely through measuring glucose, a staggering number of people with a wide array of health issues driven by chronic hyperinsulinemia but who are normoglycemic are given a false sense of security regarding their metabolic health. An abbreviated list of conditions either primarily caused by hyperinsulinemia or exacerbated by it, whether or not blood glucose is elevated, includes PCOS, hypertension, erectile dysfunction, benign prostatic hyperplasia (BPH), hyperuricemia/gout, skin tags, and more.

The lowering of insulin levels may explain the improvements in HDL, triglycerides, and LDL particle size observed in clinical trials of ketogenic diets, as well as the lowering of uric acid levels and reduction in gout attack frequency in subjects following reduced carb protocols. (Elevated insulin impairs renal uric acid excretion as well as sodium excretion, which may contribute to the connection between elevated insulin and hypertension.) Ketogenic diets have also been shown to improve non-alcoholic fatty liver disease (NAFLD), resulting in “rapid and dramatic reductions of liver fat” in subjects with obesity and NAFLD, along with downregulation of fatty acid synthesis and upregulation of fatty acid oxidation. Insulin resistance—a.k.a. hyperinsulinemia—may be a significant factor in the pathophysiology of liver fat accumulation, so an intervention that reduces insulin levels may be expected to improve NAFLD.

It cannot be emphasized enough that chronically elevated insulin is a major driver of compromised health, affecting nearly every tissue system even in individuals with normal blood glucose. Growing recognition of this led one researcher to call the lowering of insulin levels “the sleeping giant in patient care.” Reducing dietary carbohydrate via a low carb or ketogenic diet isn’t the only way to correct chronic hyperglycemia and hyperinsulinemia, but it’s certainly one of the most effective.

A future article will delve into mechanisms of action of the ketogenic diet in the central nervous system as they relate to neurological and neurodegenerative disorders.