The ketogenic diet (KD), characterized by high fat, moderate protein, and very low carbohydrate intake, has gained popularity as a weight-loss strategy and a potential treatment for various diseases, including insulin-resistant states. This article explores the intricate relationship between the ketogenic diet and insulin, delving into the mechanisms by which it affects insulin secretion, sensitivity, and overall metabolic health.
Understanding the Ketogenic Diet
The classic ketogenic diet (KD) is a high-fat, low-carbohydrate diet that mimics a starvation state with sufficient caloric intake to sustain growth and development. Ketogenic diets are generally high in fat (60%-85%), moderate in protein (15%-30%), and low in carbohydrates (5%-10%). This macronutrient distribution forces the body to switch its primary fuel source from glucose to fat.
Under normal physiologic circumstances, glucose is the main substrate for glycolysis, resulting in the production of adenosine triphosphate (ATP), the body’s main energy source. Under circumstances of starvation or dietary carbohydrate restriction, the body breaks down glycogen (i.e., the storage form of glucose) in the liver to provide the body with glucose. In a prolonged fasting or carbohydrate-restricted state (> 48-72 hours), liver glycogen stores become depleted. Without glucose as a substrate for ATP production, the liver breaks down triglycerides to make ketone bodies that travel to target tissues (e.g., brain, muscles) and ultimately generate ATP. This process of ketogenesis is regulated by insulin; low carbohydrate intake leads to low insulin levels, promoting ketosis.
When carbohydrate intake is drastically reduced, the body enters a state of ketosis, where it begins to produce ketone bodies from fat to use as an alternative fuel source. This metabolic shift has several implications for insulin regulation and overall metabolic health.
Insulin Secretion on a Ketogenic Diet: A Minimal Response
One of the key characteristics of a ketogenic diet is its minimal impact on insulin secretion. Research indicates that a ketogenic meal elicits a significantly lower insulin response compared to a meal higher in carbohydrates. This is primarily due to the very limited amount of carbohydrates provided, despite the presence of proteins and lipids that are known to stimulate insulin secretion.
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In a study comparing the insulin secretory response to a ketogenic meal and a Mediterranean meal, researchers found that glucose, insulin concentrations, and insulin secretory rate were markedly reduced after the ketogenic meal. Specifically, the glucose AUC (area under the curve) in the first hour was significantly lower, as were total insulin concentration and peak rate of insulin secretion.
These findings suggest that ketogenic meals can satisfy individual energy requirements without significant amounts of insulin secretion, which is an essential feature that could help reduce hyperinsulinemia-driven insulin resistance.
Insulin Sensitivity and Resistance: The Role of Ketogenesis
Insulin resistance (IR) is a condition in which the body's cells become less responsive to insulin, requiring more insulin to achieve the same effect. It is closely associated with obesity, type 2 diabetes, and other metabolic disorders.
Ketosis-inducing diets seem to reduce insulin resistance improving glucose and insulin levels, by requiring less insulin to be disposed of, suggesting being particularly useful in patients with insulin resistance triggered or maintained by hyperinsulinemia as well as in those with insulin secretory defects that prevent a normal glucose tolerance. Interestingly, ketogenic dietary interventions with ad libitum caloric intake or only moderate caloric restriction produce strong reductions in fasting insulinemia, HOMA-index, and postprandial insulin responses that are disproportionate to the modest differences in weight loss compared to control diets. Therefore, the reduction in insulin concentrations and the improvement in insulin resistance appear to be a direct consequence of this dietary regimen and not mediated by weight loss.
The Impact of Weight Loss
While the ketogenic diet's effects on insulin sensitivity are partly independent of weight loss, it's important to acknowledge the significant role weight loss plays in improving insulin sensitivity.
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Although not all individuals with obesity are insulin resistant, there is a well-demonstrated connection between these two phenomena, which is largely attributed to adipose and others tissues’ metabolic dysfunctions. The hormonal milieu facilitating the IR within the adipose tissue is worthy of more substantial discussion. Indeed, adipocytes secrete several hormones (adipokines) that can act on glucose and lipid metabolism as well as both anti-inflammatory or inflammatory mediators.
In response to weight loss, adipose tissue experiences quantitative and qualitative (morphological and functional) changes that lead to improvements in insulin sensitivity. In these terms, treatments aimed at reaching health glycemic targets should primarily focus on achieving weight loss.
Potential Risks and Considerations
While ketogenic diets can offer benefits for certain individuals, it's crucial to be aware of potential risks and considerations:
- Type 1 Diabetes: The clinical impact of ketogenic diets on patients with Type 1 diabetes remains unclear, as much of the literature consists of retrospective case reports and series. The subject has not been well investigated, likely because of concern about inducing ketoacidosis and hypoglycemia in patients already at high risk for these complications.
- Monitoring Ketones: For patients with Type 1 diabetes, monitoring ketones is important to identify and prevent diabetic ketoacidosis (DKA). Three types of ketone bodies, resulting from the liver metabolizing fatty acids, are measured in different ways, each with advantages and disadvantages: acetone, acetoacetic acid and beta-hydroxybutyrate.
- Adjusting Diabetes Therapies: Insulin dosages usually need to be reduced after starting a ketogenic diet; in Type 1 diabetes, this usually entails decreasing the amount of insulin received per gram of carbohydrate.
- Other Diabetes Medications: SGLT-2 inhibitors should be stopped before starting a ketogenic diet owing to the risk of DKA that often presents as euglycemic, making it difficult to recognize. GLP-1 receptor agonists can be continued with close monitoring in patients following a ketogenic diet, although some providers prefer to stop them. Metformin is generally considered safe to continue.
- Nutrient Deficiencies: Common misconceptions about ketogenic diets are that followers can consume few vegetables and must eat excessive amounts of meat. But a well-formulated diet can incorporate a variety of protein-containing foods, including fish, cheese and Greek-style yogurt. The diet may also include four or five servings of vegetables daily, which contain about 20 to 30 grams of carbohydrate in total; hence, the low amount of allowable carbohydrate may be obtained entirely from vegetables.
Practical Implications and Applications
The quantification of insulin required to metabolize a certain meal type is basic information that may help to predict or to explain the prandial response of subjects affected by insulin secretory defects or by insulin resistance, and to rationally allocate patients to personalized dietary treatments.
Knowing that ketogenic meals (even single meals) can satisfy individual energy requirements without significant amounts of insulin secretion is an essential feature that would help to reduce hyperinsulinemia-driven insulin resistance and would help patients with limited insulin secretory capability to manage their condition more effectively.
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Managing Blood Glucose Levels
By actively managing your blood glucose levels before you eat (through meal timing and nutrient-focused foods and meals), you can optimize the numbers that matter when managing your metabolic health. Rather than thinking of insulin as an anabolic hormone (i.e. it helps things to grow), it’s much more helpful to focus on its function as an anti-catabolic hormone (i.e. it prevents the breakdown of fat).
If your blood sugars after meals are elevated above 7.8 mmol/L (140 mg/dL), then you have prediabetes or diabetes and need to work to reduce your post-meal blood glucose by reducing refined carbohydrates and/or medications to reduce blood sugars.
Dietary Strategies for Stable Blood Sugar
While high-fat foods and meals will keep your blood sugars stable, they also provide a lot of energy, along with lower satiety. Foods with a higher percentage of protein and a greater nutrient density are harder to overeat and won’t raise your blood sugars significantly (in fact, they may reduce them).
In our Macros Masterclass, we guide people to reduce their carbohydrates if their blood sugars rise more than 30 mg/dL or 1.6 mmol/L after meals. In our Data-Driven Fasting Challenge, we guide people to reduce or eliminate foods and meals that are causing their blood glucose to rise more than 30 mg/dL or 1.6 mmol/L above their current blood sugar trigger.