Ketosis vs. Ketoacidosis: What’s the Difference?

Any nurse knows that ketones are bad, right? So what is all the hype over eating plans that induce ketosis? And why are ketones being labeled neuroprotective or referred to as good metabolic fuel?

Ketosis vs. Ketoacidosis: The Basics

Ketone body production, which occurs during the consumption of a low carbohydrate diet, is called physiological ketosis or nutritional ketosis. This is not the same as ketoacidosis, or diabetic ketoacidosis (DKA), which happens when there is a lack of insulin and an abundance of blood glucose. They are related, but not the same.

Humans with normal metabolic function have an alternative source of fuel to glucose that can be triggered by restricted intake of carbohydrates. Fatty acids move from adipose stores and are converted into ketone bodies. Ketosis means the presence of ketone bodies in the blood. The brain is able to use ketones as an energy source in the form of acetoacetate and B-hydroxybutyrate. This process uses ketones to fuel the body in the absence of food. (1)

Nutritional ketosis can be achieved in most adults by restricting total daily carbohydrate intake to 10 grams or less per serving for a total of less than 40 grams per day. The majority of fat for ketone production comes from a high-fat ketogenic diet, while a smaller portion comes from fat stores in the body. Both insulin and blood glucose levels remain low. (1) A recent study by Hallberg demonstrated that the decreased insulin and glucose levels on a ketogenic diet can lead to decreased fasting insulin levels and improved insulin resistance. (2)

Ketosis vs. Ketoacidosis: The Blood Glucose Level

In diabetic ketoacidosis blood, glucose levels are elevated and there is no insulin in the blood. Measuring B-hydroxybutyrate levels in the blood can differentiate diabetic ketoacidosis versus ketosis. On a ketogenic diet, serum levels of 0.5-3mmol indicate ketosis. This is below the range of starvation, which is 5-10 mmol. In diabetic ketoacidosis, ketone production rises to extreme levels of 15-25 mmol. It is rare for an individual without diabetes to experience ketoacidosis, but it has been reported when a ketogenic diet was used during lactation, after an extended fasting period, or with a diet consisting of less than 20Gm of carbohydrate per day. (1)

Hyperketosis, or high levels of ketones in the blood, may cause adverse symptoms such as nausea, vomiting, constipation, diarrhea, headache, lethargy, irritability, muscle cramps, and dizziness. These symptoms are typically related to fluid loss and electrolyte imbalance and are sometimes referred to as keto flu or carb flu. (3)

Ketosis vs. Ketoacidosis: The Bottom Line

As nurses who work in cardiovascular prevention, we are often involved in counseling patients on lifestyle choices. It is important to be aware of options that exist, including ketogenic diets. The challenges that exist in following a low carbohydrate diet, such as triggering ketosis, must be discussed in detail with our patients. Reducing carbohydrate intake to the level needed to maintain ketosis can result in a lack of nutrients such as fiber, vitamins C and D, folate, and minerals such as selenium, calcium, and magnesium. These are vital dietary components needed to maintain good immune, bone, and gastrointestinal health. We need to monitor parameters for our patients on ketogenic diets, recommend dietary supplementation, and help them with possible side effects. In addition, we need to counsel our patients that the use of a ketogenic diet is not recommended in patients with type II diabetes who are taking sodium-glucose cotransporter-2 inhibitors (4).

  1. Stefanski J. Ketosis and Ketoacidosis:They May Be Sisters, but They’re Certainly Not Twins. AADE In Practice // November 2018
  2. Hallberg SJ, McKenzie AL, Williams PT. Effectiveness and safety of a novel care model for the management of type 2 diabetes at 1 year: an open-label, non-randomized, controlled study. Diabetes Ther. 2018;9(2):583-612.
  3. “The Keto Flu: Symptoms and How to Get Rid of It”
  4. Kalra S, Jain A, Ved J, Unnikrishnan AG. Sodium-glucose cotransporter 2 inhibition and health benefits: the Robin Hood effect. Indian J Endocrinol Metab. 2016;20:725-729.

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