Ketosis and Ketones: the Keto Diet, Exogenous Ketones and How to Measure Them

The body has two main fuels: sugar and fat. When sugar is scarce – during fasting, prolonged exercise or on a very low-carbohydrate diet – the liver starts turning fat into ketones. This state is called ketosis. Biohackers like it for steady energy, and medicine has used it for decades in epilepsy. Do not confuse it, however, with ketoacidosis, a life-threatening condition.

What ketosis and metabolic flexibility are

After a longer period without food, or with a long-term low carbohydrate intake, the liver's glycogen stores run down. Insulin falls, fatty acids are released from fat tissue and the liver turns them into three ketone bodies: beta-hydroxybutyrate (BHB), acetoacetate and acetone. Muscles, the heart and the brain all use them.

I consider metabolic flexibility more important than ketosis itself – the body's ability to switch smoothly between fuels. A healthy body burns sugar after a meal, more fat between meals and ketones at night or during a fast. Constant hunger, sugar cravings and energy crashes after meals often mean that metabolism is stuck in a single mode. Occasional ketosis teaches it to use fat again.

The ketogenic diet and measuring ketones

A classic ketogenic diet provides about 5–10% of energy from carbohydrates, roughly 20–50 grams a day, adequate protein (about 1–1.5 g per kilogram of body weight), and the rest from fat. The first days often bring fatigue and headaches, the so-called "keto flu", linked mainly to the loss of water and salts. Fluids and enough sodium, potassium and magnesium help.

You do not have to guess whether you are in ketosis; it can be measured. Each method, however, measures something different:

• Blood – a meter with ketone strips measures BHB from a drop of blood from the fingertip. It is the most accurate home method.
• Breath – devices measure acetone, which rises with fat burning but is also affected by diet, exercise and breathing. Useful for tracking trends.
• Urine – strips react to acetoacetate. They are cheap and helpful at the start, but after keto adaptation they show less even though ketosis continues. Ketones in urine during fasting or on a keto diet are no reason to panic.

Exogenous ketones: esters, salts and MCT oil

There is also a shortcut into ketosis – drinking ketones directly, so that you have glucose and ketones in your blood at the same time. There are two main forms:

• Ketone salts – BHB bound to sodium, potassium or magnesium. They raise ketones only modestly and often contain half of the less active L-BHB form. At higher doses they deliver a lot of minerals, especially sodium.
• Ketone esters – bitter and expensive, but much stronger. In an Oxford study the ester raised blood BHB to an average of 2.8 mM, the salts to 1.0 mM; levels returned to baseline within three to four hours.

Eating before the drink lowered peak ketones by a third. A cheaper route is MCT oil, especially its C8 fraction (caprylic acid), from which the liver makes ketones itself. Start with a teaspoon – a larger dose sends most people on a quick trip to the bathroom.

Keto for epilepsy: the strongest evidence

The ketogenic diet is an established treatment for drug-resistant epilepsy in children. A 2020 Cochrane review pooled 13 studies with 932 participants. In children, the keto diet compared with usual care was associated with a higher chance of becoming seizure-free and of halving seizures. In some studies up to 55% of children were seizure-free after three months on the classic 4:1 diet. The authors, however, rate the certainty of the evidence as low to very low, because the studies were small and unblinded. In adults the benefit is uncertain.

For some diagnoses, such as glucose transporter GLUT1 deficiency, experts recommend it right at the start of treatment. A therapeutic diet always runs under the supervision of a neurologist and a dietitian, not as a home experiment.

Ketosis is not ketoacidosis

In nutritional ketosis, ketones stay roughly between 0.5 and 3 mmol/l and the body easily maintains blood pH. Diabetic ketoacidosis is a different state: insulin is missing, ketones rise uncontrollably and the blood becomes acidic. According to an international consensus from 2024, it is defined by blood ketones of at least 3.0 mmol/l, a pH below 7.3 or bicarbonate below 18 mmol/l, and raised glucose or known diabetes. Those mainly at risk are people with type 1 diabetes and people taking diabetes drugs of the SGLT2 inhibitor class, with which ketoacidosis can occur even at near-normal glucose. These are prescription drugs – do not change how you take them, or combine them with a keto diet, without agreeing it with your doctor.

The keto diet is also unsuitable for the following groups, or only under medical supervision:

• People with disorders of fat metabolism – inherited fatty acid oxidation disorders, carnitine or pyruvate carboxylase deficiency and porphyria are outright dangerous on a keto diet.
• People on insulin or glucose-lowering drugs – there is a risk of hypoglycaemia and ketoacidosis; the doses must be adjusted by a doctor.
• Pregnant and breastfeeding women – safety data are lacking.
• Children – outside epilepsy treatment, a varied diet with a sensible share of complex carbohydrates serves them better.
• People with kidney stones, kidney, liver or pancreatic disease, as well as after an eating disorder.
• People with familial hypercholesterolaemia – their already high LDL should not rise further.

When LDL cholesterol shoots up

The cholesterol response to a keto diet is highly individual. In some people LDL falls, in others it rises sharply. An analysis of data from 548 people on a low-carbohydrate diet showed that the largest LDL increases paradoxically occur in lean, metabolically healthy people with low triglycerides and high HDL. The authors coined the term "lean mass hyper-responder" for them: LDL above 200 mg/dl (about 5.2 mmol/l), HDL above 80 mg/dl and triglycerides below 70 mg/dl. Reintroducing a moderate amount of carbohydrate markedly lowered their LDL.

The cross-sectional KETO-CTA study from 2024 compared 80 such people, who after an average of 4.7 years on keto had LDL of about 272 mg/dl (about 7 mmol/l), with similar people with lower LDL. The amount of plaque in the coronary arteries did not differ between the groups. This is, however, an observation in a small, selected group, and the follow-up analysis from 2025 was retracted in 2026. Expert guidelines continue to regard long-term high LDL and apolipoprotein B as a cause of atherosclerosis.

In practice: if you switch to keto, have your lipids measured before you start and after two to three months, ideally including apolipoprotein B. If LDL rises markedly, discuss it with your doctor and consider less saturated fat or a milder carbohydrate restriction.

Ketosis is a useful tool, not a philosophy of life. For a healthy person it is enough if the body enters it now and then and otherwise uses both fuels flexibly.