What happens to blood sugar during fasting

How blood glucose is maintained during fasting

The body maintains blood glucose through fasting using a coordinated sequence of mechanisms. Four points explain the system.

1. Glycogenolysis (hours 0 to 24): glycogen breakdown

The liver stores around 100 to 120 g of glycogen which can be released as glucose to maintain blood levels between meals. Muscle stores additional glycogen but cannot release glucose into the blood (muscle glycogen serves muscle directly). As blood glucose falls and insulin drops, glucagon rises driving liver glycogen breakdown. This supplies glucose for the first 12 to 24 hours of fasting. By 16 to 24 hours liver glycogen is substantially depleted. Active people or those with prior high carbohydrate intake have more glycogen and last slightly longer at this stage.

2. Gluconeogenesis (hours 16+ onward): making new glucose

After glycogen depletes the liver synthesises new glucose from non-carbohydrate substrates: amino acids (alanine, glutamine) from limited muscle breakdown, glycerol from fat breakdown, lactate from anaerobic metabolism, pyruvate from various sources. This is gluconeogenesis. The liver can produce 7 to 10 g of glucose per hour through gluconeogenesis. This maintains blood glucose during sustained fasting indefinitely. Gluconeogenesis works alongside ketogenesis (ketone production) to supply fuel for the brain and other tissues.

3. Ketogenesis (hours 16+ onward): brain fuel from fat

The brain normally requires about 120 g of glucose per day. During sustained fasting ketone bodies (beta-hydroxybutyrate, acetoacetate) produced from fatty acid breakdown in the liver can supply much of the brain energy. By 48 hours ketones supply about 20 to 30 percent of brain energy. By 5 to 7 days ketones supply 60 to 70 percent of brain energy. This shift dramatically reduces the brain glucose requirement and protects lean mass from being broken down for gluconeogenesis. The shift is one of the key adaptations enabling extended human fasting.

4. Tight glucose regulation throughout

Blood glucose typically stays in the 3.5 to 5.5 mmol/L range through fasts of any duration in healthy people without diabetes or hypoglycaemic medications. The coordinated mechanisms maintain this tight range. Compare to post-prandial swings of 7 to 9 mmol/L after refined carbohydrate meals: fasting actually stabilises glucose. This stability is one of the reasons many people report stable energy during fasting compared to the highs and lows of frequent carbohydrate-heavy meals.

When the typical pattern does not apply

Five situations where blood glucose during fasting behaves differently from typical healthy adults.

Diabetes (especially type 1 and insulin-dependent type 2)

The picture is fundamentally different. Insulin therapy must be adjusted before any fasting attempt. Hypoglycaemia risk is significant. In type 1 diabetes fasting can also trigger ketoacidosis which is a medical emergency different from nutritional ketosis. Specialist diabetes team supervision is essential. Self-directed fasting is contraindicated in insulin-dependent diabetes.

Sulfonylurea medications

Drugs like gliclazide stimulate insulin secretion. During fasting they can cause significant hypoglycaemia. Doses typically need reduction or temporary cessation during fasting protocols. GP or diabetes specialist input essential.

SGLT2 inhibitor medications

Drugs like empagliflozin, dapagliflozin used for type 2 diabetes increase urinary glucose loss. Combined with fasting these drugs raise risk of euglycaemic diabetic ketoacidosis (DKA at normal glucose levels). This is a specific dangerous interaction. Anyone on SGLT2 inhibitors needs specialist input before fasting.

Insulin resistance and prediabetes

Fasting glucose may be slightly elevated. Dawn phenomenon may be more pronounced. Fasting can improve insulin sensitivity over weeks to months but acute fasting glucose readings may not look great. The improvement is in the trend over time not the immediate fasting glucose number.

Reactive hypoglycaemia post-fast

The first meal after a fast can trigger strong insulin response leading to low blood glucose 2 to 4 hours later. Breaking fasts with protein and fat dominant meals rather than carbohydrate dominant reduces this risk. People with tendency to reactive hypoglycaemia should pay particular attention to refeeding composition.

Blood glucose safety during fasting

Several specific glucose-related risks warrant attention.

• Severe hypoglycaemia in those on insulin or sulfonylureas. Medical emergency. Specialist supervision required for any fasting.
• Diabetic ketoacidosis in type 1 diabetes. Different from nutritional ketosis. Medical emergency. Type 1 diabetes contraindicates fasting outside specialist settings.
• Euglycaemic ketoacidosis with SGLT2 inhibitors. Specific dangerous interaction.
• Symptoms of severe hypoglycaemia (sweating, shaking, confusion, weakness, fainting): break the fast immediately with carbohydrate and seek medical attention if symptoms persist.
• Persistent fasting glucose above 7 mmol/L. Investigate for diabetes with GP.

Standard contraindications apply: eating disorder history, pregnancy or breastfeeding, type 1 diabetes or insulin dependent type 2 diabetes, BMI under 18.5, children, adolescents and adults under 18. Anyone on glucose-lowering medications absolutely needs medical input before fasting.

More on metabolic effects

Several pages cover related topics. Our piece on insulin levels and fasting covers the hormonal driver. Fat burning and ketone production during fasting covers the alternative fuel system. And fasting and weight loss explained covers the bigger metabolic picture.