Insulin levels and fasting
Insulin starts falling within 2 to 3 hours of finishing a meal and reaches near-baseline by 8 to 12 hours of fasting. Low insulin during the fasting window allows fat mobilisation and supports the metabolic shift toward fat oxidation. The 2018 Sutton and 2020 Wilkinson trials documented modest insulin sensitivity improvements with intermittent fasting. Insulin is one of the central mechanisms behind fasting metabolic effects. Existing diabetics should never attempt fasting without medical supervision.
What insulin does and how fasting changes it
Insulin is the central hormone of fed-state metabolism. Understanding its role explains much of why fasting produces the effects it does.
1. The insulin response to eating
Eating raises blood glucose which triggers the pancreas to release insulin. Insulin tells cells to take up glucose for use or storage. Insulin also suppresses fat mobilisation from adipose tissue (you store rather than release energy when insulin is high) and suppresses ketone production. The size of the insulin response depends on the meal: refined carbohydrates produce big sharp insulin spikes, mixed meals produce more moderate sustained responses, protein produces a smaller insulin response, fat produces minimal insulin response. After eating insulin returns to baseline over 2 to 4 hours in healthy people.
2. How insulin falls during fasting
From 2 to 3 hours after the last meal as blood glucose normalises, insulin falls toward baseline. By 8 to 12 hours of fasting insulin is at near-baseline levels (typically 5 to 8 mU/L). By 24 hours insulin is at its lowest sustainable level. Insulin does not fall to zero (some baseline secretion continues) but reaches its minimum sustained level. Glucagon, the counter-regulatory hormone, rises in parallel maintaining blood glucose through glycogen breakdown and gluconeogenesis.
3. Why low insulin matters for fasting metabolism
Low insulin allows fat mobilisation from adipose tissue (hormone-sensitive lipase becomes active when insulin is low). The liver shifts from glycogen storage to glycogen breakdown to ketone production. Glucagon-driven gluconeogenesis maintains brain glucose supply. The entire fasting metabolic state depends on low insulin. This is the hormonal switch that enables the metabolic shift described in fasting physiology. Standard 16:8 fasting achieves meaningful insulin reduction during the fasting window.
4. Insulin sensitivity improvements from fasting
Beyond acute insulin reduction repeated fasting practice can improve insulin sensitivity (how effectively cells respond to insulin). The 2018 Sutton Cell Metabolism trial of early time-restricted eating documented improved insulin sensitivity in pre-diabetic men independent of weight loss. The 2020 Wilkinson Cell Metabolism trial found similar effects with 16:8. The improvements are modest at matched weight loss compared to standard calorie restriction but some evidence suggests fasting may have a slight advantage particularly for early time-restricted eating patterns.
What this means for your health and practice
Five practical points about insulin and fasting.
Insulin resistance often precedes type 2 diabetes by years
Most people with elevated fasting insulin do not yet have abnormal fasting glucose. The pancreas compensates for insulin resistance by producing more insulin which keeps blood glucose normal. By the time fasting glucose rises significant beta cell function has been lost. Catching insulin resistance early through fasting insulin testing allows intervention before diabetes develops. Discuss fasting insulin testing with your GP if you have metabolic syndrome features or family history of diabetes.
Insulin sensitivity is highly modifiable through lifestyle
Several lifestyle factors improve insulin sensitivity substantially: weight loss (especially abdominal fat loss), regular physical activity (both aerobic and resistance), adequate sleep, reduced ultra-processed food intake and intermittent fasting. Combining these produces additive effects. Insulin sensitivity is one of the most modifiable cardiovascular risk factors through lifestyle.
Refined carbohydrates produce the biggest insulin spikes
Sugary drinks, white bread, refined cereals, sweets and pastries all produce sharp insulin spikes. Mixed meals with protein, fibre and fat alongside any carbohydrate produce smaller, more controlled insulin responses. Eating refined carbs in the middle of meals rather than starting with them blunts insulin spikes. The 2007 Hlebowicz study and similar work documented these acute effects.
Early time-restricted eating may have specific insulin advantages
Eating in the morning portion of the day (8am to 4pm or similar) appears to produce slightly better insulin sensitivity outcomes than eating later (12pm to 8pm) in some trials. This aligns with circadian biology: insulin sensitivity is naturally higher in the morning. The early pattern is socially difficult for most people so the practical benefit depends on whether you can sustain it. Late time-restricted eating still produces benefits, just possibly slightly less.
Cycle continued practice matters more than initial intensity
The insulin sensitivity gains from fasting persist as long as practice continues. Stopping fasting returns insulin sensitivity toward baseline within weeks to months. Sustainable practice over years beats intense short term protocols followed by abandonment. Match protocol intensity to what you can sustain.
Insulin-related fasting risks
Insulin and glucose-related risks are the biggest acute safety concerns with fasting.
- Type 1 diabetes. Insulin needs change dramatically during fasting. Risk of hypoglycaemia, ketoacidosis or both. Specialist supervision essential. Do not fast without it.
- Type 2 diabetes on insulin or sulfonylureas (gliclazide, glipizide). Risk of hypoglycaemia is significant. Medication doses must be adjusted before any fasting attempt. Specialist supervision required.
- Metformin alone for type 2 diabetes. Lower hypoglycaemia risk but GP discussion still recommended before sustained fasting practice.
- SGLT2 inhibitors (canagliflozin, empagliflozin, dapagliflozin). Risk of euglycaemic ketoacidosis during fasting. Many specialists recommend stopping these medications during extended fasts. Discuss with GP.
- History of severe hypoglycaemic episodes. Fasting increases risk. Discuss with GP before any fasting attempt.
Standard contraindications also apply: eating disorder history, pregnancy or breastfeeding, BMI under 18.5, children, adolescents and adults under 18. Any blood glucose monitoring you do during fasting should follow the protocol set by your diabetes team.
For the wider picture on fasting from the gentlest protocols to extended fasts plus the science behind hunger, metabolism and refeeding, our Understanding Fasting hub brings every guide together in one place.
Back to the Fasting Hub
This article sits inside our complete knowledge base on fasting covering protocols, physiology, safety and practical guidance. Head back to the hub for the full index.
More on fasting metabolism
Several related pages cover the rest of the picture. Our piece on what happens to blood sugar during fasting covers the glucose side. Fat burning and ketone production during fasting covers what low insulin enables. And how the body responds to fasting covers the integrated physiology.


Share:
What Happens to Blood Sugar During Fasting
Fat Burning and Ketone Production During Fasting