Insulin is one of the hormones most discussed in the fitness world (just ahead of cortisol). Its critical importance in carbohydrate management is often emphasized, and it is rare to see it mentioned without an association with weight management. At regular intervals, the idea that insulin “spikes” lead to weight gain resurfaces—more specifically, the idea of blood sugar “crashes” following a high-carbohydrate meal (“eating refined carbohydrates will trigger a phase of hypoglycemia with consequences X or Y”). Despite the abundance of discussion on the topic, the arguments are rarely backed by actual glucose measurements (“I feel hypoglycemic, therefore I am hypoglycemic”).
But what do the numbers and measurements actually show?
Let’s start with some context and lay down a few important foundations…
Why does the body monitor glucose so closely?
Glucose is an essential energy substrate with many functions, mainly related to energy metabolism. It fuels energy (ATP) production in many tissues and plays a critical role for the brain, which depends heavily on it under normal conditions and can neither store it nor produce it locally. This is why blood glucose must remain above a certain threshold: when it drops too low, cognitive function deteriorates (up to confusion or even coma if severe), which explains the physiological importance of defense mechanisms against hypoglycemia1.
At the same time, glucose is a metabolic “currency” and a signal. It can be stored as glycogen (liver and muscle) and also serves as a raw material for various syntheses (conversion into lipids in situations of energy excess, biosynthetic pathways). Finally, fluctuations in glucose trigger hormonal responses (insulin when it rises; glucagon/adrenaline and other counter-regulatory hormones when it falls) that maintain homeostasis and also influence sensations such as hunger.
What is blood glucose?
Blood glucose refers to the concentration of glucose in the blood. It varies throughout the day (meals, physical activity, stress, sleep), but in a healthy person it is maintained within a relatively narrow range. Blood glucose is measured in milligrams per deciliter or in millimoles per liter (1 mmol/L corresponds to about 18 mg/dL). In a healthy adult, blood glucose varies relatively little over 24 hours. Continuous measurements in non-diabetic individuals show an average glucose of ~98–99 mg/dL (~5.4–5.5 mmol/L) with low variability (SD ~17 mg/dL, coefficient of variation ~17%)2.
What is insulin really for?
Insulin is a hormone produced by the beta cells of the pancreas. Its role is not only to lower sugar: it organizes how the body uses and stores energy. When blood glucose rises, as after a meal:
- the pancreas secretes insulin;
- insulin facilitates glucose entry into certain tissues, notably muscle and adipose tissue;
- it also limits glucose production by the liver;
- blood glucose falls back toward a baseline level.
Insulin also acts on pathways involved in appetite. Experimental work (under controlled conditions) has suggested that insulin peaks could influence hunger and food preferences, but the net effect depends strongly on context (blood glucose, digestive hormones, meal composition, metabolic state)3,4. These effects on fat storage and appetite regulation make this hormone a potential candidate in the regulation of body composition, especially fat mass.
Hyperglycemia, hypoglycemia, and reactive hypoglycemia: what are they?
Hyperglycemia
Hyperglycemia refers to abnormally high blood glucose. A threshold of >140 mg/dL (7.8 mmol/L) is used when glucose is measured continuously in real-world (“free-living”) conditions2.
Hypoglycemia
Hypoglycemia is blood glucose that is too low, likely to induce symptoms related to activation of the body’s alert system (palpitations, sweating, tremor, urgent hunger) and, if deeper, neurocognitive signs (confusion, difficulty concentrating). Clinically, the classic approach relies on Whipple’s triad (compatible symptoms, low measured glucose, and improvement after correction)5.
Reactive hypoglycemia
Reactive (or postprandial) hypoglycemia refers to a drop in blood glucose occurring after a meal, classically 2 to 5 hours after a carbohydrate-rich meal in people without diabetes6.
Several subtypes are typically distinguished based on timing of onset and metabolic context: (1) an early (alimentary) form, appearing within 1–2 hours, linked to accelerated gastric emptying and/or an exaggerated insulin/incretin response (often after gastric surgery or functional digestive disorders); (2) an idiopathic form, occurring around 3–4 hours in otherwise healthy individuals, with a benign dysregulation of the insulin response (a slight shift in feedback control and insulin handling); (3) a late (pre-diabetic) form, typically 4–5 hours after the meal, associated with insulin resistance and a delayed, excessive insulin secretion after a glycemic peak; and (4) secondary/symptomatic forms, where an identifiable cause (digestive surgery, metabolic disorders, digestive inflammation) contributes to glucose–insulin imbalance.
Early reactive hypoglycemia, also called “alimentary” hypoglycemia, typically occurs 1 to 2 hours after a meal or an oral glucose load (oGTT). This phenomenon can be exacerbated by accelerated gastric emptying or an excessive incretin effect. It is plausible that rapid gastric emptying leads to an exaggerated incretin response. Following oral glucose intake, increased secretion of GLP-1 and GIP triggers excessive insulin exocytosis, with early upregulation of GLUT4 transporter regulation. GLP-1, by subsequently inhibiting glucagon secretion, leads to an inadequate counter-regulatory response in the face of potential hypoglycemia, thereby promoting the occurrence of early hypoglycemia7.
This dysregulation can also occur in individuals who fast or follow restrictive diets (often for self-prescribed weight-loss reasons). If these people periodically interrupt their diet by consuming refined sugars—such as sugary drinks, candies, or desserts8—episodes of reactive hypoglycemia may be observed. Reactive hypoglycemia can also be observed when alcohol and sugary beverages are consumed together (e.g., gin and tonic), because this combination disrupts the adrenergic response and significantly suppresses growth hormone secretion in response to induced hypoglycemia9.
Helicobacter pylori (HP)-induced gastritis can also contribute to reactive hypoglycemia; excessive colonization by this bacterium promotes glucose- and mixed-meal–stimulated insulin secretion, probably via increased gastrin secretion. After eradication of the bacterium, a reduction in the insulin response at 30 and 60 minutes after oral glucose administration has been observed, accompanied by an increase in blood glucose at 180 minutes after a mixed meal, correlated with reduced gastrin levels10,11.
Characterizing normal glycemia and hypoglycemic episodes in healthy adults
Data from recent studies using continuous glucose monitoring technology, such as Shah et al. (2019)2, provide valuable insight into glycemia in healthy adults. These studies, conducted in non-diabetic, non-obese, non-pregnant individuals, show that the median time spent with glucose below 70 mg/dL is relatively low—around 1.1% of the day (about 15 minutes). Glycemic excursions above 140 mg/dL are brief (median 2.1% of the day), and time below 70 mg/dL is even less frequent. The observed coefficient of variation (about 17%) indicates low glycemic variability, consistent with robust homeostatic mechanisms in healthy individuals.
What does 24-hour glycemia look like in a healthy adult with BMI < 27 kg/m²?
Continuous glucose sensors make it possible to quantify how much time a person spends in different zones over the course of a day.
In a landmark multicenter study in non-diabetic individuals (n = 153), the authors report2:
- Mean glucose (24 h): ~98–99 mg/dL
- Variability (SD): 16.7 mg/dL
- Time between 70 and 140 mg/dL: median 96% (IQR 93–98)
- Time > 140 mg/dL: median 2.1%, i.e., ~30 minutes/day
- Time < 70 mg/dL: median 1.1%, i.e., ~15 minutes/day
- Values > 180 mg/dL and < 54 mg/dL are uncommon
In a healthy adult, normoglycemia predominates, and “hyper” or “hypo” excursions exist but remain, on average, very brief and sporadic.
And what about the prevalence of reactive hypoglycemia?
Large CGM studies in healthy subjects quantify time <70 mg/dL well, but they do not systematically classify each episode by proximity to a meal (which would require precise meal annotation). In other words: we know that “minutes under 70 exist,” but we cannot directly infer a robust prevalence of reactive hypoglycemia in the strict sense in these cohorts2,6.
What does 24-hour glycemia look like in a non-diabetic person with obesity?
In a free-living study in adults with obesity without diabetes, the authors report12:
- Mean glucose: 99.9 ± 8.3 mg/dL
- Variability (SD): 17.5 ± 4.8 mg/dL
- Meal-related excursions (peak–nadir analysis between two meals):
- Peak: 121.5 mg/dL (95% CI 113.1–130.0)
- Nadir: 87.1 mg/dL (95% CI 81.4–92.7)
- Peak–nadir amplitude: 33.9 mg/dL (95% CI 29.0–38.7)
Overall, in a non-diabetic person with obesity, glucose remains centered around ~100 mg/dL, with moderate postprandial rises and a return toward inter-prandial values close to normoglycemia.
What does 24-hour glycemia look like in someone with type 2 diabetes?
Continuous measurement highlights a higher mean 24-hour glucose level, higher postprandial peaks, and greater variability.
In a study of hospitalized Japanese patients with type 2 diabetes (n = 294), where 24-hour CGM data are analyzed by HbA1c class13, the authors report:
HbA1c 6.0–6.9% (controlled diabetes)
- Mean glucose (24 h): 144.2 ± 31.9 mg/dL
- Variability (SD): 31.4 ± 13.8 mg/dL
- Maximum (24 h): 222.5 ± 54.8 mg/dL
- Minimum (24 h): 95.8 ± 23.1 mg/dL
- Postprandial peaks: breakfast 202.9 ± 44.5, lunch 188.5 ± 58.9, dinner 202.9 ± 48.6 mg/dL
HbA1c ≥10% (very poorly controlled diabetes)
- Mean glucose (24 h): 210.0 ± 59.6 mg/dL
- Variability (SD): 39.7 ± 11.9 mg/dL
- Maximum (24 h): 298.1 ± 66.8 mg/dL
- Minimum (24 h): 142.5 ± 47.4 mg/dL
- Postprandial peaks: breakfast 275.6 ± 70.7, lunch 263.1 ± 75.2, dinner 262.0 ± 65.7 mg/dL
Thus, in people with type 2 diabetes, the “typical” day is marked by a mean glucose level clearly higher than in non-diabetics, with prolonged periods above hyperglycemia thresholds (reflected here by high maxima and postprandial peaks frequently >200 mg/dL) and higher variability.
And how large are postprandial excursions in untreated type 2 diabetes?
In a CGM study over 24 hours in 30 hospitalized patients with type 2 diabetes who were drug-naïve (no antidiabetic treatment)14, the authors mainly describe postprandial kinetics:
- Time to postprandial peak: typically ~70–85 minutes depending on the meal
- Postprandial increase: typically ~83–109 mg/dL depending on the meal
This illustrates that, even without treatment, post-meal excursions can be large (on the order of ~+80 to +110 mg/dL), contributing to the higher and more variable 24-hour profile observed overall in people with type 2 diabetes.
Effects of hyperglycemia, hypoglycemia, and reactive hypoglycemia
Hyperglycemia
Appetite and energy intake
Under usual conditions in a healthy person, a transient postprandial rise is not harmful in itself: it is a normal signal that triggers insulin and is often accompanied by satiety signals.
Where it gets more complicated is when the peak-then-drop dynamics become pronounced (a “roller coaster”). In those contexts, it is less the peak itself than the subsequent descent (down to a lower nadir) that can promote hunger12.
Physical activity and activity-related energy expenditure
Physical activity and activity-related energy expenditure are central levers against hyperglycemia: muscle contraction increases glucose uptake by muscle (including via pathways partly independent of insulin) and, after exercise, improves insulin sensitivity for several hours. This typically reduces postprandial excursions and overall glucose exposure, which can be observed on CGM through reduced time above target. From a lifestyle perspective, increasing activity-related energy expenditure (walking more, breaking up sitting time, moderate activity, etc.) helps limit day-to-day hyperglycemia, alongside dietary and therapeutic adjustments15,16.
The other side is that the relationship is bidirectional: hyperglycemia does not spontaneously activate movement (contrary to the idea that excess glucose would push someone to move). Rather, it is associated with reduced activity and increased sedentary behavior. It has been reported17 that, in a hyperglycemic state, activity behaviors tend to decrease and activity-related energy expenditure may also drop, with increased sedentary time. Physiological and behavioral mediators are suspected (fatigue, discomfort, reduced motivation, emotional factors). This can sustain a vicious circle: hyperglycemia leading to less activity, which in turn leads to lower glucose utilization and insulin sensitivity, resulting in persistent hyperglycemia.
Body composition
In the presence of hyperglycemia, insulin promotes carbohydrate storage and limits the release of fatty acids, creating a profile favorable to energy storage. However, to actually store reserves, the organism must be exposed to a sustained energy surplus. Hyperglycemia in the presence of an energy deficit will not allow meaningful energy storage, whether as carbohydrate (glycogen) or fat. Over the long term, chronic hyperglycemia is primarily a marker of impaired glucose metabolism regulation. The link with body composition operates mainly through energy balance (total energy intake vs total energy expenditure), more than through a direct, easily quantifiable day-to-day effect.
Hypoglycemia and reactive hypoglycemia
Hypoglycemia corresponds to reduced glucose availability, which triggers counter-regulation (hormonal responses and symptoms) aimed at quickly restoring glucose levels compatible with proper brain function. Behaviorally, this response often translates into increased hunger and a tendency to ingest carbohydrates to correct the episode.
Appetite and energy intake
In many contexts, a simple correction is about 15 g of carbohydrates (≈60 kcal), which is often sufficient to bring glucose back into a normal range. However, it is common to over-correct (eat more than necessary), notably because the glucose drop can overstimulate appetite, and because non-physiological factors (stress, availability of highly palatable foods, social context) facilitate excess intake.
When glucose drops occur before a meal (which typically includes postprandial reactive hypoglycemia leading to a low nadir before the next meal), there are solid free-living data. In Kim et al. (2019)12, a lower pre-meal nadir is associated with:
- higher hunger at the next meal;
- increased caloric intake per meal.
The authors report mean nadirs of about 85.1 mg/dL (normal weight) and 87.1 mg/dL (obesity), and an estimated relationship between nadir and calories at the next meal of about:
- +20.4 kcal per mg/dL lower nadir in normal-weight individuals
- +43.6 kcal per mg/dL lower nadir in individuals with obesity
This suggests that, for a comparable glycemic signal, the increase in intake may be more pronounced in people with obesity. Extrapolating to a nadir of 70 mg/dL yields very large surpluses (≈ +308 kcal normal weight; ≈ +746 kcal obesity), but it must be interpreted cautiously: that level is lower than the observed mean nadirs, potentially rarer, and the relationship may not remain linear at those values12.
24-hour physical activity and energy expenditure
Hypoglycemia can cause symptoms (fatigue, weakness, confusion, lethargy) that reduce the ability to sustain effort and may lead to reducing or stopping activity in the short term. Over a 24-hour window, the impact mainly depends on the frequency and severity of episodes: when they are rare and quickly corrected (a common case in people without major carbohydrate metabolism disturbances), it is unlikely they will produce a measurable reduction in daily activity.
Body composition: why reactive hypoglycemia could matter
If repeated drops promote increased intake (e.g., +300 kcal on certain meals in a plausible extrapolation), then in the long term it is primarily the energy balance that becomes the driver of body composition change (more fat mass if chronic surplus), rather than a direct effect of hypoglycemia or reactive hypoglycemia on adipose tissue.
Conclusion
Ultimately, the idea that “insulin spikes” would systematically turn the day into a glycemic roller coaster (with uncontrollable hunger and fatigue) does not match what measurements show in most people. In healthy adults, blood glucose remains overwhelmingly within a narrow range over 24 hours (e.g., ~96% of the time between 70 and 140 mg/dL), and clear episodes of hypoglycemia or hyperglycemia are brief and relatively rare. In this context, it is therefore unlikely that these excursions alone are sufficient to explain persistently dysregulated appetite or a marked decline in day-to-day physical activity.
That said, exceptions exist. In some situations, a drop in blood glucose can promote dietary overcompensation (overcorrection, “safety” snacking, highly calorie-dense foods) or a temporary reduction in activity via symptoms (fatigue, weakness, malaise), and sometimes the anticipation of experiencing the episode again. These effects are real, but they most often remain intermittent and strongly shaped by context (meal composition, habits, stress, sleep, training level, food availability, etc.).
An important practical point is to avoid relying only on subjective feelings: hunger is not necessarily synonymous with hypoglycemia, and fatigue does not necessarily mean hypoglycemia. When the issue is real (recurrent symptoms, feeling unwell during training, postprandial episodes), it may be useful to confirm objectively with a glucose measurement (fingerstick meter or sensor), rather than systematically interpreting these signals as a “carb” or “insulin” problem.
Finally, in people with a disorder of glucose metabolism (prediabetes, diabetes, post-bariatric surgery, etc.), fluctuations and their consequences can be more pronounced. But even then, they generally cannot, on their own, justify chronic overeating or a very high level of sedentary behavior. Reducing weight gain or fatigue to a simple carbohydrates/insulin story is often too simplistic and downplays other determinants that can be more important: overall energy balance, fitness level, eating behaviors, environment, recovery, stress, and sleep.
References
1. Amiel, S.A. & Gale, E. Physiological Responses to Hypoglycemia: Counterregulation and cognitive function. Diabetes Care 16, 48–55 (1993).
2. Shah, V.N., et al. Continuous glucose monitoring profiles in healthy nondiabetic participants: a multicenter prospective study. The Journal of Clinical Endocrinology & Metabolism 104, 4356–4364 (2019).
3. Saad, M.F., et al. Insulin regulates plasma ghrelin concentration. The Journal of Clinical Endocrinology & Metabolism 87, 3997–4000 (2002).
4. Rodin, J. Insulin levels, hunger, and food intake: an example of feedback loops in body weight regulation. Health Psychology 4, 1 (1985).
5. Cryer, P.E., et al. Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology & Metabolism 94, 709–728 (2009).
6. Dravecká, I., Galajda, P. & Mokáň, M. Reactive Hypoglycemia. (IntechOpen, 2025).
7. Lupoli, R., et al. Role of the Entero-Insular Axis in the Pathogenesis of Idiopathic Reactive Hypoglycemia: A Pilot Study. J Clin Endocrinol Metab 100, 4441–4446 (2015).
8. Permutt, M.A., et al. Alimentary hypoglycemia in the absence of gastrointestinal surgery. N Engl J Med 288, 1206–1210 (1973).
9. Flanagan, D., Wood, P., Sherwin, R., Debrah, K. & Kerr, D. Gin and tonic and reactive hypoglycemia: what is important-the gin, the tonic, or both? J Clin Endocrinol Metab 83, 796–800 (1998).
10. Acbay, O., Celik, A.F., Kadioglu, P., Goksel, S. & Gundogdu, S. Helicobacter pylori-induced gastritis may contribute to occurrence of postprandial symptomatic hypoglycemia. Digestive diseases and sciences 44, 1837–1842 (1999).
11. Açbay, Ö., Çelik, A.F. & Gündoğdu, S. Does Helicobacter pylori-induced gastritis enhance food-stimulated insulin release? Digestive diseases and sciences 41, 1327–1331 (1996).
12. Kim, J., et al. In a Free-Living Setting, Obesity Is Associated With Greater Food Intake in Response to a Similar Premeal Glucose Nadir. The Journal of Clinical Endocrinology & Metabolism 104, 3911–3919 (2019).
13. Hajime, M., et al. Twenty‐four‐hour variations in blood glucose level in Japanese type 2 diabetes patients based on continuous glucose monitoring. Journal of diabetes investigation 9, 75–82 (2018).
14. Ando, K., Nishimura, R., Tsujino, D., Seo, C. & Utsunomiya, K. 24-hour glycemic variations in drug-naive patients with type 2 diabetes: a continuous glucose monitoring (CGM)-based study. PloS one 8, e71102 (2013).
15. Hermans, M. La prise en charge du diabète de type 2 à l’ère des capteurs glycémiques. Louvain médical 144, 21 (2025).
16. Battelino, T., et al. Clinical targets for continuous glucose monitoring data interpretation: recommendations from the international consensus on time in range. Diabetes care 42, 1593–1603 (2019).
17. Cheval, B., et al. Why Are Individuals With Diabetes Less Active? The Mediating Role of Physical, Emotional, and Cognitive Factors. Annals of Behavioral Medicine 55, 904–917 (2021).