ADHD and Blood Sugar
A Neuroendocrine Perspective on Energy, Stress, and Focus
ADHD is often explained as a dopamine issue.
But attention, mood, and focus are also influenced by physiology. The brain depends on stable energy. Stress hormones influence glucose. Hormones shift metabolism. Medication can change appetite.
When we look at ADHD and blood sugar together, we gain a broader understanding.
This article explores how glucose regulation, stress physiology, hormones, and energy availability interact with attention.
This is not about blaming food.
It is not about replacing medication.
It is about understanding physiology.
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The Brain Runs on Glucose
The brain uses a large amount of the body’s energy. Glucose is its primary fuel source (Ren et al., 2024).
Neurons require energy to:
• Fire electrical signals
• Release neurotransmitters
• Recycle dopamine and norepinephrine
• Maintain ion gradients
When glucose delivery becomes unstable, cognitive function may feel less stable. That does not mean blood sugar causes ADHD. It means energy stability supports executive function. In children, the brain uses even more glucose than in adulthood. Peak metabolic activity occurs during childhood, especially in frontal regions involved in executive function (Cacciatore et al., 2022). These areas are energy intensive. When energy supply fluctuates, behavioral variability may feel amplified.
Stress and Blood Sugar Are Connected
The body has a built-in system to protect the brain when glucose drops.
When blood sugar declines:
• The sympathetic nervous system activates
• Epinephrine rises
• Cortisol increases during sustained dips
This is called the counterregulatory response (Cryer, 2018).
Symptoms of this response can include:
• Anxiety
• Irritability
• Shakiness
• Palpitations
These symptoms are physiologic. They are not personality flaws. Stress and metabolism also influence each other over time. Chronic stress contributes to cumulative physiological burden, known as allostatic load (Ng et al., 2024). Glucose regulation is part of this larger stress system.
The Afternoon “Crash” Pattern
Many adults describe a pattern like this:
• Rapid rise in energy after eating
• Sudden fatigue or irritability
• Temporary alertness from stress hormones
• Followed by exhaustion
When glucose rises quickly and then drops, catecholamines help compensate. That temporary boost can feel like focus. But when the stress response fades, fatigue may follow (Cryer, 2018).
Individuals who are already stress sensitive may experience this pattern more intensely.
Hormones, PMDD, and Glucose Sensitivity
Hormones influence metabolism. Estrogen enhances insulin signaling in multiple tissues, including muscle and liver (De Paoli et al., 2021). As estrogen and progesterone fluctuate across the menstrual cycle, glucose handling can shift. Research shows measurable metabolic changes across cycle phases (Archives of Gynecology and Obstetrics, 2023). During the luteal phase, some individuals notice greater sensitivity to mood and energy changes. Glucose variability may influence perceived mood shifts during this time.
In perimenopause, hormone patterns become less predictable. Fluctuating ovarian hormones influence neurosteroids that modulate GABA, which regulates the HPA axis (Gordon et al., 2015). Some research also shows changes in cortisol awakening response with age (Moon et al., 2023). Hormonal transitions may increase stress sensitivity, which can influence metabolic regulation.
Stimulants, Dopamine, and Appetite
Stimulant medications increase dopamine and norepinephrine. Dopamine influences reward pathways, including appetite regulation. Randomized trials show appetite suppression and modest weight reduction with methylphenidate use (Vedrenne-Gutiérrez et al., 2024). Appetite suppression is especially common early in treatment (Al Eid et al., 2024).
For some individuals, reduced appetite may lead to irregular intake patterns. Irregular fueling can contribute to greater glucose variability later in the day. This is not a criticism of medication. It is an acknowledgment that metabolic context matters.
Energy Restriction and Cortisol
The body responds to energy deficit as a stressor. Short-term caloric restriction has been shown to increase cortisol concentrations (Abedelmalek et al., 2015). When the body senses low energy availability, stress pathways activate. Cortisol influences hepatic glucose production. In individuals sensitive to stress or glucose shifts, restrictive patterns may amplify instability.
The goal is not rigidity. It is metabolic stability.
Blood sugar does not cause ADHD. But the brain is energy dependent. Stress physiology and glucose regulation are interconnected. Hormones influence metabolism. Medications affect appetite. Energy restriction activates stress systems. For some individuals, improving energy stability may reduce afternoon crashes, support mood consistency, and enhance resilience. The goal is a flexible nervous system supported by stable physiology.
Want to Look at Your Patterns More Closely?
If you experience persistent crashes, mood shifts, or fluctuating focus, personalized lab analysis can help clarify what is driving your patterns. In my practice, I use functional testing to assess metabolic markers, stress physiology, and neurotransmitter-related pathways to build individualized strategies. You can learn more about working together at Botanical Health Clinic.
References
Abedelmalek, S., Chtourou, H., Souissi, N., & Tabka, Z. (2015). Caloric restriction effect on proinflammatory cytokines, growth hormone, and steroid hormone concentrations during exercise in judokas. Oxidative Medicine and Cellular Longevity, 2015, 809492. https://doi.org/10.1155/2015/809492
Al Eid, F., Albanna, A., Joseph, J., Talo, S., Jeyaseelan, L., & Sultan, M. A. (2024). Exploring the impact of stimulant medications on weight in children with attention deficit hyperactivity disorder in Dubai, United Arab Emirates. Frontiers in Psychiatry, 15, 1392846. https://doi.org/10.3389/fpsyt.2024.1392846
Cacciatore, M., Grasso, E. A., Tripodi, R., & Chiarelli, F. (2022). Impact of glucose metabolism on the developing brain. Frontiers in Endocrinology, 13, 1047545. https://doi.org/10.3389/fendo.2022.1047545
Cryer, P. E. (2018). Mechanisms of hypoglycemia-associated autonomic failure and its component syndromes in diabetes. Endocrine Reviews, 39(5), 719–738. https://doi.org/10.1210/er.2018-00226
De Paoli, M., Zakharia, A., Werstuck, G. H., & Shaikh, M. (2021). The role of estrogen in insulin resistance: A review of clinical and preclinical data. American Journal of Physiology-Endocrinology and Metabolism, 320(2), E214–E227. https://doi.org/10.1152/ajpendo.00455.2020
Gordon, J. L., Girdler, S. S., Meltzer-Brody, S. E., et al. (2015). Ovarian hormone fluctuation, neurosteroids, and HPA axis dysregulation in perimenopausal depression: A novel heuristic model. American Journal of Psychiatry, 172(3), 227–236. https://doi.org/10.1176/appi.ajp.2014.14070918
Moon, J. H., Kim, H. J., Lee, S. Y., et al. (2023). The cortisol awakening response and sleep efficiency in menopausal women. PLOS ONE, 18(4), e0284627. https://doi.org/10.1371/journal.pone.0284627
Ng, A. E., Gruenewald, T. L., Juster, R.-P., & Trudel-Fitzgerald, C. (2024). Affect regulation and allostatic load over time. Psychoneuroendocrinology, 169, 107163. https://doi.org/10.1016/j.psyneuen.2024.107163
Ren, W., Chen, J., Wang, W., Li, Q., Yin, X., Zhuang, G., Zhou, H., & Zeng, W. (2024). Sympathetic nerve–enteroendocrine L cell communication modulates GLP-1 release, brain glucose utilization, and cognitive function. Neuron, 112(6), 972–990.e8. https://doi.org/10.1016/j.neuron.2023.12.012
Vedrenne-Gutiérrez, F., Yu, S., Olivé-Madrigal, A., & Fuchs-Tarlovsky, V. (2024). Methylphenidate can help reduce weight, appetite, and food intake—A narrative review of adults’ anthropometric changes and feeding behaviors. Frontiers in Nutrition, 11, 1497772. https://doi.org/10.3389/fnut.2024.1497772
