Longevity 8 MIN READ

How does dopamine impact blood glucose?

When you run a marathon, complete a task or eat a slice of chocolate cake, your brain produces a chemical called dopamine in response, giving you feelings of satisfaction.

Written by Krish Arora

Mar 22, 2022
How Dopamine Impacts

When you run a marathon, complete a task or eat a slice of chocolate cake, your brain produces a chemical called dopamine in response, giving you feelings of satisfaction. It is human nature to want to replicate this feeling, so you seek out more of the behaviour that led to the dopamine production. But an excess of any of these things will eventually catch up to us. For instance, overdoing slices of cake elevates the risk of diabetes in the long run, which affects over 500 million adults globally. Integral to preventing or managing diabetes is maintaining healthy blood sugar levels.

Read our recommendations for reducing blood sugar levels here.

Dopamine Impacts BloodGlucose


  • Dopamine is a chemical messenger that forms an integral part of the central nervous system. Dopamine pathways control vital functions such as cognition, memory, locomotion and sleep, 
  • New studies are emerging linking dopamine activity to blood glucose levels. A key element in this relationship is insulin,
  • Foods rich in fat and sugar can override the brain’s reward system and inhibit appetite-suppressing hormones. This causes individuals to eat more and can lead to obesity, metabolic syndrome and, eventually, diabetes. 

Recent studies have shown a promising link between nervous system functioning and blood sugar. We present the latest findings to you here; first, the basics of dopamine, followed by its interaction with serum glucose. 

What is dopamine?

Dopamine is a neurotransmitter, or chemical messenger, responsible for several key functions in the central nervous system. Conventionally, it is known as the ‘feel-good’ or ‘pleasure’ chemical even though it does not produce pleasure. Instead, dopamine connects feelings of pleasure, gratification and reward with certain behaviours by controlling the brain’s reward centres and pathways.

Dopamine is produced in various parts of the brain: the striatum, substantia nigra, ventral tegmental area, pituitary gland and pathways of the hypothalamus. Dopamine receptors are located primarily in the central nervous system and less prominently in the kidney and vascular system. The type of dopamine receptor determines its function, but overall these receptors are responsible for:

  1. Cognition—learning, decision-making and attention
  2. Memory
  3. Impulse control
  4. Locomotion
  5. Sleep
  6. Renal function via renin secretion

Maintaining a balanced dopamine level contributes to our overall health and well-being. Dopamine-deficient or oversupplied individuals may experience any of the following symptoms:


  1. Anxiety and mood swings
  2. Constipation
  3. Hallucinations
  4. Loss of balance
  5. Low energy
  6. Low sex drive
  7. Muscle cramps
  8. Sleep difficulty
  9. Tremors
  10. Weight change


  1. Aggressive Behaviour
  2. Anxiety
  3. Stress
What is dopamine

Dopamine deficiency can also lead to Parkinson’s disease and major depressive disorder. A dopamine surplus can cause ADHD, schizophrenia and substance abuse.

Dopamine controls feelings of reinforcement and reward, thoughts and emotions, arousal and regulation of hormones and glands. The function of brain dopamine is “to coordinate cognitive and motor resources for successful exploitation of environmental energy sources.” This goal-directed behaviour supports fundamental body functions and is of crucial importance to our physical and physiological health.

Dopamine and blood glucose

Although studies have not proved a definitive correlation between dopamine and blood glucose levels, the answer lies with insulin. Insulin, a hormone produced by the pancreas and present in all mammals, controls glucose delivery to cells and regulates metabolism in the human body. Insulin controls carbohydrate, lipid and protein metabolism, providing glucose access to our cells. Together with glucagon, insulin helps maintain a state called homeostasis, an internal equilibrium. Insulin resistance is high in individuals whose cells respond poorly to insulin and have difficulty taking glucose from the bloodstream. The pancreas, therefore, ramps up insulin production to aid in glucose delivery. Over time, people with high insulin resistance develop high blood sugar levels. If you have low insulin resistance, that indicates high insulin sensitivity (beneficial for your health). People who have type 1 diabetes have inadequate insulin production. Chronically elevated insulin levels and decreased brain insulin sensitivity is linked to type 2 diabetes. The interaction between the reward system and the homeostatic system governs our eating patterns and behaviour and can determine our predisposition for conditions such as diabetes. 

The relationship between insulin and dopamine is fraught with contradictory findings. Recently, however, promising developments have been made. 

Researchers at the Institute of Diabetes Research and Metabolic Diseases in Munich examined the interaction of the homeostatic and reward systems in the striatum. They administered insulin via the nose to 10 healthy male participants to discover lower dopamine levels and a change in the brain’s network structure. Participants demonstrated a stronger increase in functional connectivity in the brain for 45 minutes after insulin was administered. The results indicated that insulin modulates dopamine release in the striatum, which affects brain activity and connectivity. The team believes that changes in this network can be a driver of obesity and related diseases.

In 2018, Dutch doctors chanced upon a potential link between the homeostatic and reward systems while treating a patient with obsessive-compulsive disorder (OCD). By placing electrodes in his brain, they could stimulate brain tissue involved in decision making, motivation and reward-seeking. Deep brain stimulation (DBS) caused him to get rid of one of his prescription medications. It also improved his type 2 diabetes—his insulin sensitivity improved as he reduced his dosage from 226 to 180 units of insulin per day. Researchers believe that DBS increased dopamine activity, which raised his insulin sensitivity.

At the Academic Medical Center in Amsterdam, endocrinologist Mireille Serlie conducted several experiments to explain the underlying reason behind this improvement. She first recruited the same patient (above, with electrodes) with fourteen other individuals, all non-diabetic. Serlie found that administering DBS increased insulin sensitivity in all subjects. Additionally, Serlie administered a dopamine-depleting drug to 10 healthy males to find that their insulin sensitivity decreased across the board. This finding further reinforced the connection between dopamine and glucose regulation. Her team also activated neurons in the striatum of mice. As these cells released more dopamine, the rate of glucose uptake from other cells increased. She concluded that the striatum plays a pivotal role in regulating glucose metabolism throughout the body.

Dr Alex Reeves, neurologist and former neurology professor at Dartmouth medical school, is not convinced. “Dopamine is just one of many things within the body that can have this effect on insulin resistance.” He continues, “You need neurotransmitters in their minimal quantity to function.” In the long term, excess dopamine can thus have the opposite effect and reduce insulin sensitivity. Reeves argues that prescribing dopamine-boosting pharmaceutical drugs such as bromocriptine overlooks the underlying reason for insulin resistance in the first place.

Nima Saedi, assistant professor of surgery at Harvard Medical School, Boston advises caution, “. . .the results the authors described here are not translatable to diabetic patients.”

DBS may be unrealistic for most patients with diabetes, but the uncovering of this pathway has opened the door for less invasive brain therapies to target dopamine in the future.

How sugars hijack the brain reward system

When we are hungry, ghrelin (a hunger hormone) is released to heighten reactivity within food-related reward centres of the brain, especially in the striatum. As you begin your meal, the first few bites taste like heaven. However, your food gets progressively less appealing. The stomach and gut begin to release leptin, an appetite-reducing hormone that slowly diminishes the pleasure of consuming your meal. 

Visually appealing foods high in sugars and fat can alter our reward system by overriding these appetite-reducing hormones. A study conducted on lab rats reinforces this principle. Rats were offered regular chow versus an assortment of fatty and sugary foods such as cheesecake, sausage and chocolate. The experimental group consumed these rich foods, while the control group continued to eat bland rat chow. The experimental group quickly became obese. Researchers then introduced the unpleasant stimulus of a shock to try and deter the rats from eating. The control group scrambled away, but the obese rats continued to eat—their desire to eat more superseded their instinct to survive. 

Food and drugs elicit similar responses in the brain by activating the dopamine cycle. An intense dopamine rush causes individuals to crave the next one. Over time, reward centres release less dopamine in response, causing people to overindulge. The obese population exhibits reduced dopamine receptor availability, motivating them to seek foods high in glucose and fat to compensate for under-stimulated reward circuits. Obesity is usually accompanied by metabolic syndrome, a precursor to diabetes.


Dopamine, the ‘feel-good’ neurotransmitter plays an invaluable role in our bodies. Pathways and receptors transmit messages to control cognition, memory, impulses, sleep and kidney function. Dopamine also associates pleasure with certain behaviours, directing us towards goal-seeking and corresponding reward. Crucially, it also modulates glucose homeostasis. Central to the interaction between our reward and homeostatic systems is insulin. The diabetic population exhibits high insulin resistance—excess sugar can override brain hormonal activity and wreak havoc on our reward system. This same brain region is activated during drug cravings in drug-dependent individuals. Over time, as habits form, sensitivity is dulled, we ingest more to compensate for under-stimulated reward circuits. Researchers are exploring neurological pathways that are activated and their correlation to blood sugar levels. Emerging studies correlate dopamine and insulin activity with varied results. Studies of dopamine and corresponding insulin response have found that deep brain stimulation can improve insulin sensitivity. Treatments like DBS, although not realistic, have paved the way for less invasive brain therapies in the future to treat and manage conditions such as obesity and diabetes.

Disclaimer: The contents of this article are for general information and educational purposes only. It neither provides any medical advice nor intends to substitute professional medical opinion on the treatment, diagnosis, prevention or alleviation of any disease, disorder or disability. Always consult with your doctor or qualified healthcare professional about your health condition and/or concerns and before undertaking a new healthcare regimen including making any dietary or lifestyle changes.


  1. https://www.verywellmind.com/what-is-dopamine-5185621
  2. https://www.healthline.com/health-news/brain-stimulation-possible-diabetes-treatment#Reaction-to-the-results
  3. https://www.science.org/content/article/could-deep-brain-stimulation-help-zap-diabetes
  4. https://www.scientificamerican.com/article/kenny-high-sugar-plus-low-dopamine-could-hasten-diabetes-obesity/
  5. https://www.scientificamerican.com/article.cfm?id=is-obesity-an-addiction

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