High-carbohydrate foods are rewarding to the mouth. Biting into a glazed donut, with the subtle crunch of the sugar coating giving way to soft, pillowy dough underneath, can instantly transform a mind-numbing work meeting into a temporary visit to one’s proverbial “happy place.” (That is, until the guilt sets in, about fifteen minutes after polishing off the donut!) Whether it’s snacks and desserts, such as chips and cookies, or healthier fare, such as fruit or granola, many people rely on carbohydrate-rich foods for comfort and a pick-me-up. New research sheds light on why insulin in the brain may enhance dopamine release, and this may, in turn, influence food choice toward higher-carbohydrate items.
It is telling that most “comfort foods” are sugar or starch-based: cake, ice cream, macaroni & cheese, French fries, etc. (Few people, it seems, gravitate toward spinach or grilled chicken when they’re having a bad day.) Increases in post-prandial plasma insulin levels activate insulin receptors in the hypothalamus, which should provide negative feedback to appetite circuitry, resulting in feelings of satiety and a decreased interest in eating more. Most of the brain’s insulin comes from the pancreas, crossing the blood-brain barrier via active transport. However, it is now believed that the brain, itself, also produces some insulin. Regardless of the source of insulin in the brain, the cells’ ability to respond to the hormone may ultimately play a role in feeding behavior and obesity.
This is not entirely new information. Studies in mice have shown that, when insulin receptor signaling is inactivated, mice end up with increased body weight, increased fat mass, and hyperphagia. Inactivation of the insulin receptor somewhat mimics insulin resistance. Insulin resistance is not limited to the periphery; it occurs in the brain, as well. Brain insulin resistance alters dopamine turnover, induces anxiety and depressive behavior in insulin receptor knockout (NIRKO) mice. NIRKO mice also have increased levels of monoamine oxidase, leading to increased dopamine turnover. When treated with monoamine oxidase inhibitors (MAOIs), commonly prescribed as antidepressants, the behavioral changes are reversible. Researchers believe the effects of insulin resistance on brain mitochondrial function may explain, at least in part, the noted association between type-2 diabetes and other insulin resistant states, and mood disorders.
The influence of insulin on the brain’s reward circuitry could explain the tendency for people to reach for carbohydrate-dense foods when they’re feeling low. It may even play a role in food addiction and/or binge eating disorder; just as with “comfort foods,” it is more common for people to be unable to moderate their intake of sweet and starchy foods than foods higher in protein and fat, such as steak or pork chops. Insulin acutely raises dopamine levels, but brain insulin resistance short-circuits this process, which may cause people to consume more and more food in order to feel the rewarding effects, similar to developing a tolerance to caffeine or narcotics, where, over time, higher and higher doses are needed to evoke the same effect. Brain insulin resistance may also explain why many people eat past the point of physical satiety. Hunger pangs are long gone, but something has gone awry in the neurological signaling that would otherwise cause someone to stop eating. The stomach may be full, but if the brain isn’t getting the message, that could lead to overeating, and, most likely, it would lead to consuming more of the foods that may be driving the process in the first place: dense carbohydrates.
That a single hormone may influence satiety and encourage feeding is not completely contradictory. According to researchers, “A dual role in signaling satiety may simply allow insulin to serve the important purpose of ending a meal, while simultaneously establishing a memory of its nutritional and thus rewarding qualities, thereby reinforcing repetition of the ingestive behaviour.”
Research on the relationship between insulin and the satiety hormone, leptin, is ongoing, but for certain, insulin’s effects are not limited to peripheral glucose uptake. The role of insulin in blood glucose management is merely one entry in an ever-expanding—and sometimes surprising—list of other mechanisms by which this hormone influences energy homeostasis. With the growing epidemics of type-2 diabetes, metabolic syndrome, Alzheimer’s disease (“type-3 diabetes”) and other conditions stemming from insulin resistance, it is critically important to further elucidate the role of insulin in the central nervous system, and how this may determine eating behavior and food choice.