Category: Brain

Appetite suppression effects have been found in two different types of brain cells, in two separate studies.

In the first study, a type of glial cell (cells that surround, support, and protect neurons) called tancytes have been found to have the same savory taste receptors that the tongue has. They sense the taste called umami, the taste of protein. That taste is what makes something taste meaty. It is activated by (among other things) monosodium glutamate (MSG), which is why MSG is put into food.

Glutamate (and its acid form, glutamic acid) is one of the essential amino acids that make up proteins. Two other essential amino acids, arginine, and lysine,  are what the tancytes in the brain detect.

The tancytes sit in the brain where they are in contact with the cerebrospinal fluid, where they can sense the amino acids, and in contact with the part of the hypothalamus in the brain that controls energy levels and body weight. When they sense that the levels of arginine and lysine are high enough, the tancytes send appetite suppression signals to the hypothalamus that decrease appetite. The tancytes respond in as little as 30 seconds to lysine and arginine. Tancytes can also generate new neurons, allowing the hypothalamus to be retrained through diet.

Foods beside meat that contain useful levels of lysine and arginine are plums, apricots, avocados, almonds, and lentils. Eating these thus reduce hunger faster than other foods. High protein foods such as these also digest more slowly, so they don’t quickly raise blood sugar levels, thus reducing food cravings and keeping you satiated longer.

Tancytes also have the same sweet taste receptor that the tongue has. They detect glucose levels in the blood this way, possibly adding another appetite suppression signal.

The second study focused on neurons in a higher-level part of the brain, the medial septal complex, which is implicated in emotion and cognition. They found that these neurons contribute to appetite suppression by sending signals down to the hypothalamus.

By activating these neurons, the researchers were able to control appetite without causing the side effects other interventions cause, such as anxiety and changes in physical activity.

Together, these two studies provide two separate targets for potential diet drugs, but also for interventions based on diet.

Odors affect what we eat. That is so obvious that we seldom give it any thought. Food aromas send signals to the brain that prepare us for digestion, secreting saliva and gastric juices in preparation for digestion. When we lose the sense of smell, food loses much of its taste and appeal, and we eat less.

A recent study looks deeper than that, however. It turns out, that in mice at least, odors also affect how much energy is burned by brown fat, the tissue that keeps the mouse (and humans) warm by burning calories to create heat.

The researchers damaged the neurons in the mouse brain that are responsible for processing olfactory sensations (smells). As you might expect, the mice ate less. But they also burned more calories in their brown fat than the control mice did. Moreover, they were resistant to diet-induced obesity, and when mice made obese by diet were given the same procedure, they lost fat mass and regained insulin sensitivity.

In another set of mice, they made changes that enhanced the sense of smell. These mice gained weight, even when fed the same amount of food as before the treatment, and the same amount of food as controls.

So the effect of food odors is not limited to changes in food intake. It directly affects the rate at which calories are burned to keep the mouse warm.

The effects of odor don’t stop at weight loss. In worms and flies, disabling olfaction leads to longer lifespans. As we have seen in other studies, metabolism and lifespan are inter-related. The smell of food (in flies and worms) decreases lifespan, but only when they are calorie restricted. So perhaps when using intermittent fasting to prolong your life, you might want to avoid the smell of food. Of course, doing so makes fasting easier, so maybe you are already avoiding Cinnabon on your fast days.

Food deprivation activates cells in the brain known as agouti-related protein neurons. These hunger neurons activate food intake, but also energy expenditure and metabolism. The smell of food can inhibit these neurons in seconds if the mouse is hungry.

Of course, mice are not people. People have a third as many odor receptors as mice, and humans lack the organ that allows mice to sense pheromone odors. But measuring the brown and beige fat activity of fasting and non-fasting humans to odors might not be a difficult experiment to try.

Fast carbs are foods that quickly turn into glucose in the body, often before you even finish swallowing. They include sugar, of course, which is half glucose, but the main culprit in the Western diet is wheat flour, which is mostly amylopectin A, the type of starch that is most quickly digested into glucose by the enzymes in your saliva. Making the digestion much faster is the fact that the flour is ground extremely fine, providing enormous amounts of surface that is then exposed to the enzymes.

We have long had a nickname for the effects of fast carbs on the brain: food coma. While the name is meant to be somewhat tongue-in-cheek, the effect is real, as a recent study  in the journal Physiology & Behavior shows.

The researchers tested the effects of glucose on simple reaction time, arithmetic, and an effect called Stroop interference, where, for example, printing the word “blue” in a color other than blue slows down thinking. In all three tests, subjects responded more slowly when given glucose or sucrose than when given the sucralose placebo. The effect was greater after a 10 hour fast (such as usually occurs just before breakfast).

The effect after fasting was a 15% slowdown in reaction time. Without fasting, the reaction time was faster, but the difference between glucose and placebo was greater, with glucose causing a 17% slowdown.

Other studies have shown that glucose induces sleep by activating sleep-promoting neurons in the brain, and that by raising insulin levels, glucose can make it easier for the amino acid tryptophan to enter the brain, where it is converted into the hormones serotonin and melatonin, both of which are involved in sleep. The tryptophan you get from that Thanksgiving turkey would not by itself make you sleepy. It is the insulin following the rolls, mashed potatoes, and desserts that allows it to get into the brain.