Tuesday, August 21, 2018

Eating Too Much? How Signaling Can Drive What You Eat (& What To Do About It)

from Precision Nutrition

Various signals within our brain can drive what, when, and how much we eat. If you’re eating too much, there’s hope, you can take back control!

It’s no secret that obesity rates have been rising in the U.S. (and other industrialized nations) for the past 30 years. It’s also no secret that Americans eat more than they used to by almost 425 calories per day since the early ’80s For decades, government officials, research scientists, and fitness pros blamed this on the inability to “push away from the table”. Diet book authors, TV doctors, and other nutrition experts tell us we’re gaining because of gluten, fats, fructose, or whatever the nemesis of the day is.

But, all this finger-wagging never really explains whyWhy are we eating so much food? And why is it so hard to stop? Part of the answer lies in our brains. Ever open up a bag of chips planning to have a small snack, only to find yourself peering into an empty bag, just a few moments later? Behind our decision-making processes are also physiological forces in play.

You see, deeper brain physiology drives what, when, and how much we eat — along with its co-pilots of hormones, fatty acids, amino acids, glucose, and body fat. For the most part, our conscious selves are less involved than we choose to be the case. In this article, we’ll explore: how our brains dictate so many of our food choices, how physiological elements can lead to weight gain, what we can do to take our power back.

Why do we decide to eat? Simply put, we eat for two reasons.
     Homeostatic eating: We eat to get the energy our body needs, and to keep our biological system balanced (aka homeostasis). (This is necessary, we have to eat to live.)
     Hedonic eating: We eat for pleasure (aka hedonism), or to manage our emotions. (This is unnecessary. we don’t have to do this, but all too often, we do, we live to eat).

Most meals are a mix of homeostatic and hedonic eating. We do know that ghrelin, the “hunger hormone”, stimulates our appetite. It peaks just before meals and falls during and immediately after eating. Yet ghrelin is not the only factor in hunger or the decision to eat.

Although taking in nutrients is as old as biology, we still don’t know why and how humans get hungry and decide to start eating. Hunger and eating is shaped by many factors, including: social cues, learned behavior, environmental factors, circadian rhythm, hormonal & genetic influences. As you can imagine, it’s complicated. Science still doesn’t have “the secret” to hunger and eating. (Yet.) We do, however, know a lot about why we stop eating.

Why do we stop eating? Once we’ve started eating, what makes us stop? This is in part influenced by satiation along with the perception of fullness you get during a meal that causes you to stop eating. When we eat a meal, two physiological factors work together to tell us to put down our fork and call it quits: gastric distension and hormonal satiation.

Gastric distension: When empty, your stomach can only hold about 2 fluid oz. When you eat, the stomach can expand to hold about 34 fluid oz, or at the extreme end, around 1 gallon. Your stomach is designed to stretch and expand, aka gastric distension. Your stomach is also designed to tell your brain about how much stretching is happening.

As your stomach expands to accommodate the incoming food, neurons in your stomach send this message to your brain via the vagus nerve, which runs from your head to your abdomen.

People who want to lose fat would do well to choose more nutritious yet low-energy and high-fiber foods, such as vegetables, beans, and legumes. Because these take up more stomach space, they can help us feel full, though we’re eating fewer calories. Unfortunately, though, gastric distension isn’t the full picture.

Hormonal satiation: While you eat, your GI tract and related organs (like the pancreas) tell many areas of the brain that food is coming in. Some of these signals travel up the vagus nerve, while others enter the brain by different routes. Some of the more important of these hormones are:
     Cholecystokinin (CCK): When we eat fat and protein, the gut releases CCK, telling your brain (through the vagus nerve) to stop eating.
     GLP-1 and amylin: Recent research indicates that GLP-1 may be the most unique, and important, satiation hormone. It seems to stimulate the production and release of insulin (a powerful satiation/satiety hormone itself) and slow down food moving from the stomach into the small intestine, among many other impressive mechanisms. Similarly, amylin is one of the few satiation/satiety hormones shown to actually reduce food intake.
     Insulin: When we eat carbs and protein, we release insulin. This tells your brain that nutrients are coming in, and eventually tells it to stop eating.

Many of these hormonal messages stick around. They can tell us to eat less at later meals, too. This is why you should think about your food choices and eating habits in the long-term — over the course of a day, a few days, or even a week. For instance, a high-protein breakfast might prevent you from overeating at dinner. Together, these physiological responses (along with other hormones and signals) help you feel full and know when to stop eating.
 
Because this is an information dense discussion, I’ll stop it here to give you time to absorb it in small chunks, but more great intel to come next week! The more you understand these types of processes, the better your chances for success in making mindful decisions about food, which of course leads to favorable weight management!


Despite their importance, the actions of various satiety hormones still aren’t the complete picture. What really matters to your weight and overall health, of course, is what you do consistently — i.e. the quality of your nutrition and how much you typically eat, day after day. Your body has a system for managing your long-term energy and nutrient needs. It’s called the leptin feedback loop.

Leptin is a hormone that’s released by fat tissue. Leptin tells the brain how much energy we’ve just consumed and how much excess energy we have stored up (as fat). The more body fat we have, the more leptin in our blood. The brain makes decisions based on leptin levels about hunger, calorie intake, nutrient absorption, and energy use and storage. Then, it cycles back to regulate leptin production in a loop that can help keep our energy (and body weight) balanced over time.


     If stored energy (fat) and leptin remain stable over time, we are more easily sated during and between meals. Smaller portions feel OK. And our metabolic rate stays high.
     If stored energy (fat) and leptin drop over time, it sends a message to the brain (mainly the hypothalamus, which links your nervous system with your endocrine system) that we need to start preventing starvation.

The brain responds to lower leptin levels with several anti-starvation strategies: We get hungry. Like real hungry. Like eat-your-own-arm hungry. We move around less. Our NEAT (non-exercise activity thermogenesis), or our daily movement like fidgeting, standing up, and anything other than purposeful exercise, goes down. The couch starts looking better and better.

We burn fewer calories through movement as our skeletal muscles become more efficient. Our metabolic rate slows down significantly (as seen in the infamous ”Biggest Loser” study). It follows, then, that if stored energy (fat) and leptin go up over time, you’ll want to eat less… right? Yes. Sort of.

Unfortunately, you can’t always count on that response. How much leptin will go up when you start eating more varies from person to person. And how your brain responds to increased leptin levels also varies from person to person.

Clearly, people’s physiologies vary a lot. In some people, when leptin rises, their brain decreases their appetite, and increases their NEAT output. In others, the response isn’t nearly so robust. That being said, most of the time, for most people: The leptin feedback loop works fairly well to naturally regulate our energy expenditure and consumption… until we disrupt it. However, the type of foods you eat can change your brain.

Assuming we’re properly nourished, that well-balanced leptin loop will tell us when we’ve had enough. It helps us feel satisfied and allows us to eat reasonable portions, comfortably. But that nicely balanced loop can become disrupted — quickly — when we eat certain types of food.

A diet filled with 
hyper-palatable, hyper-rewarding, heavily processed foods can overthrow the the brain’s “stop” signals. In plain English, this means so-called “junk foods” that are sweet, salty, creamy, and/or crunchy (maybe all at once), and full of chemical goodness that spins our pleasure dials… but contain relatively few actual nutrients. This type of diet prevents leptin from doing its job of regulating our energy balance. It can even make our brains inflamed and leptin resistant. We end up feeling less satisfied. We want to eat more, and our bodies even fight to hold on to the weight we gain.

Hyper-palatability: Palatability is more than just taste — it’s our whole experience of pleasure from a food. That includes taste as well as aroma, mouthfeel, texture, and the whole experience of eating. Palatability strongly influences how much we eat at meals.

That seems obvious: of course we eat more of the foods we like, and of course some foods are more pleasurable to eat than others. But some foods aren’t just palatable — they’re extremely palatable. They’re what you might call “too good”. Anything that you “just can’t stop eating” would fall into this category.

Reward value:  Along with palatability, some foods give us a “hit” or a reward from some type of physiological effect. We’ll go out of our way to get foods with a high reward value — in fact, we may learn to like them even if they don’t taste very good.

For instance, few people like black coffee or beer the first time they try them. But coffee has caffeine (yeah!) and beer has alcohol (double yeah!). Our brains like caffeine and alcohol. We learn quickly that coffee and beer are good things, and we learn to like (or at least tolerate) their taste. Over time we discover we like — maybe even can’t live without — them. We’ll wade through a crowded bar to buy a drink, we’ll stand in an absurdly long line for our afternoon coffee fix, and we’ll pay exorbitant amounts of money for relatively simple products.

We’ll also make room for high-reward foods even when we’re full. This is why at Thanksgiving, after moaning and groaning about how full you are, you miraculously make room for pie when it’s time for dessert.

Tasty + fun = no shutoff switch: Now, what happens when you put these two things — hyper-palatability (tasty) and high reward (fun) — together? A dangerous combination. We want these foods, we like these foods, and we’ll work hard to get them. When we do get them, we often don’t quit eating them and regulate our intake poorly..

These types of foods have a winning combination for keeping us interested and eating: energy density. i.e. a lot of calories in a small package. They have a high fat content, high refined starch and/or sugar content, saltiness, sweetness, pleasing and specific texture, such as creamy or crunchy, drugs, such as caffeine or alcohol, other flavor enhancers or additives to improve mouthfeel.

This magical mix is rarely found in nature. It is, however, often found in highly processed foods like cakes, cookies, pastries, pies, pizza, ice cream, fried foods, and so forth. Make something salty, and sweet, and starchy, and fatty, then add in some extra flavors and scents, appealing colors and a pleasing mouthfeel for good measure, and you have something that’s been scientifically engineered for us to over-eat.


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