← The Metabolic Classroom with Dr. Ben Bikman
The Metabolic Classroom with Dr. Ben Bikman
Why You're Always Hungry (Even After Eating)
00:24:01
More Knowledge, Better Health
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Why are you hungry again even though you just ate? It may not be willpower, it may be insulin. When fast digesting carbs spike, insulin fuel gets moved out of the blood and into storage. So even after eating plenty of calories, your brain may sense low available fuel. And when the brain senses low fuel, it tells you to eat. Over time, hunger can get worse. When fullness signals weaken, the leptin stops working well and the brain becomes insulin resistant. So constant hunger isn't just a discipline issue, it's often a signaling issue. The goal isn't to fight hunger harder, it's to fix the signals driving it. This is lecture 157 of the metabolic classroom.
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- [01:06]
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- [01:25]
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- [02:26]
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Foreign. Welcome back to the Metabolic Classroom. I'm Ben Bickman, metabolic scientist and professor of Cell biology. Today I want to talk about why some people feel hungry almost all the time. It's a complaint that I hear. I'm sure you either hear it or you felt it. And it's one that just seems to pop up constantly and it's usually blamed on weakness. Willpower. Now I do think willpower has something to do with it. But persistent hunger may be better understood as the output of hormonal signals that tell the brain whether the body needs fuel. When these signals are distorted, then the hunger stops, reflecting real need. And no amount of resolve or discipline or willpower can really correct the signal that has been corrupted or broken. The right place to begin is with the hormone that sits at the center of how the body handles fuel, which is, of course, my friend, insulin. Insulin's primary job after a meal is to move fuel out of the blood and into storage. It drives glucose into muscle, fat and liver and other tissues. It directs fat into fat cells, and at the same time, it restrains the release of, of fat that is already stored, whether that fat is in the fat cells or in the liver. Overall, the theme of these actions is to tell cells to store energy. This is normal and it is necessary. Without it, blood glucose would climb dangerously high and any stored fuel would be pouring out of tissues unchecked. Indeed, the output of that fuel into the blood would far surpass any ability to take it into the cells to burn for energy. Insulin wouldn't let that happen. But there is a direct consequence to this phenomenon, which is that insulin lowers the concentration of overall fuel circulating in the blood. And it lowers several fuels at once because it clears glucose while also holding back the fatty acids that fat tissue would otherwise release. At the same time, the insulin prevents the liver from making ketones, the the other fuel for the brain. Now, the brain is relevant here because it's constantly monitoring how much fuel is available in circulation. And a simultaneous fall across all of those fuels is one of the strongest cues that the brain has, that energy is running short. Now, importantly, this can happen even if the body has plenty, hundreds of thousands or millions of calories stored in fat cells. The brain can, can't really it it. I'll highlight a signal that allows it to sense that, but it's more concerned with the short term fuel use and, and the brain's ability to access fuel. And so the brain will then respond to this cue, again this low fuel cue, by generating hunger. This is the first mechanism and it's the foundation for, I think, everything else that follows. So consider with me what happens after a single meal, a meal that provokes a large insulin response, which generally means a meal high in easily digested carbohydrate, moves a great deal of the incoming energy into storage quickly, and insulin's action tends to outlast the meal's absorption. The result is a bit of a mismatch. The hormone is still clearing fuel from the blood and still suppressing the release of stored energy like stored fat or stored glucose after the meal, after the meal's been finished and absorbed. But the system overshoots into a relative energetic trough. It's this kind of rebound drop. In a controlled human feeding study, adults who had lost weight, they were maintained on one of several diets. The diet held protein constant, but it differed in carbohydrate content in the late portion of the postprandial or post meal period. Those on the higher carbohydrate diet had lower total circulating metabolic energy than those on the lower carbohydrate diet. In other words, the sum of all caloric energetic molecules like fats, glucose ketones, was lower in the blood when insulin spiked. Because the higher carbohydrate meals provoke more insulin, more of the meal's energy was directed into storage and held there, was locked in, and a few hours later, there was measurably less fuel circulating for the rest of the body to use, especially the brain. Now follow that reduced fuel availability to a, to a behavioral endpoint. There was another study similar, but it was with 12 teenagers and they had obesity. Each one was given meals that were identical in calories and matched for protein, fat, fiber and even palatability. They only differed in the glycemic index, which is to say only in how quickly the carbohydrate was absorbed into the bloodstream and therefore how large the glucose and insulin response the meal provoked. After the high glycemic meal, glucose rose sharply and then fell. And in the late postprandial period, both glucose and circulating fatty acids dropped below the levels seen in the fasting state. The body registered this as a shortfall and mounted a counter regulatory response, including a rise in adrenaline, interestingly enough, what we would call epinephrine here in the US which is the same kind of response the body uses to defend against a genuine drop in blood sugar or blood glucose levels. The participants reported more hunger, and over the following five hours, they ate substantially more food. Voluntary energy intake after the high glycemic meal was 53% greater than after the medium glycemic index meal, and it was 81% greater than after the low glycemic meal. The same calories consumed at the meal produced a large and measurable difference in the hunger and the eating that followed. So again, after they ate a meal that spiked their insulin much more than the low glycemic meal, they ate almost, I would, I want to say, almost twice as much but it didn't quite get that far. But it was getting close to that. The trigger that links the fuel dip to the eating has been observed directly in people isolated from food and from any external time cues, so that they could only eat when they felt the urge to. Small, transient declines in blood glucose preceded the great majority of hunger and requests that the study subjects had to eat. In one such study, 83% of meal requests were preceded by a brief dip in blood glucose that began minutes before the person consciously felt hungry. The brain uses a falling fuel signal as a cue to seek food, and it does so even before the feeling of hunger reaches that level of awareness. So when a meal drives a large insulin response, pulling circulating fuel down into a a bit of a reactive dip, the dip itself becomes a hunger signal. And hunger returns not long, even though the after the person just ate. This is the familiar experience of finishing a large carbohydrate heavy meal and feeling hungry two or three hours later, despite having eaten more than enough energy to carry a person well past that point. The hunger is very real. The brain is feeling it and promoting this sense. And it's not a sign that the meal was too small. It is a sign of where the energy from that meal has gone. There is a further turn to this, which is that the hunger produced by a reactive dip tends not to be a neutral desire for any food. It actually tends to lean specifically toward quickly absorbed high glycemic food, the very kind that produced the dip in the first place. You can see and and see this to its logical conclusion here. This sets up a repeating cycle in which each such meal helps create the conditions for the next one. Insulin also acts directly inside the brain in a way that bears on hunger from a different direction. And I'm going to come back to that in a moment. So we're going to leave insulin for now, having framed it in the context of a fuel regulator hormone. And when insulin goes really high, the total energy available to the brain dips low. The brain responds to that by pushing the body to eat more now. But again, we're going to come back to insulin because it actually plays another role.
- [11:37]
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This episode is brought to you by Progressive Insurance. Do you ever think about switching insurance companies to see if you could save some cash? Progressive makes it easy to see if you could save when you bundle your home and auto policies. Try it@progressive.com Progressive Casualty Insurance Company and affiliates. Potential savings will vary. Not available in all states.
- [11:56]
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Everyone treats summer like it owes you happiness. Long days, pool parties, your best life on a loop. So what does it mean when you feel worse? The summer blues are real. It's why summer is one of the busiest stretches of the year for people starting Therapy Grow Therapy is here for all the moments when you decide you want more. More support, more clarity, more tools. GROW connects you with thousands of high quality licensed therapists across the US Offering both virtual and in person sessions, nights and weekends. The therapist you want takes your insurance on Grow grow accepts over 125 insurance plans. Sessions average $21 with insurance and some pay as little as $0 depending on their plan. Visit growtherapy.com startnow today to get started. That's growtherapy.com startnow growtherapy.com start now. Availability and coverage vary by state and insurance plan
- [12:59]
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okay, the second mechanism with regards to hunger and satiety it we move from the pancreas into the gut and this one's going to be familiar. When food arrives in the intestine, the gut will release hormones that report upward to the brain that a meal is coming through the guts and that it's soon going to be coming into the blood. And these signals will help promote a sense of satiety or fullness, and it will slow the pace of eating. Now one of the most important and Most famous is GLP1. GLP1 works in both of these ways. It does slow the rate at which food is moving through the stomach so that the food lingers and you have a greater sense of fullness. But it also acts at the appetite regulating centers of the brain to promote satiety directly. Now, in a well functioning response, a carbohydrate containing meal triggers a brisk and robust release of GLP1 and that release is part of what brings a meal to its satisfying ending. But this response is not identical in everyone, and the variation is important. In a study that you have heard me describe before, it compared lean women with women with obesity. Each was given a carbohydrate heavy meal and on a separate occasion, a fat heavy meal. Then they measured the GLP1 response and they found that the GLP1 response to the carbohydrate meal was markedly attenuated or blunted in the women with obesity, while a response to the high fat meal was generally similar between both groups. So the same carbohydrate meal that produced a strong satiety signal in the lean subjects produced a very weak one. In fact, when you look at the data, there was no significant response with GLP1 in the subjects with obesity. So the food was eaten, the calories were absorbed, but the fullness message that should have accompanied it was muted in one group only. Now, Whether the weak GLP1 response is a cause of the obesity or a consequence, that directionality has not been confirmed. But the practical result is the same in either direction. A person in that state draws less fullness from the same meal than a person who's got GLP1 production, I would say intact, but that's kind of overstating. It just is. Is robust. But that GLP1 shortfall is going to repeat, based on this study, at every carbohydrate meal every day, which is how a small difference in a single hormone signal can become a large difference in how often a person feels hungry. It also helps explain a common and frustrating observation, which is that two people can eat the same plate of food and walk away feeling entirely differently about it. One is satisfied for hours, the other, the other is looking for something to eat even though they just ate an hour previously. The difference is not necessarily in the food itself, and I would say it might not even be solely dependent on the discipline of the person. Although, again, I'm an advocate of discipline. But I hope you can see that some of this difference can lie in how strongly each person's gut signals and those signals send this sense of fullness to the brain and to the body, helping them control their hunger. Okay, moving on. While the first two mechanisms can operate at a meal to meal level, the third operates at a slower and, I think, larger level. And it's more. It's based on the total quantity of energy that the body is holding in storage. Fat tissue. As you know by now, you studious attendees of the Metabolic Classroom is not an inert depot. It's not just sitting there holding on to energy in the form of fat calories. It is an endocrine organ, and it releases a lot of hormones, one of which is itself kind of famous, and that is leptin. Now, leptin is released in rough proportion to how much fat a person carries. Leptin's message to the brain is that stored energy is plentiful, that the threat of scarcity is not present, and that the drive to seek food can ease up a little bit. The discovery of this hormone reshaped how we think about appetite because it meant that fat tissue talks back to the brain about how much fuel is in reserve. So more body fat should mean more leptin, and more leptin should mean less hunger. In a person carrying a large amount of fat, the appetite signal should be turned down hard, and obesity should be close to self correcting. If this paradigm holds, the measurements show the opposite of what that logic would predict and what you would expect. In a study measuring leptin in 136 people of normal weight and about the same number of people with obesity, leptin rose steeply with body fat levels. So the subjects with obesity had more than four times the leptin levels of the lean subjects. And across all participants, the level tracked closely with the percentage of body fat on their bodies. So people with obesity are not low on leptin. They have an abundance of it. The signal is being sent at high volume, yet the hunger that it's supposed to suppress persists. This is leptin resistance, an abundant signal that the brain just cannot respond to. This is just one more example of what the body does when there's too much of a hormone. Too much of a signal leads to a down regulation in response to that signal. So too much leptin is driving leptin resistance. Now, with that concept in mind, we can go. That brings us. That brings us to the fourth and the final mechanism to help you understand hunger. Insulin is not only a storage hormone, it also crosses into the brain and acts there as a satiety signal, reporting on energy status within the hypothalamus and the regions connected to it, where it shifts the balance of activity away from the neurons that drive hunger and toward those that suppress hunger. Now, this can and has been demonstrated directly in people using insulin delivered through the nose. So you sniff, you inhale it, this nasal inhalation of insulin, and that's a route that carries the hormone toward the brain while causing the little change or no change in the amount of insulin that's in general systemic circulation, the separation between those two. So insulin in the brain versus insulin in general circulation is what makes this method useful, because it isolates insulin's action in the brain from its actions in the body. Like what I mentioned previously, where insulin is reducing total energy availability because it's pushing it all into the muscle or the fat or the liver. Well, that's not what happens here, because it's just going into the brain circulation. When healthy people were given insulin this way, in one particular study, they ate less afterward than when they were given a placebo. And when given insulin this way, after lunch, they reported greater fullness and ate fewer highly palatable snacks a couple hours later, Again, with no meaningful change in blood insulin levels. Insulin acting in the brain is a real satiety signal. More insulin signaling to the brain means less eating. Now, interestingly, it was not only the total amount of food they ate, it was also the craving. Back to this study, but the craving. As I noted for the most palatable foods, when insulin reached the brain, people ate less of the highly palatable snacks in particular and rated them as less appealing. This suggests a second role for insulin in the brain beyond what it does when I first mentioned it the raw change in energy status. Insulin dampens the reward value of food, the part of appetite that is driven by how rewarding something tastes rather than by any physiological need for the calories or the nutrients. When brain insulin signaling is intact, the appeal of palatable food is held in check. However, like so many other tissues in the body, the brain can become insulin resistant. When the brain is resistant to insulin, that check on cravings and pal and consuming palatable foods starts to weaken and these thus the palatable foods become less compelling and there's. There's less desire for them.
- [21:59]
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Everyone treats summer like it owes you happiness. Long days, pool parties, your best life on a loop. So what does it mean when you feel worse? The summer blues are real. It's why summer is one of the busiest stretches of the year for people starting Therapy Grow Therapy is here for all the moments when you decide you want more. More support, more clarity, more tools. Grow connects you with thousands of high quality licensed therapists across the US offering both virtual and in person sessions, nights and weekends. The therapist you want takes your insurance on. Grow grow accepts over 125 insurance plans. Sessions average $21 with insurance and some pay as little as $0 depending on their plan. Visit growtherapy.com startnow today to get started. That's growtherapy.com startnow growtherapy.com startnow availability and coverage vary by state and insurance plan.
- [23:00]
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- [23:18]
A
Now with insulin resistant. Of course, those highly palatable foods remain compelling at the same time that ordinary satiety is harder to obtain. You're just not getting satiated. And these two problems, of course, can compound on each other. This is where the two facets of insulin resolve into one. Insulin acting inside the brain reduces hunger, while insulin acting on the tissues of the body drives the fuel partitioning and the reactive dip described in the first mechanism. In a metabolically healthy person These are balanced and insulin's brain side satiety helps close out a meal appropriately. The trouble begins when the brain becomes resistant to insulin in the same way that muscle and liver become resistant to it. When men with obesity were given nasal insulin over eight weeks, insulin failed to reduce their body weight or body fat, even though other responses to the brain to insulin remained intact. In normal weight men, the identical protocol of providing insulin nasally reduces body fat. The appetite suppressing arm of insulin's action in the brain had been blunted by the obese insulin resistant state. So a person can have high insulin throughout the body and still receive a weakness satiety signal in the brain. Because high insulin in the blood does not guarantee a strong response in the brain or any tissue when it's become insulin resistant. So you can be hyperinsulinemic and hungry at the same time. Now, these last two mechanisms, leptin resistance and insulin resistance, are not separate because insulin and leptin act on overlapping brain circuits in the same regions of the hypothalamus. A brain that has grown resistant to one of these signals is most certainly also resistant to the other. Which is why brain insulin resistance and leptin resistance so reliably occur together. Two of the most powerful satiety signals the body possesses, one reporting on the meal just eaten and one reporting on the total energy in storage, are diminished at the same destination in the same state at the same time. Okay, now let's bring this all together. First, meals that provoke a large insulin response push fuel into storage and set up a reactive dip in circulating energy that the brain reads as hunger. So hunger returns soon after eating and pulls toward the same foods that caused it, those high glycemic refined starches and sugars. Second, in many people, the gut's fullness signal to a carbohydrate meal is weakened, so the meal registers as less satisfying than it should. That's that glp one response. Third, the signal from fat tissue reporting abundant stored energy. Leptin is loud in the blood. It's a strong signal, but the signal doesn't work at the brain. So the long term restraint that leptin should be driving on appetite fails. And then fourth, insulin's own satiety signal within the brain is blunted once the brain becomes insulin resistant. So here we have four distinct mechanisms, but there is one thread running through all of them. To a degree, a state of chronically elevated insulin combined with resistance to insulin's actions. Now that I say that, I should have also added a potential explanation for why some people have a reduced GLP1 response the L cells of the gut that make GLP1 have been shown to respond to insulin, and insulin is one of the signals that actually helps stimulate GLP1 release. But those cells in the midst of too much insulin can become insulin resistant. This has all been published. I've highlighted this previously. So even in the GLP one response or the blunted response, I should say, where you may think that insulin is not relevant, it most certainly is. So in the end, persistent hunger is not so much just a failure of discipline. We need to acknowledge that it is driven by a signaling environment, a metabolic milieu in which the body's messages about fuel are either disrupted at the source or at the destination. I strongly believe that the lasting solution is to lower the chronic insulin exposure and restore insulin sensitivity, rather than to just wage a daily war against hunger itself. Correct the state, the metabolic state and the signals that can that govern appetite can begin to just do what they were meant to do. Class dismissed. Until next time. More knowledge, Better health.
- [28:19]
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- [29:26]
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Could AI help you do more of what you love? Workday is the AI platform for HR and finance that actually knows your business. We help you handle the have to dos so you can focus on the can't wait to do's. It's a new workday. Summer smells like citrus in the sun.
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