How To Gain Control Of Your Appetite

Episode 103

Overconsumption of calories is a great way to make yourself sick. Many of us feel like our appetites are out of control. How and when we eat is under the control of many different factors, but all is not lost. We dive into those factors and end the episode with actionable tips for taking control of your appetite.

Nimbus Healthcare
Lifestyle Medicine

Episode Transcript

Dr. Richard Harris MD  00:00

In this episode of The strive for greater health podcast, we’re going to talk about something that we experience every single day. And that is our appetite. We’re going to dive into all the different things that can regulate our appetite, and then techniques that we can use to curb our appetite. If we’re trying to decrease our food intake, which is a major problem here in the US, we just over consume calories. And that’s a wonderful way to make yourself sick, especially if those calories are mainly Ultra processed foods. We’re going to talk about it. Are you ready to boost your health, EQ and IQ Cue the music?

Dr. Richard Harris MD  00:49

Join me Dr. Richard Harris as we strive to unlock the secret to the human body. Just drive for wellness strive for great health. Follow the show on iTunes, Spotify, Google and Android.

Dr. Richard Harris MD  01:16

And now a word from our sponsors. Our sponsor is Nimbus healthcare, the company that I co founded personalized medicine personalized results, I’d Nimbus we don’t believe that there’s a one size fits all when it comes to treatment. And the data is starting to show that there’s a large variety of how people respond to certain things. And we’re in the Age of Science where we can use things like genetic testing and biomarkers to truly customize a plan just for you. And that’s what we do at Nimbus healthcare. We are in the hair loss and the hormone space. And what we do is we use lifestyle medicine, supplements, and compounded prescription medication to tailor and individualize a plan just for you. If that sounds like something that you’re looking for, you can check out Nimbus Or click the link in the show notes. One of the things I get asked all the time is Richard, how can I support the podcast and the best way that you can support what we do at the strive for great health podcast is to invest in your health, with our lifestyle medicine course. The course is essentially everything that I do for myself and my loved ones that keep us in optimal health. It covers nutrition, exercise, sleep, stress management, we also dive really heavily into mindset into commitment into willpower, intentionality and habit change. This is something that has been life changing for me. And I really think if you want to support the podcast, the best way you can do so is invest in your health, or invest in the health of someone else around you. Through our lifestyle medicine course. It’s 4999. And as listeners of this podcast will give you 10% off using the code podcast, let’s dive in to this week’s episode. But first, we’re going to talk about updates, couple updates. We archive the Facebook group, we weren’t really participating much in that group. So all of the links that were relevant can be had in the strive for great health podcast, Facebook page, there’s a link to the page on our website. And you can grab our stress management guide and a link to the folder that has our clinical trials. Corrections, every episode that I think of something that I’ve missed said or that needs updated, we’re going to do a correction. One of the Corrections is from our cholesterol podcast. And we talked about that we said statins do not decrease small dense LDL. Well, I found a paper that shows that what statins actually do is they decrease the major fraction. So if the major fraction is large LDL, it’ll decrease that if the major fraction is small, dense LDL, it’ll decrease that. But unfortunately, if the large LDL, which we talked about as being fluffy and buoyant and not very sticky, is the major one. But you still have really high levels of small dense LDL, then it’s going to decrease the large fluffy LDL and not the small dense LDL. So we’ve covered statins extensively. I don’t have any other new updates about statins, just that correction, that I was wrong saying statins don’t do anything for small, dense LDL, GMO foods. This is another thing that I will admit we got wrong. There’s no actual human studies saying they increase allergies that I’m aware of. We have no human studies showing harm that I’m aware of. There’s actually studies that show benefit for GMO foods, GMO reduced pesticides by 37% and increase crop yields by 22%. And one meta analysis of 147 studies, a specific species of rice called Golden Rice was modified to contain More beta carotene for regions that lack vitamin A and low vitamin A can cause blindness. So this is a net benefit, GMO corn and a made up of 76 studies in North and South America at 29%, less mycotoxin 31%. Less. If you Mohsen, which is, both of these are byproducts of fungi that are toxic and can cause different problems in humans, depending on your susceptibility. And then another study showed that GMO has caused a reduction in greenhouse gases. And this is in 2015, alone by about the amount equivalent to 11 point 9 million cars. So I’m not saying go out there and eat GMO soy burgers, impossible burgers, because those are processed foods. But there doesn’t seem to be any harm that I’m aware of, by eating GMO Whole Foods. Next, we’re going to talk about fat cells. And before we get into this, I have to preface this hypertrophy of fat cells or fat cells increasing in size, and then hyperplasia of fat cells is making new fat cells, what usually happens is at first, you get hypertrophy of fat cells, they grow in size until they can’t grow anymore, and then you get hyperplasia, we turn over about 10% of our fat cells per year when your weight is stable. And the amount is pretty much set by adolescents and remains constant in adulthood. Now, what is this talking about? Well, there’s a myth. And I think I said this on the podcast, or maybe it was one of my talks, where I said that once you gain these fat cells, it makes it easier for them to fill up again. But that’s not true. There’s actual human studies showing weight cycling doesn’t predict weight regain or weight loss in the future. So if it was easier to regain weight, after you have hypertrophied or hyperplasia, then this study would have showed the opposite. So that was something else I got wrong glycemic index and glycemic load. We’ve talked about these things. Glycemic Index is basically how something will impact your blood sugar compared to table sugar. And if it’s more or less than that, does it raise your blood sugar more or less than what table sugar does, and then the Glycemic Load takes into account a serving size to estimate the overall impact based upon one actual serving. This really only matters if you’re eating carbohydrates in isolation. Eating protein and eating fat with your carbohydrates slows down the carbohydrate absorption and evens out the release of sugar carbohydrates into the blood. A recent systemic review examining glycemic index on body weight cardiovascular disease, diabetes, there was insufficient evidence to support incorporating low glycemic index alternatives to energy restriction for weight loss. And in controlled studies where calories are matched, there’s no difference between low glycemic index and high glycemic index diets on body weight. The moral of the story here is what I tried to do is whenever I eat carbohydrate, I eat it with protein, and a little bit of fat. So let’s say I’m traveling, for instance, to the airport, I’ll usually grab like pistachios, maybe some beef jerky, and then dried fruit and that’ll be my snack. And that way I have fat, carbs, protein together, I always try to eat protein whenever I eat excess protein. This is a myth that I propagated back when I was one of those keto zealots. I will fully admit that I was a low carb keto zealot, I’m not now we talked about that before. My current macro ratio is about 40% carbs 30% protein 30% fat in the Keto circles, it said that excess protein is turned into carbohydrates and will increase blood sugar. And the reason they say this is because some proteins like leucine are ketogenic, they will make ketones. Others are gluconeogenic. So some of these proteins can get turned into blood glucose. However, in human studies, protein intake has little impact to no impact on blood glucose levels. On average, the human body recycles about 200 to 300 grams of protein per day, if you eat more protein than you actually need. And at a minimum, we need about point seven or point eight grams per pound of body weight. I eat about one to 1.2 grams per pound. That’s what I eat in protein. So if you eat more protein than your body actually needs it gets converted to nitrogen is excreted in the feces and the urine. Very little, if not none, gets converted into carbohydrate. This is the same thing like we talked about with carbs, a very small amount less than 5% of excess carbohydrate rate that you eat is turned into fat. While people say, Well, how do I gain fat then we eat fats in our diet. And I’m not saying don’t go and eat no fat because you need about 20% of your caloric intake at a minimum, to be fat because there are essential fats. And we need fats for certain life sustaining functions. So too little fat is going to mess up your hormones mess up, organ function, brain function, all of that. But what happens is when we over consume calories, what gets stored is basically the excess fat. So again, I’m not saying go low fat, no, I’m getting 30% of my calories or so from fat, good fats. But the whole purpose of this was this myth that excess protein will turn into carbohydrates is just that a myth? And it’s unfortunately, a myth that I propagated. Obviously, if you’re listening to a lot of these things that I got wrong, most of it was about nutrition. I thought I knew a lot about nutrition. Q Dunning Kruger, I really didn’t know anything. And so I’ve really been applying a lot more scientific rigor to these podcasts. And to my talks, like this talk about appetite. I believe there’s 20 Something studies in the folder that I had to go through. So let’s dive in. Let’s dive in on appetite. The first thing I want to talk about appetite is our stomach. Of course, our stomach is where food gets digested goes into small intestine. Nutrients get absorbed large intestine pulls water and then you poop. That’s a basically a simple explanation of what’s going on. But stomach distension activates the vagus nerve. We’ve talked about the vagus nerve before, this goes to the brainstem and induces a feeling of satiety to reduce meal sizes. This actually takes some time, it’s one of the reasons why eating slower, especially if you’re trying to lose excess body fat is a good thing. Eating slowly has been associated with up to 100 calorie reduction per meal. And we’re going to talk about fiber and water in a minute. But these things can help with mechanical distension of the stomach to help you feel more full. Next, let’s go up to the brain. Because a lot of what happens with our appetite is coordinated in the brain. So there’s an area called the ventral medial hypothalamus. And this controls a lot of what we’re seeing with feeding behavior. lesions in this area can make animals or people ravenous or not want to eat it depends on which part of the hypothalamus is injured. We’re going to talk more about the hypothalamus here in a second. There’s another area in the brain called the insular cortex, the insular cortex gets signals from your mouth, about whether you enjoy what you’re eating. And this is like the tactile sensation of eating. Some people really liked the act of chewing people who chew gum or people like me, I really liked the act of chewing, I was a person who used to chew straws until they were like paced back in the day. And this can lead to something we call hedonic eating. And this is something we’re eating is uncoupled to energy reserves. We’re gonna talk about that more back to the hypothalamus. There’s an area in the hypothalamus called the arcuate nucleus. And this releases chemicals that can act as accelerators, or the brakes on appetite. Accelerators we call orexigenic. And brakes we call anorexigenic. And this just basically means does this increase your appetite or decrease your appetite? One of these areas called the PO MC neurons, we actually talked about these neurons in the stress episode, because these make something called melanocytes stimulating hormone. And what this hormone does is it reduces appetite for this activity, and these pathways go up when we have eaten, so they’re activated by leptin inhibited by ghrelin. We’re going to talk about those more in a minute. But if you’ve been listening to the podcast, you know, we’ve talked about leptin, we’ve talked about Grillon. It also stimulates TRH thyrotropin releasing hormone, we talked about that in the thyroid episode to increase metabolic rate. After you eat, you want to burn off those calories, so it makes sense to release thyroid hormone to help enhance our metabolism to burn calories. What also happens here is we helps in the browning of fat, we’ve talked about how brown fat is metabolically active. And then we also get a release of free fatty acids. This is important for a negative energy balance. You want to release the fatty acids from the fat cells. You don’t want to store more and you’ll also get an increase in thermogenesis which is heat generation from metabolism exercise, both anaerobic anaerobic can increase alpha MSH. We’re going to talk more about exercise and appetite later. UV light to the eyes can actually activate this and suppress appetite. And one of the things that you see is pretty interesting is that you see seasonal variations in appetite. People tend to eat less in the spring and summer and eat more in the winter. So you often hear in the bodybuilding circles I’m gonna do a bulk this winter, because people naturally tend to eat more during the winter because they’re outside list. Another group of neurons here are called the AgRP neurons and this stands for a gooty related protein. When you approach food or are excited about food, or in a non fed state, you get a release of this AgRP and something else called neuropeptide Y to stimulate appetite. neuropeptide Y also delays satiety and increases feeding time. This pathway is inhibited by leptin, it’s activated by ghrelin. It’s also activated by dips in our blood glucose. This pathway also stimulates the HPA access to release those things we talked about in our HPA access podcast, CRH, ACTH, and cortisol, it inhibits trht to lower the metabolic rate that makes sense if you’re hungry, if you’re don’t have the all the nutrients and the energy on board, it doesn’t make sense to have a really high metabolic rate when you don’t have the energy to support that. It inhibits the MSH. From the PMC neurons, it stimulates adipogenesis. So storage of body fat. And then obesity and chronic over eating leads to leptin resistance in this AgRP neurons, we’re going to talk about that leptin resistance is very important, because it means that we’re not getting the satiety signals that we should from food. Let’s move on to ghrelin and medical school, they told us ghrelin means growling, it’s released mostly by the stomach, about 60% of it. 40% is released by the small intestine, and the signal to release ghrelin is reduced blood glucose levels, glucose levels have arranged for all of us and they fluctuate. And then what happens is when blood glucose goes down, you release something called glucagon. We’ll talk about glucagon in a minute. And during these blood glucose dips, this may stimulate a little bit of release of ghrelin to make us hungry. And also you’ll get a pattern to your grill and release. So if you eat at certain times of the day, if you’d like to eat a particular time of the day, you will start to secrete growing around the same time as you regularly eat. And this is something that can actually help you regulate hormone signals by trying to eat around the same time each day. And if you want to try to change the time at which you eat, you have about a 30 to 45 minute window to change that time. So if you want to start eating at let’s say noon, and you eat at 10, we’ll do 1030 Then 11 Then 1130, then 12 Grohmann has other functions like it also stimulates gastric acid secretion, pancreatic output. It has numerous other effects, like promoting bone formation, neurogenesis myogenesis. So that’s nerve cell growth, muscle growth. It also helps with the sleep wake rhythm, it stimulates the release of growth hormone and in high doses also stimulates the HPA axis. Ghrelin may also inhibit adiponectin we’re going to talk about adiponectin in a minute and promote adipogenesis which is storage of fat and prevent lipid export on insulin resistance the data is mixed for ghrelin ghrelin exists as two forms ag and D ag 80 to 90% of ghrelin is D AG. ghrelin levels are negatively associated with insulin resistance and obese people with a normal fasting glucose. However, if fasting glucose was high, there was no association with ghrelin levels, procedures like gastrectomy, so removing all a part of the stomach reduces ghrelin levels by 50% immediately, but this returns to 70% of normal levels. After some time, you get a compensatory release by other tissues, we talked about how 40% of grilling was released by small intestine so it’ll increase ghrelin, release, obesity and hypercaloric. Feeding decreases grelle And this is what’s supposed to happen as you overfeed, you’re supposed to get less signals to be hungry, but we know that that doesn’t actually happen in a lot of people, and they can eat disconnected to their energy balance. Grillon seems to primarily want to induce fat intake, and it’s really suppressed by fat intake. It’s one of the reasons why you have to have a balanced intake of good fats we talked about in the intro, I get 30% of my calories from fat 40% from carbs 30% from protein, and when you eat you want to eat a meal that contains protein, fats and carbs, because that’s going to help you regulate your overall appetite pathways. As you’re gonna see, as we go through this, leptin counteracts ghrelin, so leptin reduces ghrelin secretion. Let’s talk about CCK or Colusa cytokinin. We’re gonna call it CCK. It’s made in the small intestine, but also is made in the pituitary, thyroid and adrenals. Those. What this does is it helps a gallbladder empty. It also helps the pancreas secrete the pancreatic enzymes to help with digestion. It stimulates intestinal blood flow. So if you’re one of the people like me who gets the itis who gets sleepy after they eat, you’re a person who gets significant intestinal diversion. So after you eat, your body says, Hey, there’s nutrients here that need to be absorbed into the bloodstream. So you divert blood flow to your intestines, and you get sleepy. I’m one of those people, especially after lunch. I get sleepy after lunch, and it’s one of the reasons why I have green tea, or I take a walk outside to help reinvigorate me after lunch. CCK is involved with intestinal blood flow and motility. It also delays gastric emptying gastric emptying is literally what it sounds, the rate at which food comes out of your stomach into the small intestine, where in the small intestine is where we absorb the nutrients and vitamins CCK blunts appetite by signaling signals to the hypothalamus from the vagus nerve to help keep from over consuming foods. It inhibits those AgRP neurons that we talked about earlier, it’s released is mainly governed by nutrient sensing cells in the gut. We’re going to talk about this more in a minute. So just remember that the mucosal lining of the gut and the microbiome are very important in the actions of CCK. CCK may also help facilitate leptin uptake into the brain. It’s stimulated by fatty acids, especially omega threes and CLAS. We’re going to talk about those more in a minute. essential amino acids and carbohydrates. So omegas, we’ve talked about omegas. On the podcast a lot. You can get those from fatty fish, walnuts, chia seeds, flax seeds, pasture raised eggs, CLAS, or conjugated linoleic acid. We’ve talked about CLAS before on the podcast, they’re used a lot by body builders to help with muscle and also for insulin sensitivity. You can get these from things like grass fed beef, full fat dairy, we’ve talked about full fat dairy, I get my whole milk Greek yogurt every single morning and pasteurized eggs. Amino acids, especially glutamine. Glutamine is a conditionally essential amino acid. What do I mean by conditionally essential, it means that normally we make enough glutamine to cover what our bodies need. But during periods of stress, we can’t. And so we actually need the glutamine from our diet. That’s what it means by conditionally essential glutamine. It’s phenomenal. I take five grams of glutamine every day as part of my pre workout, it can help with gut integrity gut cell health, it’s good for the immune system. Glutamine may also help reduce cravings by increasing something called GLP. One This is a molecule that belongs to a family that we call incretins. But we’re gonna talk about GLP. One more in a minute, glutamine can reduce ghrelin levels. Glutamine also seems to help normalize the f to be the Firmicutes to bacteroides ratio. Herb acuities really likes carbohydrates. And we’ve talked about this before our gut bacteria can influence our nutrient choices because they make neuromodulators Some studies show that increase FTB ratio happens in metabolic dysfunction. Others do not let’s move on to leptin. Leptin is made from adipose tissue mainly, and most of it seems to come from our subcutaneous, the adipose tissue beneath our skin and not the visceral around the organs. Leptin decreases when fasting or energy restriction and it increases with feeding or refeeding or stress. Leptin inhibits those AgRP and neuropeptide Y neurons, it stimulates the peel MC neurons to relieve alpha MSH it also reduces ghrelin secretion, as we talked about earlier, if you increase your adipose tissue since leptin is released from adipose tissue, you will get a proportional increase in the secretion of leptin. There is actually a genetic condition where you have profound leptin resistance, and this causes extreme obesity, as found that about three to 5% of people with extreme obesity. What this means is Leptin is a satiety signal, it’s a signal that we are full, these people have extreme resistance to that signal, so they don’t get signals that they’re full and they just ravenously eat insulin is a primary regulator of leptin secretion, but so does GLP one and what happens is long term hyperinsulinemia. So insulin resistance increases leptin levels, short term does not hyperphagia over eating and positive energy balance can lead to leptin resistance. So can corticosteroids and inflammation. TNF alpha can also stimulate leptin synthesis catecholamines, so things like adrenal When can inhibit leptin synthesis and so do thyroid hormones. Now, what does this mean in the picture of things, if you have too high leptin levels, for a period of time, this leads to leptin resistance. And if you have leptin resistance, it’s going to dis regulate your appetite. So leptin is very important in the overall control of energy balance, and the overall control of appetite GLP one, we’ve talked about GLP. One earlier, this is a molecule that is released in the gut, it slows gastric emptying, it decreases hepatic glucose production, it increases insulin release, and insulin sensitivity in the muscles, you probably are familiar with GLP one but you didn’t realize it. This is how medications like ozempic medications like we go v semaglutide. This is how it works, these medications can induce profound weight loss and clinical studies up to 15% of people’s body weight. How it does it is it curbs your appetite, because of slowing gastric emptying. And because of increasing for a lot of people who are insulin resistant insulin sensitivity, which is going to help with leptin signaling, this is going to help you better be able to match your energy needs with your energy intake. And so these medications are very popular now. The side effects are why people often discontinue them. And you can get profound nausea and vomiting, constipation or diarrhea, will how. So again, most people overeat to the tune of around 500 calories per day. But we also overeat when we consume meals, and we eat too fast. So if you’re getting something that’s slowing gastric emptying, and you’re over consuming food, you’re gonna feel terrible. Think about it, you just keep putting marbles in your stomach as it expands and it’s going to feel horrible and you’re gonna get nauseous, you’re gonna vomit, you’re gonna either get constipation or diarrhea. Whenever I put people on these medications, I use them short term, I tell them you have to change your eating habits. If you eat like you ate to get you here, you’re gonna feel pretty terrible. The main signal for GLP one release is carbohydrate absorption in the gut. Insulin, we’ve talked about insulin, a lot of times on the podcast released by the pancreas, and it’s mainly stimulated from glucose. When glucose levels in the blood increase insulin is released. There is some stimulation from protein it kind of depends on the protein, and there’s very little by fat. And this is a sidebar, but you’re given bread first at a restaurant, since it’s mainly carbohydrate with very little protein. And this will increase your blood glucose level and it’ll actually make you want to eat more glucose rich foods. So it Prime’s your appetite, kind of it’s a teaser for the main meal. We’re going to talk about taste in another podcast because that’s a whole different mechanism. And how insulin is involved with our appetite is it can reach that arcuate nucleus that we talked about, where it acts as a signal for satiety, it prevents the release of AgRP in neuropeptide Y. But if you have insulin resistance, it can dis regulate this pathway. So insulin resistance as

Dr. Richard Harris MD  28:24

we talked about, we talked about this. Oh no. We’re

Dr. Richard Harris MD  28:28

going to talk about this spoiler. Insulin resistance overall doesn’t change your metabolic rate. People who are insulin resistant actually have a higher metabolic rate. But what it can do is it can change your food intake glucagon, glucagon is released in response to decreasing blood sugars, and it tells the liver in the muscles to put glucose in the blood. The effects are transient. It can cause a profound increase in blood glucose and it normalizes within 40 minutes. What’s interesting about glucagon is it decreases feeding behavior by stimulating AgRP neurons. And this may be why exercise makes you less hungry. We’re going to talk about that later. In animal studies. Injecting glucagon directly into the brain lowers blood glucose, probably because it changes feeding behavior and feeding refeeding studies in animals. High protein intake increases glucagon but lowers blood sugars. And maybe one reason why high protein diets are more satiating is because you get more glucagon release to decrease feeding. overfeeding in rats is associated with hypothalamic glucose resistance. So, again, the glucose resistance in this regard is going to cause some issues. Cortisol, we talked about cortisol in the HPA Axis podcast. We’re not going to rehash all about cortisol and HPA access, but cortisol and corticosteroid stimulate neuropeptide Y release And anybody that been put on high dose steroids knows this because you get put on high dose steroids. You are ravenous, you’re starving. And so that’s what I tell people when they go on high dose steroids is it’s gonna make you hungry. But you don’t actually need more energy intake, because we all know that the elevated cortisol level, prolong causes storage of central body fat, which we know is very dangerous for us. adiponectin adiponectin is a adipokine adipokine are hormones released by fat cells. So this is a hormone released by fat cells. It’s most active on skeletal muscle in the liver where it promotes fat oxidation, we’ll call beta oxidation. This is turning fat into energy and to ATP. It increases insulin sensitivity. It inhibits the liver making new glucose gluconeogenesis. It protects blood vessels. Interesting enough high levels of adiponectin people have a lower risk of heart attack, even after adjustment of several risk factors. And it reduces oxidative stress. So higher levels of adiponectin is a good thing. It’s activated by PPE, AR gamma, and SRT one. We’ve talked about these genes. These are genes associated with beneficial changes in longevity and metabolism. It’s activated during periods of caloric restriction. It activates a MP kinase. We’ve talked about a&p kindness, that’s a cellular metabolic sensor basically, is how you can think of that. It’s decreased by insulin, and it’s decreased and insulin resistance is decreased in type two diabetes and obesity is decreased in hypertension and dyslipidemia. So these disorders, dyslipidemia, diabetes, obesity, hypertension, are metabolic disorders because they impact our metabolism. And so you have to treat these as such. And we know, we’ve talked about this on the podcast that metabolic disorders long term do not respond. Well. Two medications. We’ve talked about the medications and hypertension, we talked about the medications and diabetes. No, actually, we haven’t talked about the medications and diabetes, but we talked about the medications for dyslipidemia. For adiponectin. The ratio of our macros seems to matter, eating a high carb low protein, this was 64% carbs 18 Fat 18 protein has lower adiponectin than 46% carbs, 36% Fat 18 protein. So by having the right ratio of carbs and fats, you can increase your adiponectin levels. adiponectin is also increased by dietary fiber omega threes. It’s lowered by high intake of saturated fat adiponectin increases satiety by activating PMC neurons, and it’s synergistic with leptin, it inhibits neuropeptide Y and those AgRP neurons that we talked about. However, these effects may be reversed under conditions of high glucose. And so this could be another reason why insulin resistance is kind of a self fulfilling prophecy and a dysregulates feeding, which can lead to more insulin resistance. We’re gonna talk about peptide yy, or py. This is mostly produced in the distal intestine, it slows gastric emptying, it increases water and electrolyte absorption, and also seems to protect the pancreas beta cells from destruction. levels are low during fasting but they rapidly increase after food and remain high for several hours. It’s mostly stimulated by the short chain fatty acids produced by our gut bacteria. So in addition to the mechanical effects of fiber being satiating, this is also why fiber may be more filling. Because these short chain fatty acids are made from the fiber we eat. By our gut bacteria. We’ve covered this extensively butyrate being my favorite one, and P yy decreases appetite. infusions of poi in humans has been shown to increase energy expenditure and fat oxidation. circulating levels are associated with postprandial energy expenditure, so meaning energy expenditure after you eat, and py may be one of the things is largely responsible for the thermic effect of food that we’ve talked about. The thermic effect of food is it takes energy to make energy. So as you’re digesting things, you need to put energy in the system to get energy out, and mixed meals. The thermic effect of food is about 10% of our total daily energy expenditure.

Dr. Richard Harris MD  34:43

High protein can increase that a little bit protein has a higher thermic effect of food, animal and human studies show obesity is associated with lower py levels. And this seems to work through the arcuate nucleus in the brain playing a central role in appetite suppression. So It’s another very important modulator and we’ve talked about several modulators already so you can see how really regulated and how complex our appetite pathway is and we’re not even done yet. Androgens sex hormones, androgens may increase appetite in rats. Giving them testosterone increases the number of meals but not the size of meals. And it seems to be that testosterone levels correlate with ghrelin levels. However, giving testosterone supplementation to men in a state of energy deficit, decrease ghrelin in one study but did not change appetite. And women with higher androgen levels have been associated with dysregulated eating and more craving for carbohydrates and fat. What’s a condition and women this dysregulates androgen levels PCOS, we often see PCOS come with obesity. We also see PCOS come with insulin resistance. So these are all conditions independently that can dis regulate appetite. estrogens. estrogens may diminish appetite through actions in the brainstem and the hypothalamus. Estrogen seems to potentiate the effects of CCK and attenuate the effects of ghrelin, it stimulates the PIO MC neurons to suppress appetite and it inhibits the neuropeptide Y and AgRP neurons, progesterone and pharmaceutical doses in the presence of estrogen may stimulate appetite for some, it may do so by reducing CCK however, randomized control trials so no difference in BMI or weight with oral contraceptives versus placebo. And hormone replacement therapy may also prevent the shifting of fat from subcutaneous to visceral abdominal fat, which is a good thing. There is some variation cyclical variation depending on the menstrual cycle and ovulating women. food intake is less before ovulation when estrogen is high. And it increases after ovulation when estrogen and progesterone is high. Thyroid hormones, thyroid hormones, animal studies show that TRH and TSH decreased food intake while T three increases food intake if you want to know more about the thyroid, listen to our thyroid podcast. And this likely works the T three on peel MC bye inhibiting those PMC neurons and activating those AgRP neurons, the opioid system and the ECS both things that we’ve talked about. This system seems to be involved in the hedonistic eating basically eating for pleasure eating that is disconnected from energy needs. And this goes through an area called the nucleus accumbens, and this is an area in the brain. This areas involved in motivation, desire, reward pleasure, it plays a key role in addiction. Also, the system works on the hypothalamus, the control center, the aggregation center, and the hippocampus, which is a memory center. Animal studies show that stimulating the ECS increases appetite while inhibiting the opioid system increases appetite. And we’ve seen this in humans. So how do you stimulate the ECS in humans to THC? What happens when some people ingest or smoke THC and they get the munchies. There’s a medical drug that has THC in it that we use for cancer patients who are losing weight to stimulate their appetite, and then in the opioid system. So the drugs that we have for pain work on the opioid system, they stimulate the opioid system to provide pain relief. And one of the things that you’ll see is people who are using these medications say they’re not as hungry. But the thing about hedonistic eating is and this is very important, these systems can be regulated by higher brain systems cortical systems. So the hedonistic impulses can be controlled, you can learn to control these cravings, and dissociate, pleasure eating from actual eating because you need the energy and we’re going to talk about one of the main things that causes hedonistic eating. It’s ultra processed foods, spoiler alert, obesity, obesity causes a dysregulation and CCK and GLP one, you get less release of these in the presence of fat and carbohydrates. However, protein sensing is intact. We talked about how for CCK and GLP nutrient sensing is very important for their release. So CCK needs to sit and GOP needs to send certain nutrients coming through the GI system to be released. The neurons that release these things need to send certain nutrients is what I should say. However, in Obesity, that sensing is altered and you get less CCK and less GOP to fats and carbohydrates, but protein sensing is intact. This is important. This is why when people are trying to lose adipose tissue lose body fat, a lot of us recommend high protein intake. Because protein is more satiating, and people who are obese, that pathway is still intact, so they’re going to feel more full with appropriate protein intake. Also, the data shows that people who are obese tend to get more hedonistic pleasure from eating than lean individuals. But I’m not saying that this is a cop out. I’m not saying this as an excuse, because again, top down control. You can learn to control your cravings, you are in control, not your cravings, the gut microbiome. The gut microbiome, of course is very important in like everything that we do, and of course, it would be very important in appetite, gut microbiome metabolites can induce the secretion of GLP one, what happens if you have dysbiosis is you can get a disruption in the mucous layer certain bacteria. If they overgrow, will eat the mucus that coats our intestinal lining. So that mucus is there to help for protection is to help keep bacteria and other things that aren’t supposed to get close to ourselves from getting close to ourselves. And disrupting that mucus layer is going to disrupt the release of these intestinal peptides like CCK and GLP. What also happens with dysbiosis is you get a preference for gram negative bacteria. We’ve talked about this before. And these bacteria have something called LPS lipo polysaccharides. They’re on the outside of the cells of the bacterial cells. And these LPs are toxic to us they induce inflammation. And what happens with LPS is especially if they LPS is able to break free and get out of the gut. So leaky gut, it can reduce vagal nerve sensitivity to CCK and leptin.

Dr. Richard Harris MD  42:19

So it’s going to reduce satiety signals. This is one of the reasons why dysbiosis is associated with obesity, and ultra processed foods. Personally, I don’t eat much Ultra processed food and if you’re wondering what an ultra processed food is, look at the Nova classification. That’s a classification that most studies use Nova and OVA, ultra processed foods disrupt our appetite for several reasons. Number one is the emulsifiers emulsifiers are found in processed foods and even some of the processed meats and there are natural ones and there are manmade ones. The natural ones are things like locust bean gum, pectin, starch carrageenan. xanthan gum, the soil ethicist is another one. The man made ones are things like CMC, carboxymethylcellulose and polysorbate 80. The role of emulsifiers is to help keep fat and water together. fat and water don’t like to be together. You put something fatty like olive oil and water, what happens it floats to the top they don’t mix. These emulsifiers are not well absorbed. And they’re mostly excreted in the feces. So when they first did safety studies, they’re like, well, they’re not absorbed, they’re non toxic. Well, a study from this year it was a feeding trial with carboxymethylcellulose and healthy participants for two weeks. found some interesting things. Now, it was a short study that didn’t find any difference in weight, inflammatory markers, gut permeability, there was an increase in abdominal pain. One of the number one things that we hear as primary care physicians is bloating. People come in with bloating all the time. You’re not always supposed to be bloated. I mean, something’s going on with your gut. So this study did finding an increase in abdominal pain for the people who were in the carboxymethylcellulose group. There was also a change in gut bacteria. There was a loss of a bacteria called F procs. Nitze and I probably butchered these pronunciations. I’m not a pronunciation guy. I’m sorry, that just is what it is. This podcast is real. You get the real meat, which makes short chain fatty acids. And what did we talked about earlier that short chain fatty acids help with the release of py peptide yy, which is an important satiety signal.

Dr. Richard Harris MD  44:50

Source chain fatty acids are associated with metabolic improvements. They also found in this study that the CMC group had decreased microbial richness So diversity of species There’s no change in one inflammatory marker in the feces. They also showed a decrease in overall short chain fatty acid levels. And they also showed a decrease in essential amino acids by the third and then two out of the seven people in the CMC group had reduced microbial mucosal lining. So these are all things that could impact our satiety. We talked about short chain fatty acids, we talked about how amino acids nutrient sensing is necessary for release of things like GLP and CCK. We talked about how disrupting the mucosal lining could impact the release of these intestinal peptides. The main caveat with this study is the dosage likely exceeds what all but the highest quartile of ultra processed food intake would have. But the average American gets 65% of their total caloric intake from ultra processed foods. And it’s really hard to tell how much of these things are in foods the information is very sparse. Animal studies, with emulsifiers showed damaging to mucosal lining, increased gut permeability, changes in nutrient sensing, so you get less CCK less GLP one less py why it theoretically from these changes? Now there’s no human studies showing that things like polysorbate 80, for Carageenan, or Leveson are dangerous. People who will say these things are dangerous are quoting animal or mechanistic studies. I couldn’t find any human studies saying that these other ones are dangerous. I only found the one on CMC. What else about Ultra processed foods, there’s lots of refined sugar. And these refined sugars can make you want to eat more simple sugars. And we talked about how in the presence of high glucose, the effects of adiponectin, which is a satiety signal is blunted. We also talked about how Ultra processed foods are linked to dysbiosis. And we’ve talked about in this podcast, how changes in gut microbiome can be associated with changes in appetite. These foods also are easier to eat. Like what’s easier to eat a Snickers bar, or broccoli, Snickers bar, that stuff like literally melt in your mouth, it’s actually more pleasurable to eat because of the way it’s composed. So it activates this hedonistic eating, and it’s going to dissociate, eating from energy balance. If you will not eat broccoli, I don’t care how much you like broccoli, if you’re not hungry, it’s just not gonna happen. But you will eat chips, or Snickers or something if you’re not hungry, which is why I don’t care how much willpower you have. If you’re trying to make changes, get him out of the house, one of the things I recommend is if you know you have problems making good decisions at the grocery store, when that stuff is right in front of you, because visual cues are very important. We’ll talk about that in a minute. If you order your food online, you get rid of the visual cues at the store, you will make better decisions if you use Instacart. than if you are actually in the grocery store with that item right in front of you. I guarantee it. What else about these ultra processed foods? We talked about how your gut neurons can detect sugar and will tell your brain to eat more of these types of foods. And the problem with Ultra

Dr. Richard Harris MD  48:23

processed foods is they’re devoid of nutrients. We’ve talked about this. They’re low in protein, they’re low in fiber, they’re high in refined fats, they’re high in refined sugars. One study from 2019 had people on a isocaloric nutrition plan. The only difference was one was from ultra processed foods. And the other one was from Whole Foods. And they matched calories. They met sugar, they match fat, they match fiber, they match macros, and the people were told eat what you want, like how much you want, and the ultra processed foods group ate 500 more calories per day and had negative body composition changes. This is human study prove that eating Ultra processed foods is linked to overconsumption of calories and over consuming calories is a great way to make yourself sick. Let’s talk about things you can do to help balance your appetite. Exercise. I mean, we’ve talked about exercise with like every single condition on the strive for great health podcasts exercise is so important to our overall health. And you would think that exercise would make you more hungry, right? Wrong. Overall short term exercise seems to induce energy deficits without stimulating appetite. Long term exercise seems to enhance meal induced satiety and these are based on meta analyses. Chronic exercisers are better able to regulate their energy intake based upon differences in activity levels. So your energy needs per day are going to be different. But if you exercise you’re better able to sense the cues that your body makes. In fact, a recent study came out and said that for people who have diet resistant changes to body fat percentage, if they exercise, that resistance went away, likely because people who exercise are better able to regulate their energy intake plus there’s a whole bunch of other metabolic benefits that happen when you exercise you sleep better, your moods better, things just improve overall. A 2015 meta analysis showed acute exercise reduces ghrelin increases py GLP. One. These are all things that are going to improve satiety. A meta analysis looked at hunger and energy intake in obese individuals with exercise and found no increase in energy intake with exercise. They found a small increase in fasting hunger, and they found a decrease in disinhibition. This is really important. The decrease in disinhibition also came with a small increase in dietary restraint, as well as an increase in mealtime satiety. The authors theorized that exercise may also help improve food reward and food preferences. And it may also decreased compensatory effects seen with dieting alone. And this is likely due to exercise being a keystone habit. We’ve talked about this when you start exercising, other things in your life typically start to improve. And you start to layer beneficial habits you just layer positive habit, positive habit, positive habit. This is why I am so keen on exercising if you’re someone who struggles with their appetite and you’re not exercising, start exercising. Now one of the things that people will talk about is fasted exercise versus non fasted exercise. Let me back up for a minute. There’s one more meta analysis on this with exercise, and people who are older than 60. And it showed similar results. So age is not an excuse. fasted exercise versus non fasted exercise. You have higher energy expenditure during exercise when you’re fasted, but you’re more hungry throughout the day and you have lower energy expenditure later. This was proven in one study. So I tell people do your exercise how you feel most comfortable doing exercise. fasted exercise, fasted cardio is not better than being in the Fed state. Now me personally, if I have food in my stomach, I’m gonna have a horrible workout. So I have a pre workout, I make sure I get some protein, some ketones in my pre workout, the proteins, leucine and glutamine. And then I have my Greek yogurt with protein powder and peanut butter and chia seeds, a little bit cacao powder afterwards. Now there is a caveat with this whole exercise and appetite thing. There can be large variability between people and exercise intensity and exercise type. Which means that not everyone will get less hungry. But overall, the data shows overall, that it helps regulate our appetite pathways positively, what are some dietary changes that you can make to make sure that your appetite is in line with your energy needs. So

Dr. Richard Harris MD  53:18

your energy balance, eat slowly. It takes time for these signals to be generated. It takes time for that mechanical distinction to happen. How many times has that happened you where you ate super fast, and then you get to a point you’re like, oh, I shouldn’t have been that much and then it gets worse. Eat slowly. Let the signals come enjoy your meal enjoy your company. Another thing that you can do is pre drink water. One study show that pre drinking 500 milliliters which is 16 fluid ounces of give or take of water within 30 minutes of a meal decrease the amount people ate and a meal again that mechanical distension is equivalent to about 1.5 cans of soda, you know as a reference, not endorsing you to drink soda. We talked about soda here on the podcast plenty of times, eating more fiber. We talked about fiber mechanical distension. We talked about fiber and short chain fatty acids made from our gut bacteria and py how much fiber you need about 14 grams of fiber per 1000 grams of calories that you eat. That’s how much fiber you want to get protein. We talked about how nutrient sensing is very important in that protein is the most satiating. It makes us feel more full of all the macronutrients. At a minimum you want point seven grams per pound of protein, daily. The only caveat here is if you have kidney disease, I eat one to 1.2 grams of protein per day because I’m very active. I’m still lifting I want to maintain my muscle mass. Here’s one, let’s turn off the TV and pay attention to what you are eating. You are less likely to overeat so many people distract themselves while they’re Eating. One study had people eat in the dark and in the light, and some people got a supersize meal. Those who ate in the dark 830 6% More food. However, they had the same desire for dessert and satiety was unchanged. They 36% More food because they couldn’t see their meal. They weren’t paying attention to it. And then their desire for dessert and their satiety were unchanged. So pay attention to your food, slow down your eating, listen to those brain signals. And I love this one because this is exactly what I do. eat dark chocolate after meals I do the Endangered Species dark chocolate, I eat one piece with a date after meals cuts my sweet cravings you will not have sweet cravings if you eat a date. Eat a piece of dark chocolate. One study found energy intake was 8% Lower after eating dark chocolate compared to milk chocolate. And this may be due to the higher healthy fat content and protein content and dark chocolate which could lead to an increase in some of those intestinal peptides. We talked about CCK GLP one NPY there’s a lot of benefit to the molecules, the flavonoids the antioxidants in dark chocolate. There are studies linking improve brain function, lower cardiovascular disease to dark chocolate now you have to be careful because it does contain a lot of fat so you can overeat it. Pay attention to those serving size pay attention to those calories. What about supplements This is our final portion of this long discussion you have Amati your MATA is a herb from South America It stimulates the release of GLP one and helps regulate leptin. It also has electrolytes and has caffeine. One study showed that two grams per day was associated with improved measures of appetite. As a powder, you can take one to two grams per day it has caffeine so be aware of your caffeine intake. But caffeine is also beneficial for our appetite. Caffeine increases beta oxidation, fat burning and suppresses appetite. So caffeine consumed 30 minutes to four hours before meals lowers appetite, daily caffeine consumption, and one study had a slight decrease in energy intake by about 50 to 100 calories doesn’t see much per day, but that’s 700 calories per week. That adds up caffeine also increased energy expenditure by about 100 calories a day. And I suggest if you’re gonna do this, do it as coffee or tea not something loaded with sugar, not something like an energy drink. Because the caloric density of those may outweigh the benefits. You could also just do pure caffeine is like a caffeine tablet if you want it to caffeine may slow gastric emptying and may also increase GLP mpy. It may also work by increasing dopamine and serotonin so beneficial effects on mood. However, the dose for this seems to be high, it may be around 300 milligrams of caffeine for effect, which is close to the maximum daily recommended amount 400 milligrams. I don’t take that much caffeine I do about 100 in the morning, and then 50 after lunch. I’m really sensitive to elevated caffeine I get super jittery, but increasing serotonin has some benefits. So actually taking five HTP, the precursor to serotonin. There are also other serotonergic herbs on the market that have been used for this purposes that had clinical data behind them. But a randomized controlled trial and humans have shown that supplementation with five HTP can decrease sweet cravings hunger levels, lower appetite and increase fullness. Serotonin activates those peel MC neurons and inhibits the neuropeptide Y and AgRP neurons. Another way you can get serotonin get some sunlight. However we talked about earlier sunlight activates the PIO MC neurons as well as the dose in the studies was 750 to 900 milligrams a day at five HTP. And we talked about how CLAS can stimulate satiety. So you can take it as a supplement 3.2 to 3.6 grams per day of CLAS and clinical studies lowered appetite and improved satiety. It may also help reduce body fat, and it helped with insulin sensitivity. And the mechanism here is increasing CCK okay, this was a long episode, there was a lot of information, but I really wanted you guys to understand the science of appetite, because over consuming calories, especially over consuming Ultra processed foods is making a lot of people sick and how can you make better decisions about eating and controlling your eating if you don’t understand how the pathways work? So now you understand appetite. You’ve been given some tools that you can use to improve your appetite if you’re someone struggling to lose body weight or maintain a healthy body weight.

Dr. Richard Harris MD  59:59

Again, I hope this was helpful. I hope this was useful. If you want to support the podcast, you got the tips in the beginning on how to do so. The link to our course will be in the description. It’s 4999 you get 10% off by using the code podcast. You can use it for yourself or gift to someone who could use lifestyle medicine to optimize their health. Thank you for listening to strive for great health podcast with your host Dr. Richard Harris. It’s our mission and goal at the podcast to impact as many lives as possible to empower individuals to take control of their health, and live a life full of joy and purpose. You may help us achieve this mission by leaving a five star rating and review on your preferred podcast platform. And by sharing this podcast with anyone you think it may help. If you want to support the podcast, the best way is to invest in your health or invest in someone else’s health through our five pillars of great health lifestyle medicine course. A link to that courses in the show notes. Thank you for listening and God bless

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