Click on “Chapters” at the bottom of the video frame above, to go directly to:

• strategy for shrinking fat cells is lower insulin
• 40% of this drug-induced weight loss is lean mass
• helping people getting off these drugs
• unimate increases fasting levels of GLP-1 by 60%
• unimate makes fat cells less efficient
• the next wave of these weight-loss drugs

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Transcript:

(00:24):
Now most people with the best of intentions, but born from total ignorance believe that it needs to start by cutting calories. That's the first step This person will take on their fat cell shrinking journey. They say, I got to cut the calories. Now there's a problem with this, which is if your first step on that fat cell shrinking journey is to cut calories, hunger will start to rear its ugly impassable head. Now let me, and you'll go right back to where you were. You'll make a little progress on the journey and you'll find yourself solidly back where you were before, if not even a little further back, and maybe your fat cells are even bigger than they were before you ever started. Now why is that? Let me just explain why that happens by using a metaphor. Let's imagine that Rob and Trent are hosting the most delicious buffet you can possibly imagine, and they have invited the world's best chefs to come and create the most delicious delectable foods you could imagine.

(01:29):
And on their invitation, Rob and Trent are saying, come hungry because you're going to want to eat some of everything. And we're all very excited to come to their party, not only because we want to see a big fancy house, but we want some delicious food. So we are determined to come hungry. What two things would you do? Would we do to make sure we went to their beautiful buffet as hungry as possible? There are two strategies. Just think about it in your mind for just a moment. But I bet if you narrow it down to two, you're going to come to two ideas. You're going to eat less in some period of time before you come to the event and you're going to exercise a little harder, a little longer. And sure enough, it will work perfectly. You will become very, very hungry. But can you see the problem with that two prong advice?

(02:20):
Remember the question I asked was, how can you come to the party as hungry as possible, eat less, exercise more? Does that advice sound familiar? Because for the past 60 70 years, that's all we've been telling people who struggle with their body weight, we tell 'em, you're overweight. You need to lose weight. In order to lose weight, you need to eat less, exercise more. Why does it fail? Why has it failed so miserably for the past three generations? It's because you start fighting hunger. That is a perfect recipe to tell the brain to panic and to have to eat. Now why does that happen? So many people don't understand this. If you have a scenario where the first step is cutting calories, but you have not addressed the high insulin, a weird metabolic response occurs within the body because insulin's main effect is to store energy.

(03:19):
That's what it wants to do what it does, and it affects every cell of the body. Every cell of the body has insulin receptors and its theme is telling every cell of the body store energy, take it in and store it because you don't know when we're going to need it later, which is a good thing. It's not a bad thing. So I don't mean to vilify insulin completely, but it's just most people have too much for too long. So in this scenario, a person just starts cutting their calories in order to shrink their fat cells, but they haven't addressed the fact that they also have elevated insulin. Now if there's less energy coming in, but insulin is trying to store the energy, guess which tissue insulin stores energy in the most? It's all this pinchable jig bowl energy, the fat tissue. So it's no surprise, and this happens, we know this happens in humans and animals.

(04:08):
If insulin goes up and energy coming in is down, it will start, it will still. Insulin isn't care. That energy is down, it doesn't know if it's elevated. It just continues to push the energy to be stored. Now, that's not bad for tissues like fat tissue or the liver or the muscle, even the kidneys a little bit. All of those tissues have the ability to store some energy that they can rely on, but there's one very important tissue that doesn't. And this tissue has a very high metabolic rate, and that is the brain. The brain doesn't have a reserve of energy. And so if insulin's telling all the other tissues of the body to store energy, the overall energy that's available in the blood, guess what happens? It starts to go down, but the brain must constantly be getting its energy from the blood. It needs to be pulling in these nutrients from the blood.

(04:59):
But if insulin's elevated, it can't because the total available energy has gone down. And so the brain panics and how do we sense that panic? It's hunger. Now in the most extreme circumstances, it's actually losing consciousness If it continues, that scenario continued. It's incompatible with life and the person goes, basically the brain says, it's better for me to shut down and lower my energy demands than keep operating at this high rate and then die. So in between that area is hunger. The brain is saying insulin has been forcing all of the energy into the fat and the liver and the muscle, and I'm left to get none, so I need to drive appetite. So the key then is to flip the paradigm around rather than start a fat cell shrinking journey by cutting calories, let the calories take care of themselves. Let that get addressed later and start my lowering insulin.

(05:56):
If the step on the weight loss on the fat cell shrinking journey to improve metabolic health and reduce the risk of all those chronic diseases, if the first step is lowering insulin, then the person starts to make a very sound journey. First of all, their metabolic rate will go up and not even their little we know in humans is that if people eat the exact same number of calories throughout the day, but the macronutrients particularly the carbs and the fats are different. Specifically lower carb people will have about 300 calories in excess with their metabolic rate. Anyone who tracks calories knows that's a lot. That is a lot of work to do. That's like an hour on a stair step I think, right? Has anyone attracted calories? That's a lot. That's a meaningful amount of time. Nobody wants to do it. I don't want to to do that.

(06:46):
I want to be in the lab doing some cool experiments or teaching a cool class for shaving my beautiful head. Oddly enough, I should take more time doing my hair now than I did anyway, true story. But nevertheless, I have time. I don't have time to be spending an hour on the stairs study, but if I just lower my insulin, I will burn the same number of calories as I would. So metabolic rate will go up if insulin is down. Second, we start to shift our fuel use over, and I've talked about this before. Many of you have heard me talk about it, where the body is a metabolic hybrid where it can rely at any moment on the two primary fuels, glucose or blood sugar or fat. So we're sugar burning or fat burning, and it is the hormone insulin that dictates which fuel is being used.

(07:33):
If insulin is low, the body's in fat burning and good luck shrinking your fat cells. If you're always sugar burning, it doesn't work that way. You must have times where your fat breaks. So that happens. We begin to use our own body fat for fuel. And just think about it, where I am in Utah, it's very popular for people to hike the mountain in Provo where I live, very common. They're hiking up this mountain to see this big letter for the university where I work, why mountain is called, and you'll be at the base of that hiking trail and I will see people who are overweight or obese and they have energy bars and energy drinks, and I just look at that and think that's what this is for. This is your energy bar. This is your energy drink. You just never let yourself use it because you're always shoving in insulin spiking energy sources.

(08:29):
That is what those fat cells are waiting for. And so if those people were to flip the script around or flip the paradigm, they would come to that state to that hike in a low insulin state and now all of a sudden distort fat is like a band of leader of energy bars where every time they need it, they're opening up another fat cell to tap that energy. Even a lean person has hundreds of thousands of calories stored on their body is fat. You can do a two mile hike without taking in some or three miles or whatever it may be. Let there be some takeaway for you when you are exercising, unless it gets to the order of hours, you shouldn't need to be eating energy or drinking energy. That's what this is for. Let your body use its own energy for fuel rather than you constantly putting it in.

(09:19):
Okay? Now also at the same time, the brain begins to enjoy using a new fuel or one that it's a little unfamiliar with. Namely ketones. I've talked about this before. I'll revisit it very briefly here. I'll mention it again, but I'm mentioning it now, which is the ketones actually induce a sense of satiety in the brain. If the brain is used to using ketones, if it has adapted, and it does take a little bit of adaptation for the brain to build up its mitochondria in order to use all those ketones for fuel. After the brain has gotten accustomed to it, hunger starts to go down. And then lastly, indeed hunger is down and that is when calories will take care of themselves. So what I'm not saying is that energy doesn't matter. I'm not saying calories don't matter. What I am saying is start, don't even build a fat cell shrinking journey with a calorie centric view in mind. Let the calories take care of themselves. Start with a low insulin approach. How can we lower your insulin to shrink your fat cells? And then a personal will just start going on this journey without even doing it on purpose. The calories will take care of themselves as hunger gets reduced.

(10:41):
Okay, now here's the overall paradigm. Again, we've got to shrink fat cells to lower insulin resistance. So what is the best wave? Then let's get into strategy now. And so we have these two levers that we can take advantage of manipulating insulin and manipulating calories. So I presented this before and I've indeed presented a longer version. There are two fundamental ideas that I wanted to revisit, albeit briefly, control carbs. Control carbs is the best way to laureate. Then the best way to handle calories when that time comes is by structured fasts. Now remember, remember, if you have a client or a loved one, someone a friend or family member who is interested in engaging in frequently fasting, that's wonderful. That's a nice way to control calories. Remember how you end a fast matters more than how long you fast have a very solid plan in mind.

(11:38):
What are they taking during the fast to help control hunger? How are they ending the fast when it is time to eat? It should be very well planned. Less they get into a cycle of binging and purging and binging and purging. It becomes a sort of fasting version of the eating disorder where they fast, fast, fast, get hungry, and then binge and eat all kinds of junk. They are uncomfortable, they have shame, they regret it and they say, I'm going to do better tomorrow. And they're doing the same thing. Have a firm plant in mind. How you end your fast matters more than how long you fast. But fasting isn't always easy. It is natural to want to eat. It is difficult to deny ourselves, albeit it's a very important lesson to learn in discipline. So as you were talking to people and you tell 'em how healthy fasting is and they say, oh, it's so hard.

(12:27):
I find it so hard to fast. It's prudent for you to have some strategies in mind. So what is the best way to reduce it over? I mentioned previously in the talk that I gave, and I hope many of you have seen that by now. If you haven't, Trent and Rob can find a way to get it to you. I'm not supposed to have recording by know. So they'll have some way to sure you these details with you. I'm sure the topic I gave in May. So I highlighted three molecules in particular, theod, bromine, ketones and short chain fats. Now these each have myriad metabolic effects throughout the body, but the one thing they all have in common is that they induce a sense of satie and reduce hunger. And at the time I had mentioned to you that there are some very effective tools in your toolkit in order to help people take advantage or access these things and these are it. So my day has been shown, yes, you can give a little round of applause. It's appropriate.

(13:25):
So

(13:26):
With their distinct mechanisms in mind, these two supplements have the ability to increase the levels of these molecules in the blood, thereby promoting a greater sense of satiety. And that is so important to improving metabolic health. Just getting off the cycle of eating every hour or two hours and with the people have been told, we've been told that we should do it. We've been told you need to graze throughout the day and eat six meals a day. What insane advice. Look how well it has worked. We are fatter and sicker than we've ever been before it. It's not a North American problem, not at all. As you know, many of you, I'm given versions of my metabolic focused talks around the world because this is a global problem. So this has clearly not worked. We need to break the cycle of eating all the time.

(14:16):
So it is certainly in our best interest to find ways to control hunger. Alright, now what else? This is now getting into the new topic for the day because a lot of what I've just shown is review. Thanks for humoring me. Okay, now we're going to talk about the gut. This is an area of research as I know there that I have really been paying attention to since literally its origins. When I got my PhD, my dissertation was focused on people who had just gone through gastric bypass procedure. Have you all heard of that? Yeah. So sometimes, in fact I'll revisit this more in just a moment and what some of the effects of that work was the birth of the discovery of these hormones in the body that come from the gut that have very powerful metabolic effects. The incretins are a classic hormone that was discovered at the time gastric bypass became very big and it's still very big.

(15:10):
It's only getting bigger. And again, that was the whole focus of my dissertation. So I'm extremely familiar with this area of research. At that time, they found that there was a new group of hormones that had been discovered. Mind you, they'd always been there. We just didn't know about them yet. But the incretins can be defined as such. These are gut derived hormones that are having a metabolic influence. In particular, they're generally thought to be just lowering glucose. That was their initial, that was the initial discovery. Now let me just present to you why that was initial discovery. So here is a cartoon version of what goes into what's called rule Y gastric bypass. This is still the most common one and it was kind of the big one at the time where you can see what they do to the stomach. They take what should have been this really big stomach that is capable of taking a certain amount of food and churning into Health digest and sitting there for a few hours to digest and get really mixed up well, and then the food would leak down into the duodenum, the first part of the small intestine to be further digested and then absorbed.

(16:16):
So the body then pulling in what it needs to pull into sustained life. Now what happens in this surgery is they shrink the stomach to the size of a small, a bunched up teeny little fist, and then so the food doesn't stay there very long, it just passes through. But by bypassing, bypassing the stomach as a duodenum, the food not only moves through the intestines to do quickly, but we don't digest it very well. We don't absorb it very well. So it's basically at its core a way of forcing starvation. That is the frank takeaway of gastro bypass. Now this is what happens though. We found that the metabolic response, you can take people who have profound diabetes, significant insulin resistance, which is what this is measuring on this axis, and correct it in a week, within a week, they are as insulin sensitive as an athlete and yet they're still morbidly obese.

(17:12):
They've only lost the green modest amount of weight in just six days, and yet there's insulin sensitive as a healthy college student. It's crazy. That's a remarkable turnaround. Mind you, it is in fact just a testament to the power of fasting because they're basically not eating this whole time. But even still, there were some other changes that were curious, including my PhD mentor when I got my PhD. So this is why I've been in tune with this topic for so long because my lab was one of the first funded labs by drug companies to study the incretins. So naturally, clinicians and scientists ask the question, what on earth has happened in these people to pull apart the obesity from the diabetes and insulin resistance? And among the many things they found, that was the discovery of the hormones called the incretins. Now, what are the incretins themselves?

(18:05):
There are many. The guts are actually a very active endocrine organ or a hormone secreted organ. It's not just the adrenal glands or the goads or the thyroid gland anymore. Every single tissue of the body is an endocrine organ. So what are the impotent? The most famous one is GLP one. We're going to talk about it in more detail because I want you to know this. I want especially GLP one, you need to know that because that's the medication class that is just taking over the world. That's mind blowing. But then there are other ones that I want you to be familiar with because you don't know it yet, but it actually should be part of what you're talking to people about because you have a unique opportunity to influence these levels in your friends and family. Alright, so here are some of the bigger, more well-known in incretins that again, there are many, many more, but this is what happens to GLP one levels and someone right after gastric bypass when you give them a meal, which is normally when GLP one gets released, along the bottom was the non bypass population, the GLP one barely moves post bypass.

(19:08):
Look at that effect. Enormous. That's part of what went into discovering what was going on. They would look at the blood samples of people and find, boy, there's some protein here that's changing. We don't know what it is yet. They didn't at the time. And then later it got the name GLP-1. This is what goes into these two very, very famous drugs, Ozempic and Mogo. Is there anyone here who has not heard of those drugs? Now if you have, you should feel a little sheepish. If you haven't heard of them, I mean you should get a little shish because they are the, it's unlike anything I've ever seen. I've never seen people bragging about being on a drug. You know what I'm talking about? No one brags about being on an erectile dysfunction drug. No one brags, especially the drug. No one brags about being on a hypertension drug and yet people are bragging openly even just as recently as the latest Saturday Night Live, although no one watches that nonsense anymore.

(20:07):
But the host joked about being on Mogo ozempic and these are actually the exact same drug, just used a different doses. And I hope I'm not wrong in focusing on this a little bit because I think it is important for you to know these. You undoubtedly have friends and family who are on these drugs now or who are interested in them. I want you to know a lot about them so you can talk intelligently about it and provide perhaps alternative solutions or way out because they want to get off it yet. Alright? Now, what is the main effect? The main effect of GLP one as it is used? So these drugs, what GLP one has done or doing these drugs are called GLP one agonists. And agonist is a very precise term, meaning it activates the GLP one receptor. So it's mimicking GLP one now because GLP one is what's called a peptide, it would get digested in the stomach if we took it orally, although more and more that's an option with some clever chemistry, but it's an injection so it goes right into the blood.

(21:13):
So they won't activate GLP one and at its initial dose, but it was called ozempic, it still is, that's the lower dose. It only works well, primarily works by lowering the level of the hormone glucagon and glucagon is insulin's opposite with regards to glucose, whereas insulin wants to lower glucose. Guess what glucagon wants to do? Raise it? Yeah, it wants to bring it up. Now that's a problem if you're a diabetic and you have high blood sugar levels. So this there then is the solution because if you can lower glucagon when mimic one, you lower blood glucose and the diabetes starts to go back. However, there was notice another effect to these drugs, even at that lower dose at the so-called pic dose, namely that it slowed the movement of food through the stomach. Normally when we eat a meal, we're all going to go have lunch in a couple hours.

(22:14):
The food will sit there for a few hours, three to four hours mixing and breaking down into small parts, and then it will start trickling down into thein into the small intestine to be further digested and somatically and then absorbed into the body. You don't do any absorption in the stomach for nutrients. It happens through the small intestine. But what happens now with these drugs is rather than taking three to four hours to clear out, it may take eight hours or so, which is okay, that's not inherently a problem. In some instances it can take a lot longer, but by doing so, the person just feels a little fuller for longer. Does that make sense? If the food is sitting there naturally, your stomach has an empty, you're not going to want to eat. So hunger goes down and that is when they noticed even at that formal modest dose of what we call ozempic people were losing weight.

(23:05):
Now of course that became the focus, the obsession, which turned into, well, if that dose of ozempic slows the guts so much to weight loss, let's times it by five and then call it something else, file a new patent even though it's the exact same molecule, we just have five times more of it and we'll call it govi. So when gov's strategy was to slow the guts down even more and induce an enormous amount of weight loss and avoid as it become popular, this is just looking at the market trends here. And you can see this is what happened to the weight loss market with ozempic when it was used in its original diabetes dose. Yeah, some buzz about it, some buzz, but then once they timed it by five and called it something else, oh boy, the sky's the limit. Indeed, the sky's the limit financially where the manufacturers, one of the manufacturers of the most commonly used indeed these ones is now the single most wealthy company in all Europe.

(24:06):
And I'm going to show you some more Starling statistics at the very end just to make sure you're ahead of the next wave of these drugs coming. So what this is done now at this forgo V dose, if you will, is really amplify the effect of slowing the intestines down. Now there's a problem to that, which is that you may paralyze the intestines. This is known to happen in people and it can be life-threatening very quickly. So it has to go immediately to emergency services. So some people are sensitive enough to it as a side effect that rather than just slowing down, it stops. And now the food even before it stops completely, there are reports of people who have food staying there for a day or more. You guys know that with surgeries, when you go for a general surgery or when you're going to go under general anesthesia, they'll have fast so that your stomach is empty so that you won't vomit up food and then somehow breathe it back in and kill yourself with pneumonia.

(25:06):
That sounds kind of gross. But what they find is that people who are on these drugs, they have to tell 'em to fast longer or get off the drug because there will be food sitting in their stomach from to 48 hours and they'll notice this because people who are on these drugs will know that they'll burp or their breath stinks. It's because they literally have petrified food just sitting in their stomach because it's not moving, it's just kind of rocking. It's pretty shocking, a little repulsive, but that's what starts to happen. So it's a very real concern that people should have. This is just one of the reports of physicians documenting this phenomenon referred to as an ileus or just the frozen intestinal tract.

(25:57):
Now, another concern is how the person is losing weight. It's how they lose weight and it is substantial. But we know now that when people are losing weight as a result of these drugs, slow delaying, gastric emptying, compromising digestion, eliminating food entirely basically that what they find unfortunately is that when you're starving through weight loss, you start to lose fat mass, they lose muscle mass. Up to 40% of the weight loss that they're losing is muscle or lean mass, I should say, to be a little clearer, it's muscle and bone. Now if you are a young 20-year-old man, no problem, you can gain that back. You, it wouldn't be easy, but you could still gain it back. But if you are a middle-aged woman in particular whose bones are going to have a harder time than normal gaining back, good luck, you will never gain that back.

(26:56):
Now why is that a problem? Because there are more and more reports of people getting off the drugs and this is an opportunity for you to help, I believe. I think this should very much be part of what's on your mind. As you look at these trends, people are getting off whether they're getting off because they are tired of literally feeling sick in their stomach all the time or whether it's because their insurance provider have to pay for it anymore, which is also happening a lot, particularly here in the us. More and more insurers are stopping the coverage and people can't afford them anymore. So whether they want to or not, a lot of people in their own volition or not are getting off the drugs. Now the consequence of this, of course, is that their intestinal system wakes right back up and what they thought was then learning to control their cravings was nothing of the sort.

(27:46):
It was a drug induced cravings control. And they find that in reality, they're hungry and craving everything that they ever were. And so it's no surprise that the moment they stopped the drug, the weight starts to rebound significantly. Now, some people like to point out the fact that after in this study, they didn't gain it all back. Mind you, if they kept going, guess what keeps happening? It does in fact continue to trend up. But even still, if we just looked at this, we would say, all right, well they stopped about 10 pounds off from where they were before. And so that's a bit of a win. So there's no concern here. However, mind the gap. What is responsible for that? What weight? If you're looking at fat mass or lean mass, guess which they regain very, very easily. Fat, fat mass, and there's one they don't. And in some instances, especially someone who's middle aged or older, that lean mass will probably never come back. It is so difficult as we get older to put on substantial bone and muscle mass that if you actually look at their percent body fat compared to here to here as a percent of what they're made of, they're fatter than they were before they ever started. So this is something to be mindful of because again, whether they choose to or not, people are going to be getting off these drugs.

(29:14):
Now, how can you get then some of the benefits without the risks? How can you get some of the benefits of the incretin without the risks that appear to come with it? Some of which I've been showing you? Well, you have some strategies here. Some of the ways whereby products you have access to and can help people with can take advantage of some of these same processes. Now remember, I'm a scientist. Nothing I'm presenting to you is made up. I'm always sharing the citations. So as you need to share these things and you only see my little numbers at the bottom, that is always my hope that you're then going to somehow find the manuscript that I'm sharing as I'm doing. So that or if your friends or your family's challenge you on something, always go to the data. Always go to the data. Alright, so we know that uni is enriched with particular molecules more than just what I'm showing here, but I'm highlighting these three deliberately.

(30:13):
So chlorogenic acids, EGCG, and ferulic acid, each of these are known molecules that have been enriched deliberately, inane, and among their many effects throughout the body is a direct effect at the intestines to induce the release of incretins. So this is unique because generally the incretins, when they were first discovered were thought to only be released in response to food, calories, energy. But these are calories, there's no energy here, but these are molecules whose structure is such that as they're moving through the small intestine, they start to induce the same response of the same hormones, the same incretins coming up. Now let's talk about each of them in just a little detail because they're pretty cool hormones. The first one is C, CK or cholecystokinin. Cholecystokinin has multiple effects. One being it inhibits the level of hormone called somatostatin. And that's important because somatostatin inhibits insulin glucagon.

(31:19):
The lowered glucagon means that glucose levels can improve the lowered insulin means the body can learn more fat more readily and have a slightly higher metabolically. So that's generally metabolically beneficial. Also, this one seems a bit odd, but C, CK will help the gallbladder contract. So not only is that a very, very good way to ensure you don't get gallstones because the best way to prevent prevent gallstones is to empty the gallbladder, which normally that only happens when we eat fat. But with that in mind, it helps digest fat a little better. The person will have just a healthier feeling intestine and back movements. Also, it delays gastric emptying a little bit. So there's that subtle effect of C, c, k just slowing down the stomach to help you feel fuller a little longer. And then lastly, one of my favorite topics, which is that it will stimulate the activity of brown adipose tissue.

(32:13):
Have you guys heard me talk about brown adipose tissue before? This isn't something I've focused on ever in a ity based event, so I want to just mention it very briefly, but before I do, I want to bring it back to two unexpected characters that have a direct relationship. When you have bile getting released from the gallbladder, that bile goes into the intestines to help digest fat. Most people don't know that we actually reabsorb some of that bile into our bloodstream and that bile will have a direct effect of increasing the activity of brown pose tissue. So it's a very overlooked effect of bile. So bile goes into the guts, we absorb some back into the blood and then it will stimulate the activity of this very high metabolic fat tissue. This is what brown adipose tissue looks like. We just did some experiments actually looking at the size of fat cells in response to diesel exhaust.

(33:08):
It was a very cool study. Remember as the fat cells get big, they become problematic and look at the difference. This is fat tissue, but it looks totally different and the size, this is not at all in scale. Mind you, the brown adipocytes are much even smaller than the white adipocytes. But white adipose is what we have most of that's what we pinch and jiggle and curse, although in reality it is healthy in its own way. But brown adipose tissue is something that we can't really control much of unless we know how to turn it on. We want to turn it on because it's so dark, because it is loaded with mitochondria. It has tons and tons of mitochondria and mitochondria, unlike in the white adipose tissue where we have so much, they are the engine that's the powerhouse. That's where we're burning nutrients to let the cell work.

(34:02):
Now, just as a brief tangent, there were some papers that have been published and made a lot of headlines and making the rounds on social media about microplastics and nanoplastics. One aspect they have, they can directly get into a fat cell and prevent the fat cell from being able to break down its fat. So it's a pretty interesting tangent, just fyi, be mindful of the source of your plastic. Alright, now here is a direct comparison between the two for the sake of time, I'm going to go through it a little quickly. Brown adipose tissue is a type of fat we have that wants to be burned and it wants to create heat. White adipose tissue, which is the abundance of fat that we have. It wants to store energy, it wants to hold onto energy to use for later as adults. That's mostly what we have.

(34:52):
Most of what we're storing in our bodies as adults is white adipose tissue. However, that wasn't always the case because when we were babies or the darling little babies we have whose baby was here, you and your beautiful little son, adorable. You'll notice when your baby was just a little baby coming out of the bath. If you were to come out of the bath, a warm hot bath, you'll shiver a little bit because you have enough muscle to shiver and that shivering will create some heat. A baby doesn't have enough muscle to shiver, but the baby has really hot fat cells. So these fat cells are just producing a lot of heat, wasting energy, chewing through fats, burning glucose just to create more heat. Now, adults do have some brown fat. You can see imaged here. We typically have a little more of a sort of tip of tucked through our rib cage throughout our thoracic and the clavicular area, the thoracic in cavity.

(35:47):
But humans who have more brown fat are more resistant to gaining weight. They're more insulin sensitive. And that's what this study among many others found that if you either had more brown fat or your brown fat was turned on more often you would've an easier time controlling body weight and being a little more resistant to insulin resistance. So that's something you want so that matters. So the fact that CCK will turn on brown fat, that's good. It's a smart metabolic move if you can take advantage of it. Now, PYY peptide YY, I'm not going to talk about any more than just this just to show that it is one more incretin that is known that have a direct role on someone's preponderance or likelihood of gaining weight for staying lean. So this is another one that acts through similar mechanisms, delaying gastric ene, and now this one's a little unique compared to C, c, K because it has a direct effect of the brain telling the brain to stop eating.

(36:43):
And then once again, a direct effect on the fat cells enabling the burning of white fat. So stimulating the oxidation of the burning of body fat. Now let's get to the big one. GLP one is the big one and for good reason, this is the hormone that when they looked at all of the incretins and said, which one do we really want to take advantage of for these drugs? It was GLP one because it has all of the best effects. It's kind of the all star. It delays gastric emptying. It's activating the satiety centers in the brain to induce that satiety. It's burning. White is stimulating the burning of white fat more and activating ground fat. So it's doing all the best stuff that we want. So it makes sense to focus on GLP one. Now, as a reminder, GLP one has a normal response to food in particular fat.

(37:33):
Fat particularly will activate GLP one release. I wanted to share with you though a very cool human study that compared different types of fat, saturated fat, monounsaturated fat and polyunsaturated fat. And while the saturated and monounsaturated fats induce a substantial increase, several times higher increase in GLP one polyunsaturated fats from refined seed oils like safflower or nut oil or corn oil or soybean oil, they don't have any such effect. So just another reminder to focus on the natural fats that we as humans have been eating since time of memorial animal fats and fruit fats, fruit fats being coconuts, olives, avocados. If it's from the flesh of the fruit, it's going to have more mono monounsaturated and less of the more problematic or omega six polyunsaturated. Anyway, just an interesting little tangent. Okay, now what about insulin secretion? You'll very likely hear if you haven't yet that GLP one has a main effect of increasing or improving her glucose because it increases insulin secretion.

(38:42):
If you haven't heard this yet, you probably will at some point, but how could you be losing weight and shrinking fat cells if it is in fact increasing your insulin? You couldn't. That would be antithetical. That would be a response that would be impossible because it's wrong. The earlier scientists that claim the GLP one worked by increasing insulin, were doing it in isolated cell culture experiments. But when you actually look at the effect of humans, it has no such effect. In fact, it appears that GLP one as published here actually lowers an insulin response into a certain meal. So that's just not true. If you ever hear GLP ones lower glucose because it increases insulin, you laugh politely in their face and then teach them the truth.

(39:36):
Alright, now as we start to really near the end, let's just revisit the tool that you have in your toolkit and it is one that you should be using readily and you're very justified in talking about it promoting. I was delighted to have my lab paper just last year that look at some of the UN here to unexplored aspect of Y in particular, and we explored that by using uni. So the UNICITY specific version with all its unique concentrates, and the first thing that I wanted to share with you that we haven't shared before is that it increases fasting levels of GLP one by not double, but in a solid 60% increase in GLP one. So that is a known statement that you can make. You can state that this will increase your GLP one levels significantly because it was very statistically significant.

(40:42):
Now beyond this effect, very relevant to the conversation, let's go through three specific tissues that all have a very important metabolic role. Let's just briefly look at what did to fat cell metabolism, to muscle cell metabolism and to liver. Now first let's start with fat. I want to actually just bring your attention to one particular. There's a lot going on here as we did multiple experiments measuring numerous aspects of mitochondrial function. The one that is the money maker, if you will, is this cool salon, this cool image right here. What we find here is looking at the amount of energy the cell is making based on how rapidly its metabolism is running. And so the general conclusion is I want you to appreciate the wording here is uni makes the fat cell less efficient with its energy. That is a good thing because that is exactly what's happening in brown fat cells.

(41:45):
So imagine if you will, just until recently I drove a 1998 Subaru Outback, there is a five speed manual transmission. I never even locked the doors because I knew no one could steal it on campus. There's no way a 20-year-old is going to know how to drive. So anyway, I had three pedals, right? One is my clutch and so I could be in gear, but riding my clutch, revving the engine. So the RPMs are really moving, but the car isn't going anywhere. We're not moving at all. I'm being very inefficient with my fuel use. But what if I want to be? We want to be inefficient in the metabolism, our fat cells because if our fat cells are less efficient, they're burning energy, not because we are exercising, but because they just can't stop. That's a good thing because if the fat cells is burning more energy at any moment, not because it needs to, but just because it is, then it's a very, very good way to shrink fat cells.

(42:44):
Does that make sense? So if you ever hear a radio ad, which I have and a chuckle say, you need to take this supplement because it will make your metabolism more efficient. That is the worst thing you want. You do not want your fat cells to be very miserly with their energy. Being more deficient in a fat cell means your fat cells will only release or burn as much energy as they absolutely must. It doesn't sound very good. You want fat cells that are inefficient. You want fat cells that are happily burning energy, not because they need to, but because they just like being wasteful. That's the perfect tissue to be wasted. So I hope that this leaves a cruel impression on you. In fact, this is reflective of white fat cells behaving more like brown fat cells. We are pulling these two processes apart.

(43:36):
Let's call mitochondrial uncoupling. That's the technical term. It sounds awesome. So find a way to use it. Mitochondrial uncoupling of the fat cells. It means the fat cells are less efficient with how they're using energy, which means they're going to shrink better and faster. Now, this is not a globally good phenomenon. Imagine if you are unfortunate enough to be on the stair step for an hour. You don't want your muscles to be inefficient, then they're wasting energy and it's going to be very hard to get work done because you need a lot of a TP to get work done. Remarkably, this effect does not happen at the muscle. In fact, the muscle is more tightly coupled. So while the fat cells are less efficient, muscle is more efficient. This was completely unexpected. I expected, if anything in the fall of the same trend as saw in the fat cells or perhaps be inert, it is better.

(44:34):
This means that fat cells are able to produce more work for less energy. That's a pretty good bang for the buck. Or to say another word, the bang for the buck just got better in these animals. Now, the liver, you'll see in this first one here, the liver had no effect at coupling or uncoupling the mitochondria. They work the same as they ever did. However, the liver, unlike the other tissues, is capable of handling oxidative stress better. That's one of the livers. Many, many effects. And there are many. The liver does everything for everyone in the body. That's why I call it the metabolic soccer mom. It's just constant sacrifice. So the family of tissues and cells within the body, it will take oxidative stress molecules. And this is a technical term, in fact, it is. It will squelch, it will get rid of them, it will make them inert by actually turning them into water just metabolically inert water.

(45:33):
It will just negate the oxidative stress. So that was another effect we found with ate improved the body's ability to handle oxidative stress. Pretty deep, powerful and just one more reflection of how ate is affecting mitochondrial health within the body. Now, I appreciate the fact as I wrap up in just a moment, you have more than just one tool at your disposal. You also have arguably the best way of getting healthy fiber in the diet. So let me not leave that stone unturned, albeit very briefly. So first of all, I wanted to share with you in-house data that I hope changes the way you're talking about balance. In the past, it is always been part of the story to say, just take it 15 minutes before your meal. But look what happens when you take it with the meal. You have about a 20% improvement.

(46:27):
And in fact, if we look at the entire area under the curve, it's even more about 30% improvement. So I do think there is some justification to change the story a little bit of when balance is being used based on the data that it perhaps is going to have a bigger bang for the buck if it's consumed with the meal rather than 15 minutes before. So just something to keep in mind that is pretty significant. But also why might be acting like this. Once again, we have anin story here, which is that the soluble fiber has been shown to increase the L cell secretion. And guess where GLP one comes from? The L cells of the intestine. So the soluble fibers will activate the L cells to reduce the release of GLP one. Now mind you, there's another point there about intestinal integrity. So that's a comment that refers to the permeability of the leakiness of the gut, but that's outside the scope of this lecture. That'll be a topic for another. But nevertheless, even once again with the impotence in GLP one is you have family and friends who are either considering the GLP one negative drugs or wanting to stop considering them get off them. Another thing to say, Hey, I have a way you can take advantage of the effects of this hormone without all the negative side effects that come with it at these ridiculous doses.

(48:00):
Now, very briefly, my final thought, what is the future? This is absolute cutting edge stuff that I want you to get ahead of still taking advantage of GLP one. But as the GLP one, specific drugs are going to start to fall out a favor, and they are drug manufacturers are getting pretty clever and they are combining GLP one with a pancreatic from a beta cell, a beta cell hormone called lin. This is the new thing that's coming out. And in fact, with the announcement of this drug, Nova Nortis has become more valuable than Tesla with this single announcement. So this is a drug that's going to be released soon and you'll be very, very familiar with it. It might have a different trade name, but the operating molecule name is Retin. Retin is the name of the drug molecule, and it is just combining amylin and GLP one agonists like SLU into one and it will work.

(49:00):
I mean, in fact, what they found in early reports is that it induces double the weight loss at the early stage compared to just the GLP one agonists alone. And that's because of its effects once again, on some redundant pathways, redundant but additive, it's increasing the response. But mark my words, they're going to be the same consequences of slowing down the guts. You're just adding one more way, eventually floating the guts down to the point of stopping, which truly is a lethal scenario. But you're familiar with this. Now, you may say, alright, I'm going to have a family member who's going to be familiar with this analog or mimic, and how can you then work that into your idea, helping them when they ask about, oh yeah, all right, well, you're telling me not to take the GLP ones. I'm going to take one that combines both of these, and you say, I have a better idea. I've already walked you through these in the past friend and family member. And if you want to take advantage of amylin, then just remember this other principle, prioritize protein. Protein will give a substantial release. So you just fit this into your story. There is a natural way to beat what the drugs are trying to do with the benefit in hand and without the side effects, the negative side effects in the other. And you are uniquely positioned to take advantage of that.

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