Can THIS Plant Extract Activate GLP-1 Like Ozempic? (Sarah Kennedy) | Ep 427
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Why does hunger sabotage weight loss even with perfect macros? Is appetite control really about discipline or hormone health?
Body recomp, weight loss, and building muscle get complicated fast when appetite refuses to cooperate. I dug into the real biology behind hunger with Sarah Kennedy, founder and CEO of Calocurb, to explore how the gut and brain regulate appetite through GLP-1 and other hormones tied to metabolism and nutrition. We unpacked why calorie deficits trigger powerful biological pushback, how bitter compounds can naturally influence appetite signals, and where these strategies fit alongside lifting weights, protein intake, and evidence-based nutrition.
This conversation reframes appetite as a physiological signal, not a personal failure, and shows how strength training, nutrition, and smart tools can work together. If you’re navigating fat loss, women’s fitness, or strength training over 40, this adds a missing layer most fitness podcasts ignore. It’s a practical lens on appetite control.
Today, you’ll learn all about:
0:00 – Why hunger overrides willpower
4:10 – Appetite hormones explained
8:45 – GLP-1 beyond weight loss drugs
13:30 – Bitter compounds and gut signaling
18:55 – Appetite control during fat loss
23:40 – Women’s hormones and cravings
28:20 – Using tools without dependency
33:10 – Long-term appetite strategies
Episode resources:
Website: calocurb.com/witsandweights
Email: hello@calocurb.com
Instagram: @calocurb
Facebook: @calocurbglobal
Youtube: @calocurb
Real hunger is not a character flaw. It is a biological signal rooted in evolution and governed by hormones like ghrelin, GLP1, CCK, GIP, and PYY. When we cut calories, the hindbrain pushes back to protect us, often doubling hunger over months and derailing most diets. Our modern food environment only amplifies this pressure: fast meals, low fiber, and constant cues lead us to overeat before our gut can send fullness signals that typically arrive 45 to 60 minutes after eating. Understanding the timing and pathways of these hormones reframes appetite as a system we can influence, not fight. High protein, slower eating, and fiber help, but for many people, a targeted nudge to gut receptors can shift behavior in a meaningful, repeatable way.
The surprising key lies in bitter taste receptors that line the gastrointestinal tract from stomach to colon. These receptors evolved as a defense against toxins: extreme bitterness in the mouth prompts spitting, in the stomach can provoke ghrelin to dilute the perceived threat, and in the small intestine triggers a powerful satiety cascade to stop intake. New Zealand government-backed research mapped these receptors with 300 human biopsies and screened over a thousand compounds. Only two families meaningfully activated the satiety pathway; the safe and effective winner was a specific hop extract. Delivered to the upper duodenum in delayed-release form, this extract super-stimulates L-cells to release CCK quickly, GLP1 next, and PYY later, creating a 4 to 6 hour arc of fullness signaling without relying on synthetic hormones.
Clinical data makes the case concrete. In a cannulated human trial, the hop extract boosted post-meal GLP1 roughly 600 percent above baseline signaling and produced an average 18 percent reduction in ad libitum calorie intake compared to placebo. That is below the 25 percent average seen with semaglutide but achieved by amplifying the body’s own hormones. A women-only study synchronized to the menstrual cycle found striking results during a 24-hour water fast: no rise in reported hunger by hour 24 compared to hour 16, a 120 percent reduction in cravings, and a 14.5 percent drop in rebound calories when food returned. Because women appear more sensitive to GLP1 signaling, this suggests tailored potential across cycle phases and life stages, including the luteal phase and menopause when appetite and energy needs shift.
Mechanism and delivery matter. If bitter compounds release in the stomach, they can raise ghrelin and backfire. The delayed-release capsule ensures the extract reaches the duodenum, where it engages receptors to send fullness signals to the hindbrain. The extract is produced with supercritical CO2 to remove phytoestrogens, leaving alpha and beta acids plus a trace of essential oil, and shows minimal systemic absorption in bioavailability studies. Less than one percent reaches blood, and only a fraction of that is metabolized in the liver, minimizing drug interactions and focusing action in the gut. Most users take one to two capsules an hour before a main meal; some “super tasters” find one capsule enough, while a transient laxative effect signals an excessive dose.
Positioning this tool within the broader landscape is crucial. Lifestyle still leads: protein-forward meals, fiber, resistance training, and slower eating increase endogenous satiety signaling. The hop extract can serve three roles. As a natural alternative for those avoiding injections, it reliably reduces food noise and portions within an hour. In combination with GLP1 agonists, it can help patients remain on the lowest effective dose and blunt midweek breakthrough hunger. As an off-ramp after discontinuing injectables, it supports the reactivation of the gut-brain axis when endogenous GLP1 is downregulated, reducing the fear and rebound appetite many report. Practical timing helps: morning dosing supports intermittent fasting, while midafternoon dosing curbs evening cravings for sweets or ultra-processed snacks.
Beyond numbers, the psychological relief matters. Many listeners describe calmer meals, less fixation on treats after dinner, and fewer urges for alcohol, likely because the appetite center sits near the addiction center in the hindbrain. While formal trials on alcohol intake are pending, the anecdotal pattern is encouraging. Most importantly, this approach restores a sense of agency. Hunger does not vanish, but it softens into a manageable cue rather than a command. In a world engineered for overconsumption, working with physiology—rather than white-knuckling against it—may be the most sustainable way to eat less without feeling deprived, whether you are navigating a cut, stabilizing at maintenance, or simply seeking peace with food.
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Philip Pape: 0:01
If you've been struggling with uncontrollable hunger, whether you're at maintenance or a calorie deficit to lose weight or body fat, but your appetite keeps winning, maybe you've looked into GLP1 drugs like Logovi or Mandaro, and for some people, they're a great fit. But maybe you're curious about whether there's another way to work with your body's own appetite signals without a prescription. This episode is for you. Today we're breaking down how your gut controls hunger at the hormonal level, what happens when you stimulate GLP1 naturally versus pharmaceutically, and how one particular plant extract is showing results in clinical trials when it comes to meaningful appetite control. Welcome to Wits and Weight, the show that helps you build a strong, healthy physique using evidence, engineering, and efficiency. I'm your host, certified nutrition coach Philip Pape, and today we're going to continue our series on appetite with a conversation about something that most people don't realize that real physiological hunger is closely related to specific hormones, and there are more ways to address it than you might think. My guest is Sarah Kennedy, the founder and CEO of CaloCurb, who is sponsoring our appetite series. And Sarah is a veterinarian by training with over 20 years in animal and human nutrition, an MIT slone fellow, and she led the development of a natural appetite compound backed by over 30 million in research and 15 years of clinical study. We're going to get into details behind that in a bit. Her product works by stimulating your body's own GLP1 production through bitter receptors in your gut. These are the same hormones targeted by weight loss drugs, but through a completely different mechanism. Today you're going to learn why hunger is a biological signal that you can actually influence how bitter compounds trigger a powerful hormonal cascade that reduces appetite and how to think about the full landscape of appetite tools from lifestyle strategies to natural supplements to pharmaceuticals so you can make an informed decision about what fits your situation. Sarah, thank you so much for joining me on the show today.
Sarah Kennedy: 2:11
Thanks, Renew. It's great to be here.
Philip Pape: 2:13
And I'd love to jump straight into the science just to set the stage for my audience of, you know, what is happening in the gut when someone is really hungry or just hungry in general. And then I want to connect that to why bitter things, why compounds related to hops and specifically can connect to that and then affect our appetite. And then we can get into the research as well.
Sarah Kennedy: 2:35
Sure. You know, it is, as I said, I loved your introduction because there are so many things that affect us. And, you know, Calicobe, like many other things, is a tool in the toolkit for you. So hunger, what most people don't realize is our appetite control center is in our hind brain. So this is our primitive primal hindbrain, really important through evolution, because this is what made us get out of the caves and go and hunt. So I love this fact. If you reduce your calories by 25%, your hunger will double over four months. And as I said, that is the way to get us out of the caves and to go and hunt something. Because we'd all be lying in our caves going, oh, you know what, it's raining, I'm not going out. So this was driving us forward. So this is why 99% of diets fail. You know, you're really good for a week, maybe two weeks, maybe more, but that primal urge to eat, which is driven by griolin. So grielin is a hormone we call it your hunger hormone. And then when you eat, you know, the grielin goes down. And what most people don't realize is 45 minutes later, when you've eaten, um it your digestion goes into your um upper digestive tract, into your diet out of your stomach, and that's when it signals these receptors to release appetite-suppressing hormones. And there is more than one, uh, in fact, I think, well, there's a lot more, but the ones we know are CCK, which is cholycystokinin, which is a very powerful but short-acting GLP1, so we all know that, GIP and PYY. And these all go to the brain and say, you know, you've eaten, it's okay, you're full. But of course, what happens in a lot of well, all of us really, is we actually eat on the run. How many of us eat on the run? Uh, you know, we eat too fast because that takes 45, at least 45 minutes to an hour to signal your brain. So you eat on the run, you're throwing food down, and of course you eat more, and suddenly you go, oh, I'm full, right? So you remember how your mother used to say, chew 10 times, you know. So those are those things. Uh so you know, and then high fiber foods will give you more of those signals as well. So we don't sit down and eat that much. I look, I'm just as bad as anyone else, always grabbing something sitting at my desk. I'm not listening to my body. So your appetite is actually in your hindbrain. It drives you to go and get something to eat, which was important in evolution, but it is a bit of a liability for us now, uh, because we're so, well, in modern-day developed worlds, we're surrounded by food.
Philip Pape: 5:30
We are indeed surrounded by lots of calorie-dense foods. And a lot of the stuff you just mentioned, if the listeners go check out two episodes ago, we got into some of those hormones. But I love how Sarah, how you brought up the evolutionary reason for this and the fact that when we are trying to diet, our body's essentially pushing back, saying, wait a minute, something is lacking. Exactly. Which unfortunately, many of us, you know, we've gained the weight over several decades, most likely, especially around the holidays, right? We gain the weight, and it's like all of a sudden we look at ourselves and we're like, wait a minute, I need to do something about it. And this is where the challenge becomes, okay, crash diets can set you back. Also eating on the run, also just rushing and not being mindful about it, and then not having enough fiber. And I know there's other things like protein that trigger these gut signals as well. So once we understand that, we start to say, okay, there may be some tools we can put in place, which you've already alluded to, like, hey, maybe if we don't rush and we chew our food, potentially. I want to connect that to bitter hops specifically, because I've mentioned to my audience like all the hacks, you know, drinking water before you eat, eating spicy foods, like beyond just the fundamentals. And now that I've met you guys and invited you on the show and we did this appetite series, I looked a lot more into it and was pretty excited about how it works specifically with receptors in the gut. So tell us about that. Where does bitterness come in?
Sarah Kennedy: 6:55
Yeah, so um, I'll just go back to the start. So it was 2009, 2010, a group of very talented scientists in New Zealand. So just to give you a little background, all primary research in New Zealand is sponsored by the government. So this is so we get what we call blue sky research. So about 15 years ago, a group of talented scientists, but employed by the government had a hypothesis that they would find a plant-based extract that suppressed appetite. Now, why did they have that? They had that because of historical reasons. Historical reasons were in the um in the times of famine in the Scottish Highlands, Scottish people chewed very, very bitter berries, heath berries, to suppress their appetite. Also, interesting enough, in the Kalahari Desert, our tribesmen will chew very, very bitter cactus before they go hunting to suppress their appetite. That was in fact the origin of Hoodia. So they had this and a few other, and then there'd been some recent work on uh washing mouse stomachs with bitter substances to reduce appetite. So they had this hypothesis, they put into the government a grant called, it was called Foods for Appetite Control, and got $20 million back for a six-year program to look at this. Just some extraordinary work. So what they did was first of all, they took 300 biopsies, 300 human biopsies, to show that we actually have uh we actually have taste receptors in our stomach and guts. Now, no one had actually proven that before. And when these taste receptors are stimulated, they will release different hormones. So these little taste receptors sit in the L cells and they are our receptors. So they literally map from the stomach right down to the lower colon, these bitter taste receptors, and then could show what they released. Hilarious story getting these human biopsies because Dr. Edward Walker, the senior scientist, had to go and hang out in hospital for about two years and go and approach people and go, hey, because you actually needed someone with a normal physiology who was either having an inter a colonoscopy, or I always get it wrong, an interoscopy. And so finally they got these samples, but you know, hanging out in hospitals to get them, uh and showed them all. So once it showed that we do, they mapped them right down through the gastrointestinal tract. They then and what they expressed, they then tested over a thousand extracts, uh natural plant and some and some pharmaceutical ones to test what expressed what made these express when um when something was put on them. Not surprisingly, only two things did. One was a potato oxalate, which is fantastic, but it's poisonous, so you'd be thin and dead. But the other one was hops. And um, because they're plant and food research, they then tested another 50 varieties. Why I say not surprisingly, this is a secondary evolutionary mechanism to protect us. So if you ate something very, very bitter, you would spit it out. If it went to your stomach, you would probably vomit it up, or if it wasn't so much, it would encourage you to release ghrelin because that would say eat more and you will dissipate that potential toxin. But if it goes past the stomach into the upper duodenum or the upper intestinal tract, it's too late then. So what it does is it stimulates these bitter taste receptors to release these appetite-suppressing hormones to go to your brain to say, you're full. So stop eating, you're full. So basically, what they were trying to do is super stimulate these bitter taste receptors. So we're telling the brain, you're full. Only one was the the sort of what they called the eureka, and that was this hops. And then they found the specific hop, which was really the one that was the strongest and the best. Then they did a whole lot of things like dose dependency and so on, like that. So that was sort of the background, which I think everyone skips over, but so incredible to map this whole thing in our physiology and to explain why we had it.
Philip Pape: 11:45
Yeah, that is incredible. I I do love understanding evolutionary biology and how the context because we're in a different environment today, as you mentioned before. And if we can kind of leverage, take advantage of, in some cases, quote unquote hack, you know, our own bodies to our benefit, which in an artificial world, sometimes you have to do things that are a little different, you know, just to give yourself an advantage. I wonder how how does so you said bitter and then the hops specifically, and that these super stimulate um the appetite or super stimulate appetite suppressant, I guess, right? Where do other compounds fit relative to this? And before we recorded, I mentioned things like capsicin and saffron, because there's other things people talk about for appetite suppressant. Is there kind of a spectrum of how stimulant stimulating they are?
Sarah Kennedy: 12:29
Yeah, um, so what I will say is some of them will stimulate. It's more likely to be in the stomach, um, and that's when you'll get the ghrelin. So with our beta hops, we deliver them to the upper duodenum. So they're delayed release capsules, and they go down to the upper duodenum where they release, and that's where we get this super stimulation. If they released in the stomach, we'd be more likely to get ghrelin. The other thing is a lot of things will say they stimulate GLP1, and yes, they will, but unless you stimulate GLP1 and the other appetite-suppressing hormones over 400%, you will not get a behavioral change. You might get a drop in blood glucose, but you will not get a behavioral change. We stimulate GLP1 and or CCK and GLP1 at 600%, and that's why. So, going on with the story, they then knew that they could get this, they could stimulate these in the lab, but then they took it into a human clinical trial, so the first human clinical trial. And uh it was 20 males, which doesn't sound a lot, but it is what you needed for this clinical, and they cannulated, so they had blood coming out of these people, I think it was like every 20 minutes. So it was a very expensive trial, and they cannulated them and they gave them uh calicurb, it was in those days, it wasn't called calicurb, it was um they gave them the capsule, uh, an hour before an ad libutin or an eat till you full lunch and an eat till your full dinner. Sorry, eat till full lunch and eat and snack. And then they measured the bloods over the next um, I think it was two hours, and they measured these hormones in them. Um, and what you see is this enormous, you see placebo, where when you eat, you will release your own GLP1, and then you see this huge spike where we have super stimulated it to get this 600% increase in GLP1, or twice what we call the postprandial amount or post-eating amount, and then we got an average of an 18% reduction in calorie intake. So the control group ate 18% less than the placebo group. Now, just as a comparison, a semiglutide, which is like an ozempic, will give you around about a 25% reduction. So you can see the difference 18% or 25%. So there is nothing, and I, you know, and I look all the time, but there is nothing in the world that super stimulates like americate, the active ingredient, all this hop stars at 600%.
Philip Pape: 15:25
Okay, so that answers a question I had about the threshold and the quantity of how these get stimulated. Related to that compound, americete, what makes it unique? Like, is it regarding what you can tell us? Because I know it's patented, what makes it unique versus just me going and finding these hops in the wild and just crushing them up and eating them?
Sarah Kennedy: 15:44
Yeah, well, there's two, there's actually quite a few things with it. It is a specific variety, it is very high in what we'd call alpha and beta acids. So, but what most people don't realize, this is what we use to flavor beer. It was actually used as a preservative and to flavor beer. So very high in that. The other thing we do is we extract it using supercritical extraction, CO2 supercritical extraction. So we take all of the flavonoids, so um, all of the um phytoestrogens. So you're left with no phytoestrogens because we often get asked, well, what about the phytoestrogens? They're all gone. All you're left with is the elferin beta-off acid and a small amount of essential oil. So guys don't really mind that because if they get a burp, it'll be like a beer burp. And they're like, oh, I just had a beer. So um, so that's sort of it's how it's it is it is the variety, it is how it's extracted. The other thing is we put it in a delayed release lycat. Um, so a delayed release catch that does release in the upper duodenum or the upper gut. So it releases 45 minutes later. So you wouldn't want to crush it up, you wouldn't want to eat it. And um, yeah, so there is a number of things that go into it.
Philip Pape: 17:01
Right, because like you said, if it gets digested too early in the tract, it actually can release ghrelin, and then you actually get hungrier to try to uh dilute the the poison, the toxic. I get it, cool. That that's explaining a lot. So what about, and by the way, I'm not a big fan of IPAs, I don't drink much at all anyway, because you know, alcohol's not great for you, but uh now they have a good use for those hops, it sounds like, uh, other than IPAs.
Sarah Kennedy: 17:24
We always get asked, well, if I drink beer, will I get the same? No, because when you put hops in beer, you actually isomerize them. So you actually cook them, so you've taken away that activity. So unfortunately, beer won't do it either. Might make you.
Philip Pape: 17:42
Always looking for that angle to drink. Um, what now, are there other hormones that are triggered through this process besides GLP1? Is it all the other uh appetite-suppressant hormones as well?
Sarah Kennedy: 17:52
Yeah, so what's fantastic about it? It first of all releases CCK. Now, CCK, as I said, is a very potent but short-lived uh appetite suppressing. So it does that first. That's the first part of the gastrointestinal tract. Gastroenterologists love it because it actually squeezes the gallbladder. CCK squeezes the gallbladder. So often on the synthetic GLP1s, um, you'll get stasis or your gallbladder won't squeeze, which can lead to gallbladder stones. So gastrointestinal, um, on the gastrointestinal, they love it. The next part it goes down, it releases GLP1, which is your appetite suppressing as well, and much longer lived. And then lastly, in the lower, in the lower part, it releases PYY. So, and that is so you're getting three gastrointestinal hormones, you're getting three appetite suppressing hormones, literally three for the one pill, uh, and it's it has a persistency, so it lasts for four to six hours. So a lot of people say, hey, these hormones get broken down in two minutes. Well, they do, but the thing is, as it travels down, I kind of liken it to a pinball machine, you know, in a pool, it's going down, it's banging against these taste receptors, and it's activating them as it goes down. So it lasts for four to six hours. And I will tell you about the following clinicals, which we know why it lasts for four to six hours with it. So think of this pinball machine. The other thing we get asked a lot was, well, do I have to keep taking it? You know, am I doing this? What we're actually doing is we're upregulating your brain, your gut brain access. So if you think about it, when you inject yourself with a DLP1 um injectable, so the synthetic, and nothing wrong with those. But when you inject yourself, you are down regulating your hormones because your hormones go, ah, you know what? I don't need to do anything. I'm going on holiday now. And you know, we know that. Happens and you know, if you think of it like testosterone, if you inject testosterone, your own natural testosterone goes down. So whenever you use a synthetic hormone, your own hormones decrease. So they go on holiday. So this is why when people come off the injectables or the synthetics, they get this intense hunger because they don't have any natural left and and you know and often regain the weight. So a marisade or calicurb is upregulating. So we like to say we're actually improving your gut brain access. And as we get older, your gut brain access is less because your little taste receptors die, you know, everything we've done to our bodies over the years, uh then so we are improving that gut brain access.
Philip Pape: 20:50
Yeah, that's incredible. Upregulating hormones, we're talking, like you said, the GLP1, the CCK, the PUIY. Oh, and and then just to reiterate for the listeners what Sarah was saying, you know, just normal eating increases those roughly, it sounds like 300%-ish, and these double that, and you get 18% reduction in calories consumed versus 25% for GLP1, or zero for placebo, right? Roughly, or maybe it's a little more if you think you're in the study. I think one of the trials, correct me if I'm wrong, showed that females had a stronger response than than men. Is that true?
Sarah Kennedy: 21:25
Yeah, that was a fascinating trial, and I'm really proud we did it because less than 30% of clinical trials are done on females, and literally because females have hormones. And I was a bit grumpy. I was a bit grumpy when we had to do it. I was registering in Australia, and if anyone says I've got an Australian accent, I'll be very, very upset. It's New Zealand. No, no, but um, we had to do it for registration, and so it's it was an appetite, it was on hunger and craving. And interesting, when we did it on men, uh, we needed 30 men, it probably took six weeks, right? In females, it took 18 months. The really the and and it was a quarter of a million dollars. The reason is that you had to sink women on exactly the same day of their menstrual cycle, uh, on the same day of their menstrual cycle each month, uh, and on the same day of the week. And you had to do three times with the same woman because, and it was over COVID, because we did placebo, low dose, high dose. So this was a huge trial, and I'm really proud we did it, but I was a bit grumpy at the time, but I'm so proud of it because women are more sensitive to GLP uh stimulation, and they think we don't know, but they think once again it's evolutionary because it protected the fetus, if you could have potentially protected the fetus. So this is sort of the the suggestion behind it. But what we did was a 24-hour fast, so no a water-only 24-hour fast, and we gave calicurb at 16 hours into the fast and 20 hours. So these are the times when you'll be the hungriest in that last eight hours, and we measured hunger, craving, and then rebound eating. So in that last hour, uh eight hours, we got a hundred percent decrease in increased hunger. So at 24 hours, they were no more hungry than they were at 16 hours, and we got a 120% decrease uh in craving. So they were craving less at 24 hours than they were at 16 hours, and then we um we also gave a rebound eating, which was once again an ad libitin, and they ate 14.5% less calories, and that was after 24 hours. So you can actually equate that to, you know, we say a 30% reduction over 24 hours. You can say a 30% reduction in hunger, a 40% reduction in craving, and you know, an average of an 18% reduction in calorie intake. So yeah, it was a superb, absolutely superb response in the woman, and you know, and and leads it on to how it can be used. It doesn't always have to be used for weight. Certainly, you know, in a woman in a menstrual cycle in her luteal phase uh will on average eat 200 calories more a day. And and really, it's normal, it's natural. Your body is preparing in case you're going to implant an egg. So it's preparing and doing all of that. So women can eat up to 600 calories more a day, and you know, it's like that calling PMS, I just want chocolate. So incredible, you know, in that week um of the menstrual cycle. And the wonderful thing about Calicoop, you can come in and out of it because it works in an hour. You know, you don't have to build up a dosage, you don't have to do anything like that. So, yeah, you can say, I'm just gonna take it then. Of course, the other thing is in um menopausal women, uh, just so not fair, is it? I mean, and not only, you actually have to eat 200 calories less a day just to save the same size, because you'll do up an estrogen. So lower metabolic rate.
Philip Pape: 25:30
Yeah.
Sarah Kennedy: 25:30
Yeah. So, and as I said, you can come in and out of it. So, yeah.
Philip Pape: 25:36
No, that that's power. Yeah, I was curious about that, right? Because I mean, I have a lot of clients, women, and I know it individual variation is is large, you know. Some women don't notice much of a change, and others big cycles with their training, with their recovery, and with their um appetite. And that's really powerful. Like you said, it's not just to lose weight and be in a deficit, it could just be to offset periods of hunger. I could see this being a tool when you have specific moments or events where you can use it as well. I've been telling my audience that I'm gonna use it for my next fat loss phase as well to show them what it how it can be used as a tool. And then uh the other thing is I was gonna ask you, have there been any uh long-term cohorts studied with like calorie deficit, you know, or weight loss phases or extreme approaches of that? Like, have there been anything like that?
Sarah Kennedy: 26:24
Oh my god. So I'm just smiling at that. And I can't say too much, but um, I raised $3 million three years ago for our largest human clinical, which was a long one. Uh, and it was just done blinded in November, and the results were amazing. And I'm not allowed to say them yet because it has to be published, so we're waiting for it to be published in April, but yeah, I'm over the moon, and um, and that's a long term. So it was 150 patients, men and women, BMI between 25 and 35, uh uh six months, and very little intervention. So they had a group, um, this is what the scientist told me, they have a group tutorial once a month by Skype. So that was the only intervention. No diet, no exercise, no nothing. So yeah, it was unblinded, and I got the top line in um December. So very, very new, and um you really promising result, amazing results. So I'll be able to talk about them in April.
Philip Pape: 27:34
What a tease. Uh and of course, and of course I ask, right? Because everybody knows the numbers from the GLP1 agonists, where it's anywhere from I think uh the the basic semaglitide, something like 15, 17% or something, up to like terzepatite and the new retratite, I forgot to pronounce it's like up to 30. Yeah, up to 30 percent. You know, and so the kind of range I think in people's heads are like 15 to 25 percent ish. And so whatever your number is, if if it's even five or ten percent, it's still an improvement. So uh it sounds like you're optimistic. I'm excited for that. Maybe we have you on back again when that happens. I love it.
Sarah Kennedy: 28:08
It's it's an amazing result, and I'm not allowed. I'll be absolutely flat, but I can say it's so promising, and I'm over the moon. But you know, it's really interesting. Anecdotally, we get thousands of people coming back and going, this has really helped me. I've lost weight, I've done this, and you know, we know anecdotally uh it's um amazing, but however, to have this long-term cohort and it to be published uh in April uh is is fantastic. So that was it was worth, you know, for three years I'm going, yeah, we're doing it, yeah, we're doing it, and I'd raised all this money and yeah, we're doing it. And then suddenly it was like a month away, and I'm like, oh my god, oh my god. But anyway, yeah, so uh all good.
Philip Pape: 28:55
So so the natural next question is will there then have to be a follow-up on uh what happens when they come if they stop using Calicrum for a while, just like when you stop using GLP1s, and you know, we talked about the weight regain and you talked about upregulation of hormones. Is there gonna be a study for that as well?
Sarah Kennedy: 29:10
Yeah, we we did, yes, we did. We did a three-month follow-up, and that was um a great result as well. So, but that's all I'm allowed to say.
Philip Pape: 29:21
No, it's okay. Listeners, I don't know anything about this. I'm totally asking questions that I'm curious about, so obviously you're you're trying to answer them and they'll be answered shortly, so you guys just have to wait.
Sarah Kennedy: 29:30
Everything we do at Calico, we have four values, and the first one is uh we are we are science-led. So everything we say and do uh is science led, and we have a US regulatory consultant that we consult in every well, we have our own scientists here, but we have a US regulatory consultant, so everything we say is legal and backed by a clinical study. Our second value is customer success because if they're not successful, you know, we're not successful. So we always get this little whoop in the office if we get an amazing email back. Um, the other one is simplicity. We literally use all of our money for science. We don't try and expand our product range, we don't try and do anything like that. We are about Calicurb. So, you know, I always say we're a tool in the toolkit. And like you said, protein, protein, protein. You know, I can't talk more about that. Those are other tools, but we don't expand on that. So yeah, we have pretty um, and then our last one is uh passion, but with integrity. You know, it's such a sensitive product, it's such a sensitive area that you, you know, you we have to, and you know, my own story is why did I get into it? Um, you know, I'd battled with food my whole life, and you know, yo-yo dieting always on. And, you know, I don't think I was ever, you know, I'd sort of go in and out. I was never terribly overweight, but just battled that food noise, loving food but hating it, this love-hate relationship. And then I um calico came along, so obviously it resounded with me, and then um I took it for the first time, and I'm like, this is incredible. So now uh what we've been around six years, I can say I've got this absolute um I'm I'm at peace with food. I can eat, but I just don't eat as much. I mean, I still take calicurb. I we used to say, you know, gin is mummy's little helper. I say it's not gin, it's um calicurb because it doesn't matter what you're doing, as I said, you are surrounded by food every day. So you just want to you want to eat it. You just want to eat less of it. You don't want to not eat, you just want to eat less of it and have that control mechanism.
Philip Pape: 31:51
Yeah, you mentioned food noise, and and that has become more of a topic of conversation with the GLP ones. When they first came out, um, many of us in this industry were, you know, either skeptical or kind of jumped on that bandwagon of judgment and criticism of, hey, this is a shortcut, this is a quick fix kind of thing. And I think the nuance has come into the equation over the last, you know, couple of years. Obviously, Ozempic came out 30 years ago, people don't realize that or something like that. But but the more recent ones, and we had a I had a guy on this um show, his name is Jamie Sellsler, and he he was 650, approaching 700 pounds. Wow. He just recently got under 300, and he talked about how he needed to cut out that food nose. Now he he didn't he went the pharmaceutical route as he needed to. It was so extreme of a situation. He was at death's door. But I think you bring up an important point in that there's body image, uh, there's the weight loss industry, there's the whole spectrum of like, do you do this naturally? Where do supplements fit in and where does all that fit in? And I'm a big fan of looking at these things as tools, um, not look using them as a crutch necessarily. So having said that, you said you still take Calicurb. What are the experiences of some people taking Calicurb in conjunction with lifestyle changes? And maybe that's from an education standpoint on your end or something else.
Sarah Kennedy: 33:11
Yeah, look, there's a number of ways to use Calicurb, but you know, the first one is if you want to use it as an alternative. You know, you just want to go that natural route. You don't want to inject yourself, you can't take the side effects. So absolutely. But once again, as you say, you've got to put lifestyle changes in. You know, I say if you go from eight donuts to if you go from ten donuts to eight donuts, it's really not going to make a lot of difference other than two donuts. But so, you know, you want to be thinking about that, you know, your diet, whole foods, protein is a fabulous, fabulous thing because it does fill you up, particularly as you're getting older, because we do our muscles degrade by 0.5% a year. So absolutely, and and exercise, strength exercise. So as an alternative, just quieting that noise down, allowing you to eat less. A lot of physicians are using it in combination, and that's a really interesting one because they actually interesting, they will start them off on calicurb, and if they're not getting the exact result, they'll then put them onto an injectable so they can start at the lowest dose, but stay at the lowest dose. Because if you think about it, when you're injecting your synthetic hormone, right? But you're using calicurb at the same time, so you're stimulating your natural hormones, so you're getting both. So you don't need because you have to keep up in your dose on the injectables because you're desensitizing your body. You know, you're bathing your body in this high, high, high, high synthetic hormones 24 hours a day for seven days. So you want to keep it lower if you can and increase. And what they're finding is in day five, that it stops that breakthrough hunger. So use it in combination, really great usage like that. And then the third one I say is not an if, it's a must. When you come off an injectable, remember, I said your own natural GLP1 levels are at zero. You know, they're like, hey, I'm still on holiday, I'm not coming back. So T-Trate off using Calicurb and stay on Calicurb until that brain access keeps work, it starts working again. And this is why you just see this enormous rebound, because you know, the hunger comes back. So you've got to restart or kickstart that gut brain access. And interesting, I read a study the other day, um, you know, because we look at the physiology, and I talked to you about the physiology dampening down that natural GLP one or making that go to zero. But there is a there, that's a physiology, but there is a psychology as well. You know, they did this um um measurement on people coming off GLP1. A hundred percent had um fear. Um, fear and hopelessness coming off. You don't want your patients to feel that. You don't want people to feel fear and hopelessness because they've come to depend on them. So, yeah, three alternative uh in combination uh and and absolutely, absolutely coming off.
Philip Pape: 36:28
Yeah, I didn't even think about the fact that you could use them in combination, but that makes total sense. And it makes me think of, you know, when we've had members in our in our group who come in on turzepatide, for example, and they're lifting weights and they're walking and they're eating better than they have before, and they want to titrate off of it. And and I have seen that situation where even if they slowly do that, uh the hunger's really ramping up. And I can see Calicurb as a solution, even because one of the solutions I've had to offer is let's just eat more and get back to maintenance or even shift into a bulking phase timed with you coming off because now you're gonna eat more, or doesn't necessarily address the root cause with the hunger. So that's that's fantastic. Speaking of food noise, then I know with the medications, some people have other types of noise and addiction reduced at in the brain. Does it does it have a similar effect because it comes down to GLP1 or is that another mechanism happening in those?
Sarah Kennedy: 37:25
Well, no, once again, um we think it does because your appetite center is right by your addiction center, really, in your hind brain. And so we have had a lot of people coming to us and going, you know, I just drink less alcohol. You know, I just drink this. So we think it does, but we haven't done any clinicals on it. So I think it's gonna help. And of course, um, you know, if you feel fuller, you know, um I do know it takes away that sweet craving. So many people say that after dinner treat, you know, when I'm watching television or something like that, I eat less. But yes, we have heard about it with alcohol.
Philip Pape: 38:01
Well, now you that brings up another question. You mentioned the the craving. So on GOP1s, some people find like fattier, ultra-processed foods kind of repulsive or they get sick. Uh, do we see again? Do you see some of that as well? Even if it's anecdotally, I appreciate your nuance that we haven't studied all of these.
Sarah Kennedy: 38:16
Well, we do, you know, we do know the craving. You know, we did do that clinical in woman. Uh, we were showed 120% less in craving, and it was actually a sweet craving. So we do know that. Um, so yes, and absolutely what we're finding is a lot of people say to us, hey, you know, after dinner I would always sit with my husband and I'd have, you know, some chocolate or something like that. It's sort of a reward for the end of the day. Um, they're like, I don't need it. So I always say, you know, if that's when you're getting your worst cravings, remember with Kilacoube, you must take it at least an hour before a main meal. The reason being is nothing particular, it's just got to go into your, it's got to get past your stomach and go into your upper duodenum. So take it with water. It doesn't matter if it's two hours, it doesn't matter if it's three hours. We only say an hour to make it easier. Like eye intermittent fast. So I take mine about eight or nine o'clock in the morning, and then I can go through till 12 or 1 o'clock, and you know, and I'm I can walk past that muffin, I can walk past that, and I'm fine. But you know, you can take it. But if you're trying to reduce your cautions, take it at least an hour, an hour and a half. And how do you remember that? I always say, look, you know, 10:30 in the morning, you know, if that's when you get your cup of coffee, we get your morning tea. Um I'm very English in saying morning tea, isn't it? That's what we have in um have our morning tea is have your calicurb then. And in the afternoon, you know, about three o'clock, you'll get that slump or you're a bit tired, take your calicurb then with a large glass of water.
Philip Pape: 39:55
So that's that's the protocol. And and it make the timing makes sense because you mentioned before it takes about forty five minutes. And it's with the time released to get in there. And then it lasts four to six hours, meaning you have a big window. So I like that. My man is already going to not just a typical like calorie deficit type fat loss phase, but sometimes I'll run with more advanced clients, something called rapid fat loss, which there's different forms of that out there, right? Like protein modified fast. Uh Lyle McDonald has his version of that, kind of this evidence-based, you know, two-week or three-week approach where you're eating almost exclusively protein for like four days and then you refeed, you know, back all the way up to your maintenance calories for a day, kind of recover some leptin and get a little psychological boost and all that. This could be a really powerful tool for that as well. Because now you're talking about slashing calories by like 45% from your maintenance just for a short duration, but some people can't even handle that and they want to give it a shot. So it's in my head, uh, Sarah, as a possibility.
Sarah Kennedy: 40:49
It would be fantastic for that. And that's why I say, you know, people use it for all, you know, like people use it when they're going on holiday. Um, you know, because you're on a cruise and they just don't want to eat too much. You know, they use it, but you know, you can come in and out of it. That's what I love. If I've gone to a degastation dinner or something like that, uh, I'm like, I'm not gonna take my calico, you know, because I want to eat my dinner. So, you know, these are these, um, you know, the ways you can use it. Uh, we do say when people start on it, just start, um, there is a a ramp up like and really like everything. Remember, this is a biologically active product. You, um, some people, around 5% of people are what we call super tasters, so super gut tasters. So they will just need one capsule. So we just say start low and slow and build up over two to three days. The the the dosage is two capsules, you know, before a main meal, uh, before lunch and before dinner, if you're reducing calories, but you may be one of the super tasters, the five percent, and you may only need one. And you will know if you've had too much because you'll get a laxative effect. That's all. You will get, you know, it'll be an hour after you've taken it, and it's a laxative effect. So nothing to stress about. The other thing we could ask is to just to let you know, it's incredibly safe. We did some human biome bioavailability trials, and less than one percent is absorbed, well, one percent is absorbed in the bloodstream. So, and of that one percent, less than five percent of that one percent, so 0.001, is metabolized in the liver. So really important because people go, well, I'm taking other drugs, you know, and sometimes supplements can either speed them up or slow them down. We don't do any of that. We work exclusively, we're exclusive to the gut.
Philip Pape: 42:47
I'm glad we have this conversation because you covered, I think, all the bases, but I want to give you the opportunity, Sarah. Is there a base that we haven't covered that we should address before we uh before we sign off about Calicurb or about hunger or anything we talked about today?
Sarah Kennedy: 43:02
No, I think, you know, I'm I'm terribly proud of it. As I said, it's it came from and it's still owned by the government. Most people don't realize that, and we have the worldwide license to it. Uh so everything we do has to be totally um correct, uh, is because they own the technology uh and they veto um, you know, all well, they do all of the clinical trials and so on like that. So there's no um uh yeah, it's it's really above board. So I'm very proud of it. Uh as you can imagine, I think what it does, it assists us in the modern world. We have a primitive brain that hasn't evolved with the modern world. So it is, it is just really, and once again, to your point, a tool in the toolkit. You have to do other things with it. But you know, these are all things that are controllable if you take that noise out of your head, which remember is evolutionary. It was driving you to hunt. So don't blame yourself. It is it is what we were designed to do.
Philip Pape: 44:09
Well, thank you, Sarah. Um, yeah, I think it's a powerful tool with a lot of upsides. And if you're listening or if you're watching on YouTube, feel free to comment below. If you have questions, we'll get them to Sarah. And I will include a link in the show notes to get 10% off CalloCurb, by the way. You guys can go to witsandweeights.com/slash calocurb to try it out. Definitely just give it a shot. You don't even have to subscribe, just grab one, try it out, and you'll know pretty quickly, I think, if it helps you out. So, Sarah, besides that, where can people reach you or the company to kind of learn more about this or just say hello?
Sarah Kennedy: 44:39
Yeah, just go to our website, which is www.calacurb-c-a-l-o-c-ur-b dot com. So calacurb. Uh, and look, people always say, why did you name it that NAF name? But the thing is, when you go to name something, it's really, really hard to get something that you can trademark globally. So um, anyway, so Calicurb, or you can just go hello at Calacurb and we'll literally answer your questions um the same day.
Philip Pape: 45:10
When I first mentioned this to my wife, she's like, Oh, like curbiocalories. I'm like, Yes, exactly. Because I didn't even notice it the first time. She's just like, boom.
Sarah Kennedy: 45:18
Yeah, she's well, because we call the hop extract a marisate. And as I said, never ever let scientists name anything. Because it was named that when they brought it to me, an a marisate, meaning um bitter in Latin and satiation um in Latin, so bitter satiation. But of course, no one in the world can pronounce it. And and but the scientists still love it. They're like, oh yeah, it's such a good name. So I'm like, look, you guys stay with the science.
Philip Pape: 45:48
I I hear you. The hormones are hard to pronounce, they're all hard to pronounce. At least I think of my country, America, and I'm like, America America. There we go. That's how I remember it. Okay, cool. That's how I did it. After I listened to like three other podcast episodes and make sure it's said the right way. All right, Sarah. Well, this has been a pleasure. Um, I learned a ton, which is is my first goal because then I know the listeners are gonna learn a lot. And um, thank you again for being on and and thank you for this partnership as well. I'm looking forward to using the product myself personally and then maybe experimenting with different ways that clients and um listeners can use it as well. So thank you, Sarah.
Sarah Kennedy: 46:19
I can't wait to come back and talk to you about the um the longer. Yeah, I can't wait to.
Philip Pape: 46:25
Yes, yes, yes. That's a great hook. That's a great hook. We're gonna be dying to hear about that. All right, Sarah, been a pleasure. Thank you so much for coming on, Wits and Wait, four, four, four, four, five, five, and then, four.
