Paul Saladino, MD: The Big Lie & The Real Reason You Can't Lose Weight | TUH #082

I believe strongly that there is a ton of evidence that not all calories are created equally.

Look at the data. In the United States, we eat the highest consumption of processed foods. We're the most obese.

So they came out recently and said that there is not enough evidence to say that ultra processed foods contribute to obesity in humans. What calories in, calories out means for weight loss. And I thought, okay, this is really interesting. There are studies looking at markers of metabolic syndrome, and the studies would suggest that 88 to 93% of the US population have at least one marker of metabolic dysfunctions. Calories are king. You know, calories are what make you fat or make you lean. Yes and no. I want people to know it's not that complicated. If we just understand that negative effects of ultra processed foods are amplified and the positive effects of unprocessed foods are amplified in our physiology. And if we just simply.

Hey, guys, welcome back to the ultimate human podcast. I'm your host, human biologist Gary Brecker, where we go down the road of everything anti aging, biohacking, longevity, and everything in between. And a very, very close friend of mine who's usually in Costa Rica hit me up last week and was like, hey, I'm gonna be in Miami. And I, I was like, we definitely got to come by the house. We'll do breakfast together. We'll, you know, we'll do some videos. You know, we'll pick a couple of topics and we'll. And we'll put them out on social media and we'll do some educational things. And we, as always, just started eating each other's face and we're doing a bunch of biohacking. Today we did sauna and red light and cold plunging and a little bit of a light workout. Connect with our community. Let's do this together. Now let's get back to the ultimate human podcast. So many things that we could talk about. You know, we're having a great debate about seed oils earlier out on the balcony. And then we started this conversation about calories in, calories, calories out, and how there's an oversimplification in, in my opinion, in the market about calories in general. So talk to me a little bit about the research that you've been digging into lately on calories.

So I was mentioning to you that on Twitter, Kevin hall, whose study we'll mention in a second, posted something from the U. S. Governmental dietary guidelines Committee, and they.

Well, there's an entity I really trust.

I know, right?

Yeah, yeah, yeah, that's super. True already, I'm suspect.

Yeah, but the U.S. dietary Guidelines Committee, these are the people who made the 2020-2025 U.S. dietary guidelines. They shape food lunches, they shape food stamps, they shape a lot of things in our country. You know, not everyone is accepting what they say is canon, but it affects policy in the United States. And then they're about to make the 2025-2030 guidelines for our country's health foods. And these are the people who brought you the infamous super healthy food pyramid, you know, etc. Etc.

Lucky charms.

Exactly. Well, yeah. So they came out recently and said that there is not enough evidence to say that ultra processed foods contribute to obesity in humans. We need more research, guys. We don't know. And I thought, okay, this is really interesting. This is. And, and Elon Musk commented on this tweet. He said, calories cause obesity. Calories are king. And I thought, okay, this is an interesting jumping off point. Two things I want to mention about this. The first is, I hope that this isn't the US Dietary Guidelines Committee sort of giving themselves license to include more ultra processed foods in the guy in the, in the dietary guidelines, because I think this is very confusing and this is insidious for us as Americans, because I think it's really important that we understand what calories in calories out means for weight loss. And I believe strongly that there is a ton of evidence that not all calories are created equally.

Hmm.

And what I mean by this is if you really look at the data, and Kevin hall, who retweeted this, has actually done a great study on this in a metabolic ward, a completely controlled study looking at humans who are fed. Fed certain foods. And they were. They were completely control. Everything they were fed was controlled. They were in the hospital. And what they did in Kevin hall study was they gave people the same amount of calories for every meal. They presented the same amount of calories, and one group of people got ultra processed foods and one group of people got unprocessed foods. So people got ultra processed foods and they presented the same calories. They matched for fat, carbohydrate, protein, salt. They matched for as many things as they could. But one group of people got ultra processed calories and one group of people got unprocessed calories. So one group of people is getting like salad and fish or chicken, maybe some beef, maybe some grains that are unprocessed, and the other group is getting more processed versions of all these things. A McChicken sandwich, a fish fillet. Sandwich, McDonald's, you know, chips. And what they found, and this was an ad lib study, so they let people eat as much as they want, so they gave them a certain amount of food and then they looked to see how hungry people were. And the study was two weeks long, I believe. And over those two weeks, not surprisingly, the people on the ultra processed food diet ate an average of 500 calories more per day.

Dr. Hyman, talking about this, it was the, it was the lack of satiety and the hunger response was significantly more intense. And they not only ate more food, more calories and gained more weight, but they also reported being hungrier faster. Yes, I, I, I, I, I, I didn't read it to the depth that you did, but I did, did gloss over it. And, and I think this is opening up a really interesting conversation because you know, I, I've long since held the position that some of the worst research we do on human beings when we study things in isolation. Yeah, right. So they, we say, okay, let's deprive this person of calories, put them in a caloric deficit and they lost weight. So the way to lose weight is to go into a caloric deficit, which I, which I agree with. And then this myth in my opinion emerged that a calorie is a calories calorie. So you could eat a th000 calories of donuts or you could eat a thousand calories of grass fed meat, or you could eat a th000 calories of, you know, soda water and, or soda. And it doesn't matter because those are just calories. And see, here's the proof because we gave these people that drank nothing but soda and ate donuts, but only ate 1500 calories a day, they lost weight. Sure, they lost weight and they're being ultra processed, high carbohydrate, sugary foods. But we're not looking then at downstream consequences. What are the consequences on inflammation, what are the consequences on hormones, what are the consequences on, on hunger, satiety, all of these things. So I'd love to hear your comments on that.

Yeah, this is exactly it. And it's the idea that not all calories are created equally. Right. A thousand calories of donuts are not going to have the same physiologic responses in my body as a thousand calories of ribeye. And we know this to be true. There are plenty of studies that show us this. A thousand calories of donuts, we know that's going to make me hungrier sooner. Which in Real life, not in a study where they're limiting people and they're only giving them a certain amount of food in real life. Makes me hungry and it makes me crave food or it makes me just. It can have other physiologic effects. You mentioned hormones. It can potentially affect endothelial function at the level of our blood vessels. Mood.

Mood. Motion. Yeah.

Emotion. Whether we sleep, whether we're on a computer, or doing things that are going to affect us in terms of circadian rhythms. And so what was interesting was that, you know, Elon Musk responds to this comment from Kevin hall saying, the diet, The Dietary Guidelines Committee says ultra processed foods, we're not sure they really cause obesity. Kind of opening the door.

Yeah.

For Coca Cola and these ultra processed food companies, which, by the way, spend millions of dollars a year lobbying Congress.

Right, right.

To have some sort of get out of jail free card in the, in the health space or from the government to be included in, like, food stamps projects. You know, you can buy ultra processed food with food stamps.

That's insane.

It's crazy, right? And so this is how it all kind of works that the Dietary Guidelines Committee can say, well, we're not completely sure that the calories from ultra processed food are uniquely obesogenic. And then you have studies like Kevin hall saying, well, they're definitely making people hungrier and they're definitely not full of the same nutrients that a steak is. And they're definitely full of more pesticides, more oxidized oils, more gut disrupting compounds.

Preservatives.

Preservatives, yeah. So how can you not. It's just, it's crazy to me that we don't understand this. And I wanted to just, I, I wanted to respond to, like, Elon's tweet and say, because Elon said calories are king. You know, calories are what make you fat or make you lean it. Yes and no. So this is. We go round and round. You know, we chase our tails about this. Calories in, calories out. And yes, you're right. And this is what the proponents of calories in, calories out model say. You can lose weight eating junk food. You can absolutely lose weight eating junk food. But will you keep that weight off long term? Will you be satiated? Will you be hungry? What will your mood be? What will your hormones do? What, what will your blood vessels look like? How inflamed will you be overall long term? And those are not the same. And the reason I want to think it's so important to talk about is because I want people to know it's not that complicated. It's really pretty simple.

Yeah.

If we just understand that ultra processed foods are going to have a reverberating effect in our physiology, they're going to be the negative effects of ultra processed foods are amplified and the positive effects of unprocessed foods are amplified in our physiology. And if we just simply kind of discard all the tribalism around which foods are best and we focus on unprocessed animal and plant foods at the exclusion of ultra processed foods, realizing I probably shouldn't eat 500 calories of Doritos today because that's going to have an amplified negative effect bigger than those 500 calories in my physiology.

Right.

You know, if I exclude as many ultra processed foods as possible and I just eat unprocessed meat and plant foods, you're going to lose weight, you're going to feel better, you're going to get healthier. That's what the message should be. And the fact that the U.S. dietary Guidelines Committee can't take that stand and that, that, that even Elon is a little confused or doesn't understand this and that there are a lot of people in the health space who want to amplify the message that you can lose weight eating donuts, it just drives me crazy. And I'll mention one more study also. So I talked about the study from Kevin hall, but there's another study and this is an a pilot study. So it's a small study of eight people, but they gave people a, an oleic acid rich meal. Oleic acid is a, an, is a monounsaturated fat prominent in tallow or olive oil. And they gave people a linoleic acid rich meal. That's an 18 carbon polyunsaturated fat prominent in seed oils.

Okay.

So linoleic acid.

This is another whole argument that people are like, seed oils aren't bad for you. Processed, industrial, processed seed oils are not bad for you. They're not causing inflammation. There's no signs that, you know, these have negative consequences. I see that all over. I know it's social media.

Yeah. It's frustrating. So they gave people these two meals, Right. And what they found, they actually looked at two hormones. Ghrelin, which is kind of a hunger hormone. It's anti satiety and resistant. And we know that as levels of resistant rise in human body, we get more insulin resistance. And so the levels of ghrelin and the levels of resistance were higher when they gave people a linoleic acid rich meal. So this is a small study, but. Yes, it's a small study, but it is a study in humans. It is a controlled trial in humans.

And.

And we need bigger trials showing that linoleic acid rich meals may make us hungrier and more insulin resistant. And this is just to emphasize this concept that not all calories are created equally. These are equal caloric meals. One of them has 18 carbon monounsaturated fat oleic acid. One of them has 18 carbon polyunsaturated fat linoleic acid. They're supposed to both be 9 calories per gram. But this linoleic acid rich meal, again, linoleic acid rich in. Is usually found in seed oils, things like corn, canola, sunflower, safflower, soybean is making people hungrier. It's changing the hormonal profile, and it's.

Also causing damage to the endothelial lining, which is the genesis of the cardiovascular disease that we blame on cholesterol. Right. Cholesterol is at the scene of the crime, not pulling the trigger, but very often it's there because it's trying to repair damage. So I think that it's like, you know, we used to think that Alzheimer's disease was the presence of amyloid plaques in these neurofibrillary tangles. And we're realizing now that the amyloid plaques are the byproduct of the inflammatory process. Right. So that the. The culprit is not the amyloid plaque.

Right.

That the culprit is the inflammatory process. Right. And so I think you're getting to the root of another issue, which is are we really getting atherosclerosis, arteriosclerosis because of cholesterol or. Or are we getting it because of damage to the endothelial lining, of which there's strong evidence to indicate that insulin resistance causes this inflammatory process and that cholesterol is just being called there. It's like, somebody gave me the analogy the other day that every time there's a fire, firemen show up.

Yeah.

And, you know, to put it out. And. And so we're not blaming the firemen for the fire, are we? Because they're actually there to try to put the fire out. And it's kind of like what happens to, you know, when there's damage to the endothelial wall, to the. To the lining of the artery. You know, the firemen show up, the cholesterol shows up, and. And we're like, we need to keep the cholesterol down. Right?

Yeah.

And so, like, we need to suppress the firemen and fires will stop happening.

Yeah, it's interesting. And if people are confused about seed oils, because there's a lot of conflicting data. Yes, I would say look at the data regarding seed oil consumption and oxidized ldl. So LDL is low density lipoprotein. It's this quote unquote, bad cholesterol. Obviously that's an oversimplification, but it's pretty darn clear from multiple randomized controlled trials in humans that when you feed humans seed oils versus olive oil versus butter, we get more oxidation of ldl. That is very, very difficult to argue that point. So I do not know how individuals in the health space can argue and.

Tell, tell my listeners. Like, what does oxidized LDL mean? Right, right. Why is that so bad?

Yeah, LDL is, is low density with a protein. It's like a balloon or a bus that floats around our bodies and moves, moves cholesterol and triglycerides. So it's, it's a ball and it's a transporter. It's a transporter, it's a ball. It's. It has a membrane and the membrane is full of phospholipids and the membrane is full of cholesterol and the membrane is full of proteins. And when LDL becomes oxidized, it means that the phospholipids in the membrane have become oxidized and oxidation is akin to rust. Right.

Okay.

You can think about rust as oxidation. Technically, oxidation is loss of electrons. When a molecule loses an electron, it begins a free radical type cascade. In the case of lipids, we call this lipid peroxidation. And these are lipid peroxides that get formed in the membranes of our cells or in the membrane of an LDL particle, a low density lipoprotein particle.

So now I've taken an LDL particle, I've oxidized it, so I've damaged its phospholipid bilayer.

Right.

And now what is that damage causing? Just because the phospholipid bilayer is rusted, now what's the next consequence of that?

So when, when electrons are stolen from the phospholipids in the membrane, there's a chain reaction. And eventually that free radical cascade, that lipid peroxidation reaction damages the proteins on the surface of the ldl. And when the proteins at the surface of the LDL are oxidized, they look differently. And then we know pretty clearly from medical studies that that makes the LDL particles look like foreign Invaders. And your macrophages, the immune cells that live in your body but also live in your arterial walls, are more likely to take up that LDL molecule and form the beginning of an atherosclerotic plaque, which is called a foam cell or, you know, a fatty, or a fatty streak. So macrophage is more likely to ingest LDL particles when the LDL is oxidized. That's how atherosclerosis begins. So oxidized LDL is probably, you know, potentially making this LDL more atherogenic, or I would say atherogenic de novo from the beginning. Because, as you say, I also don't believe that the case that LDL is atherogenic in and of itself is shot yet. I don't think it's very clear, right. I think that ldl, low density of protein, is moving cholesterol and triglycerides around the body and it is at the scene of an atherosclerotic plaque, like you say, like firemen. But that doesn't mean that it causes it because there's.

And the ones that are at the scene are these usually the oxidized versions.

Of, of ldl, very often within the plaque.

Right? Because, because, you know, what you're getting to is that not all LDL is created equally. Maybe it's all created equally, but not all LDL is the same.

Not all LDL is the same. And you can change your LDL based on what you eat, right? You know, you can change the size, you can change the membrane composition, you can make your LDL more likely to oxidize, right, when you eat seed oils.

And then once it oxidizes, it's more likely to be the culprit of plastic. Now why is that? Does it increase how sticky it is? Is it more likely to clump and, and, and stick together and group and narrow the artery?

I don't think we fully know it could be that. So this is a whole sort of not fully fleshed out within the lipid space. It could be that there's, there's a lot of changes that can happen to LDL that damage ldl. You can get desalated LD desalated, you know, ldl, you can get oxidized ldl, you can get all sorts of changes. But basically, I would say high level, it looks like LDL is this particle that moves around your body carrying substrate, carrying building blocks. And it probably moves in and out of your arterial wall on its own, naturally, because it has to deliver things. But if your LDL is More likely to oxidize, then it's. And again, this is all sort of hypothesis. We don't fully have this worked out within lipidology, that the LDL that's more likely to oxidize gets stuck in your vessel wall. And when it gets stuck in your vessel wall on a proteoglycan matrix inside of your arterial wall, then it's oxidized and then the macrophages come and clean it up. Because it's a, it's a foreign looking particle and that's how you get atherosclerotic plaque forming. So native ldl, ldl. It's not oxidized. It's, it's not an easy case to make that. That is actually atherogenic or injurious to the endothelium.

Right. But oxidizing without endothelial damage. I don't know that you have atherosclerosis.

I would say that you don't.

Yeah. Because if we look at where atherosclerosis starts, you know, it's, it, it, it starts in, in, you know, in and around the heart, usually. And why would it concentrate there?

Well, it concentrates there because there's more, more turbulence and more damage to the endothelium. But we can get atherosclerosis other, other places. Sometimes people get it in the, the bifurcations of the femoral artery. The femoral arteries. But we do get atherosclerosis in places where there tends to be more turbulent stress denuding the endothelium. And I think that individuals who are insulin resistant, metabolically unhealthy, they don't repair those wounds as well. I think you and I, all of humans are getting endothelial damage. That's just part of being a human. You have this, you have this delicate layer of endothelium lining your arteries and you have pressure in your arteries is very high. 120 millimeters of mercury is a lot of pressure every time your heart pumps. Yeah, right. And so you're going to strip that endothelium even in a healthy individual. And I think that my theory, I think the hypothesis here would be that in a healthy individual you can repair that. Just like you scratch your knee, you know, you repair it. But in a diabetic, somebody that's metabolically unwell, the repair of the endothelium is delayed or it's impaired. We know that wound healing is impaired in diabetics. And so this is why I believe diabetics have more of a predilection to Atherosclerosis, because they skin their knee and sometimes you have to amputate the leg.

Right.

You know, I mean, diabetics, you know, when I was working in the hospital, you would see diabetics come in and you would do foot inspections on diabetics because sometimes they don't even see they have a little cut on their foot. So a diabetic can, like, stub their toe and they might lose their whole foot because the infection becomes so rampant they don't know it's there. And wound healing is so impaired. So when we become insulin resistant, also known as metabolic dysfunction, I think that we're probably just not repairing the endothelium. We're all skinning our knees, we're all getting some denuding of the endothelium, but we're not repairing it as well in diabetics. So we come back to square one. How do you prevent atherosclerosis? Don't be diabetic.

Yeah. Don't be diabetic.

Don't be metabolically unhealthy. Let your body repair it. And so I think that what's happening probably is that diabetics, people with metabolic dysfunction, which is a spectrum. Right. Of metabolic dysfunction, you're getting some damage to the endothelial wall. And this could be from cigarette smoke. Secondhand smoke could be from diesel exhaust, probably alcohol could do it.

Yeah.

Lipopolysaccharide might be involved. Endotoxin.

Lots of things can damage seed oils.

Yes. Lots of things can damage the endothelium. And it's. It's all about how well you repair it. And if you're not repairing it, well, then, yes, it's possible that LDL could get involved and become connected to that proteogycan layer in the arterial wall. It's more likely to get oxidized if you're eating a bunch of seed oils. Macrophages come, pick it up, make a foam cell, making a fatty streak, and atherosclerosis. There it goes.

There you go.

So I'll take you this one thing and then I'll pause. I think about ldl, like wood. And wood is valuable, but you. Wood doesn't make a fire on its own.

No.

Right. Wood is valuable because you can build a house out of it. And we know that LDL has valuable roles in the human body. It has immune roles. LDL participates in the immune response. It moves precursors for hormones around our body.

Yes, precursor for cholecalciferol.

Exactly. And it actually can bind up LPS in the human body and decrease it along with other lipoproteins. So it protects us from injury. Wood is valuable. And if you live in a place where you don't have a lot of sparks coming out of your oven and you're not like hammering metal and doing things with lots of fires, having a bunch of wood in your woodshed is great, it's valuable for you. But if you're in, in a house, like if you're in a forge and you're, you know, you're making iron and you're flying sparks everywhere, having a bunch of wood sitting around, it's going to give you more atheroscleros, it's going give you more fires, you know, more LDL in the setting of sparks, which is, I'm drawing a metaphor with inflammation or metabolic dysfunction. Could look like it's causing more fires, but it's just a substrate. It's involved, it's in the causal cascade, but it's not causing the issue. You need sparks to make a fire. Wood doesn't spontaneously combust.

Right, yeah, no, very, very true. So just around this out, you know, and get back to our calories in, calories out. Where do you stand on the calories in, calories out theory?

So you can lose weight eating anything. It's been proven you can lose weight eating Twinkies.

And I think that's the detriment. I think that's where, you know, the pundits, you know, get us and they go, yeah, if you ate two donuts a day, you'd lose weight.

You can lose weight.

Yeah.

But we know from studies, there's so many studies that show this, that caloric restriction more than 85, 90 of the time fails long term because you get adaptive thermogenesis. Your thyroid metabolism. Yeah, your thyroid turns down your metabolism. I mean, look at the biggest loser.

TSH drops. Yeah, right.

Look at the biggest loser. They all gain the weight back plus more. So calories in, calories out works in the short term and fails in the long term. And I think that the, really the only strategy that I've seen that's successful people to lose weight long term is to improve food quality because that's how you get satiety, right? You improve food quality. You need less ultra processed foods. And the Dietary Guidelines Committee needs to just check themselves because they're absolutely crazy to say that, that we don't know that obesity is caused by ultra processed foods. You can't leave that door open because.

Then look at, look at this data. In the United States, we eat the highest consumption of processed foods, and we're the most obese. And I know it's just correlation, Gary.

Correlation.

Yeah. You know, it's like we also do the highest number of randomized clinical trials. And, and in health care, we did 150,000 of them since 2008. And you see the byproduct of taking randomized clinical trials and just applying that narrow science to an entire populace. Yeah, right.

And it's, it's crazy. And so I think that, yes, you can lose weight if you want to restrict calories, but I think that if you want to get healthier, that will be nearly impossible to achieve unless you improve food quality. So I think the, we should not be thinking about calories in, calories out. We should be thinking about how good, how, how, how high quality can I make my food? And if that sounds like a nebulous concept to people, just think unprocessed meat, beef, chicken, fish, lamb, pork, eggs, you know, cheese, milk, preferably raw, like unprocessed animal foods and unprocessed plant foods shop around the outside of the grocery store.

Right?

Just don't, just don't do ultra processed foods. And then that's, that's the key to success. Because I think that if you think calories, then you're just going to say, I can eat this pizza today and I'm going to eat less calories tomorrow. But I want people to understand like my, the problem I have with that is it's very difficult for us to quantify or qualify how the negative effects of that ultra processed food reverberate throughout our physiology. And that's where calories in, calories out fails. The qualities of calories in can affect calories out, it can affect your metabolism.

It can affect your satiety, the downstream consequences. We used to see this in the mortality space, you know, pushing LDL cholesterol down because it was linked to cardiovascular disease, but not realizing that it's also, for lack of better words, a construction material that's used to build cell walls, cell membranes, hormones, you know, vitamin D3. So now if you, if you, if you remove construction material from the job site, doesn't matter how good your contractor is, they're not going to assemble anything without the construction material. And the body's no different. You know, it has, it has to make cell walls, it has to make cell membranes, it has to make hormones, and it, it makes vitamin D3 from, from sunlight and cholesterol. And if you deprive it of those resources, you get other downstream consequences. And if the study didn't look at those things, then you would just draw the conclusion that, well, it's bad because people with higher cholesterol have these higher rates of cardiovascular disease, but maybe it's because people with higher cholesterol are having the endothelial damaging things like the oxidation and what have you that actually leads to the damage that is calling the cholesterol there.

I agree. There are studies looking at markers of metabolic syndrome. There's one from a few years ago and one more recently. And the studies would suggest that 88 to 93% of the US population have at least one marker of metabolic dysfunction. So if we have a population in the United States where 85% plus of people have at least they're on the spectrum of insulin resistance, it's not surprising that LDL might look like it, quote, causes atherosclerosis. But there are so many studies now that generally get ignored by people in the apob causes atherosclerosis camp that show a discordance between apob levels and atherosclerosis. So I think that it's. But and again, like it's causal until it's not. Exactly it's causal. It's causal unless you're healthy.

Right, right.

You know, and maybe some of the behaviors you do that are healthy might actually raise your apob, like eating grass fed meat and eating less seed oils. That's going to raise your apob. And so this is where I really run into problems here with the ideology is I think that unless we really help people and we're very precise about the way we describe cholesterol and cardiovascular disease risk in terms of a context, people are just going to be confused. I can't tell you how often I get DMs saying I'm eating an animal based diet, I'm eating meat and I'm eating organs and I'm eating fruit and I feel great and I've lost weight and my diabetes is better. But I went to my doctor and they said my LDL is high and I need a statin. And it's just like there's no context here.

Right.

And if you, if you don't, you know, you don't have to look much further than the side effects of statins to understand the benefits of, you know, in terms of their signal for potentially increased dementia, potentially increased diabetes. I mean, I can tell you because I work as a pa, so before I was a doctor, I was a physician assistant in cardiology and I worked in cardiology. The idea that 3%, like Pfizer says of people get side effects from statins is bunk. It's more like 30% from what I've seen in my clinical practice and I saw hundreds of patients and the, a lot of them get side effects from statin. So it's the whole eight. The cholesterol piece is probably one of the single greatest hurdles for people getting healthy because we have not described it properly. Because I think the paradigm is wrong. Because most, at least if people are listening to what I'm saying or listening to what you're saying, people are going to eat more meat and they're going to eat less seed oils. And in 40 to 60% of people that might raise APOB. And so there's just, there's so many roadblocks people are putting up for people actually getting healthier and becoming, you know, more vibrant individuals because we're not thinking about calories properly, we're not thinking about APOB properly. And these are nuanced, complicated discussions. So hopefully that helps people understand the content.

Yeah, I think it does. I think it does. Man, I really appreciate you coming on. We ran a little bit over the time, but I mean, I just talk a lot. No, no, no, no. And I'm so interested. I actually am. I've got 50 other questions that I want to ask and the audience is probably really interested. So you will come back on.

Right?

Okay. So next time you're in Miami, we're definitely going to run another full, full podcast. But for, for those folks that don't know you and, and would like to find out more about you or your books or your supplement line, how can they find you?

I met Paul Saladino, M.D. on every platform.

Okay, Paul Saladino, M.D. On every platform. He has unbelievable line of products, organ organ meats and you know, dissected dried organ meats that are, that are, that are in a capsule form. If you don't like to eat raw.

Liver, that's hardened soil. Heart and Soil and Lineage is our newest company and we make grass fed beef sticks with organs and we just release an all in one out of.

Testicle called the whole package.

That's a hardened soil. Yeah, we don't make beef sticks with us Capsules test really help. You know, it's interesting. You would think tasted and the reviews on that one are amazing. We can do a whole another podcast on organs next time in my kitchen. Amazing. Yeah, like the, the, the benefits of organs for humans are incredible. And that's a whole separate podcast probably related to like Micrornas or something, but they seem uniquely beneficial for humans and that's why we built hardened soil just to make them easy to get.

So yeah, and you've been sending me some great research where which I've been digging into lately on I want the cat out of the bag, but target specific or organ supplementation for target specific organ results. And it's very, very interesting. I'm not ready to comment on it yet, but I've been been reading a lot of what you sent me. It's very, very eye opening. So guys, I hope you enjoyed this podcast. Follow Paul Saladino. Check him out. Look, look for his supplements, heart and soil. And as always, that's just science.