Why A High-Fat, Ketogenic Diet Chock Full Of Saturated Fat, Coconut Oil & Butter Could Be Destroying Your Brain (& What To Do About It).

Wakey, wakey. I slipped down in my office. I had to get up early this.

Morning.

Which is why I'm drinking my coffee. I know people hate that when I consume things on the show. I think it just makes the show more intimate. And fireside y Personally, I have to go in for a big blood draw this morning. My quarterly Wellness FX longevity panel. So I'm gonna go in and give them, like, 19 tubes of blood. But I figured I'd come down here and talk to you first. This has been Greenfield. You're about to hear me talk to my friend Max, Max Lugavere, a really cool guy, and we have a chat about making yourself smarter with food. We talk about Alzheimer's, dementia, take a dive into cholesterol. This one's actually quite a thrill when it comes to cognitive stimulation with two bros talking like they're smart. At least he's smart. I try to play catch up.

In.

This episode of the Ben Greenfield Fitness Show.

You know, I mean, if I could give my mom a pill tomorrow or put her on a diet tomorrow that would reverse her disease, I would do it, but I just don't see that as happening. I think getting a normal, healthy person to adhere to a ketogenic diet is hard enough, right? But like getting somebody with dementia, and especially a person with dementia who's cared for by caregivers who are completely uneducated, to adhere to such a rigorous dietary protocol when their brains are actually crying out for sugar and things that are anything but ketogenic clinic, it's like a major, major stress.

He's an expert in human performance and nutrition, voted America's top personal trainer, and one of the globe's most influential people in health and fitness. His show provides you with everything you need to optimize physical and mental performance. He is Ben Greenfield.

Power, speed, mobility, balance, whatever it is for you, that's the natural movement get. When you look at all the studies done, studies that have shown the greatest efficacy.

All the information you need in one place right here, right now on the Ben Greenfield Fitness Podcast.

Hey, folks, it's Ben Greenfield. And I guess it was. It was a couple months ago now that in a weekly roundup, I send out these weekly roundups on Fridays where I talk about stuff that I found interesting. And often those recommendations and takeaways include books. One of the books that I commented about was written by my friend and a guy who's been on the podcast before to talk about a documentary that he made called Breadhead, but he wrote a book, and it was called Genius foods. Genius foods. I figured it would probably be another like egg and walnut and fish make you smarter kind of book and thought I might get through in like five minutes, just flipping through, but it actually wound up pleasantly surprising me. It takes this deep, deep dive into things like specific genes that affect intelligence and how to pair them with food. You know, mouth watering recipes for everything from like liver to avocado, salmon bowls, and actually a lot of science that I hadn't yet seen discussed, particularly when it comes to either A, getting smarter or B, taking care of your entire central nervous system intelligently or C, even staving off your risk of something like Alzheimer's or dementia, which I can legally say because I'm not a doctor. Anyways, this book is, in my opinion, a must read for anybody who wants a better brain. And as I usually do, I don't like to get guys on the podcast and just talk about guys or girls and just talk about things that you could find if you were to just go freaking read the book. I like to take kind of a little bit of a deeper dive and unpack, so to speak, some of the more cutting edge concepts that I discover within the pages of wonderful books like this. So I got Max on the show. He's here with me and like I mentioned, he was on the previous podcast episode called the surprising facts about what bread does to your brain. And he created this documentary called Breadhead, much to the chagrin of anyone who likes my wife's slow fermented sourdough bread recipe, which I still have to get you to eat. Max. You may have also seen max on the Dr. Oz Show, Rachel Ray show, the Doctors. He's also been on like Vice and Fast Company and CNN and the Daily Beast. He's all over the place. He even has a podcast now he has a podcast called, of all things, the genius life, just like his book, Genius Foods. So I will link to everything Max and I talk about if you go to BenGreenfieldFitness.com GeniusFoods that's BenGreenfieldFitness.com genius. Let's just say it like that every time. Genius Foods. And you can just grab the book everything else that Max and I talk about today. Max, first of all, welcome to the show. And second of all, have you yet recovered from the severe beating that I gave you at the gym in Arizona a couple of months ago?

Dude, thank you so much for having me. It is a pleasure and a privilege. There's nobody better than you. You are simply the best and an inspiration oh, Dar, I just launched. Yeah, no, I, I, I just launched my podcast. And you are, you're a master. And yeah, I'm still recovering. I've still got doms from that workout that we had three months ago.

Well, that was my go to, that was my. So my go to gym workout subtracts anything that requires any amount of coordination or focus because I know when I travel I have an incredible amount of decision making, fatigue and lack of cognitive willpower from traveling. So it's a very simple workout. You simply choose five exercises. Upper body push. Upper body pull. Lower body push. Lower body pull. And something for your core. And you just hammer all of those out for as many rounds as you can fit in to the amount of time that you have. And after every round, you do two minutes of intense cardio. So it's like concurrent strength and cardio training? No, it's not snatches or cleaning jerks or anything remotely functional, but damn, for, for like you mentioned, Max doms. It works, doesn't it?

It works. It works. Yeah. I mean, I, you know, I consider myself to be in very good shape. I'm really interested in, you know, physical performance, body comp, stuff like that. But being around you and watching how you work out, I mean, definitely, you know, it's good motivation. So thanks for that.

You're welcome. I'm also a masochist, so that helps. Helps a little bit. What'd you call it? A sesh? That's what the kids are calling these days, huh? By the way, you're incredibly well spoken and I've seen you speak on stage a few times. You know your way around this science pretty well. How old are you?

I'm 36.

Okay.

And yeah, so I, you know, I've been interested in fitness and nutrition my entire life. It began in high school. I wrote my high school senior thesis on creatine, so. And you know, I was also kind of obsessed with the ketogenic diet. I read the Ketogenic diet by Lyle MacDonald back when I was 17. So I'm an early adopter, if you will, of many of these nutritional concepts which seem to be really entering the zeitgeist lately. But for me, they've been a part of my life for as long as I can remember. So if it seems like I know what I'm talking about, it's just because I've been kind of obsessed with nutrition science for the longest time, more than pretty much anything.

Why this book? Why didn't you write a book about. I know you kind of got on the bread soapbox for a while. But what made you decide to write a book book about foods in your brain instead?

Yeah, that's a good question. So I used to work for a TV network that was a news and information network that reached 100 million homes in the United States. And it was called Current tv. Some of your listeners might remember it. Al Gore was the co founder of it, but it wasn't a political platform for him. It was really just sort of like a news and information network meant to bring forth a new kind of journalism that was meant to ultimately make the world a better place. And I was one of the journalists for that network. I was sort of handpicked out of college by this guy who gave many, you know, well known journalists, journalists that are household names at this point, their first jobs. And I was one of them. So I got to do that for six years, cutting my teeth with some of the best of the best in the field. And I was very young, but nonetheless I learned a lot. And when I left that job in my late 20s, I started spending more and more time with my mother in New York City, which is where I'm from. And I really seized the opportunity to catch up with my family, spend more time with my mom. I'm the oldest child of, you know, I've got two younger brothers and I'm the firstborn. So, you know, any. Anyone who's the oldest in the family listening can relate. You tend to have a special relationship with your mom, and there's no question that I do. So I began spending time with her. And you know, Ben, it was really strange. My mom was 58 at the time and youthful, blonde haired, had this vibrancy about her that, you know, my mom is really kind of known for. And nonetheless it seemed as if her brain suddenly had downshifted and had almost as if she had had a transplant, a brain transplant with a much older person. It really came to a head when I would be cooking dinner with my mom, which is one of my favorite things to do, and I would ask her to pass a spice that was maybe in the overhead cabinet where, you know, that she was standing by. And it would take her a few extra beats to register that command. I mean, almost like to a point where, you know, I was taken off guard and it left me with a knot in the pit of my stomach. But ultimately I kind of just wrote it off to aging. And in tandem with that, there was a change to my mom's gait, which is the way that she walked. Now my mom is a New Yorker, I'm a third generation New Yorker, and New Yorkers walk pretty fast. But what had previously been a very healthy stride suddenly had transitioned to more of like a shuffle. And me and my brothers actually coldly would joke amongst ourselves that it looked kind of like my mom had been bitten by a zombie because of the way that she began to walk. And, you know, we were completely ignorant of movement disorders, of neurological disease of any sort. Dementia didn't run in my family tree.

Yeah. And by the way, I should throw in there too. I don't know if you've seen some of the NIH studies that you can find. They go back as early as 2010 on Pubmed about the pretty significant link between walking speed and survival, or walking speed and risk of mortality. That's like one of the things to kind of pay attention to if it's declining dramatically with age. Kind of like walking speed and grip strength are two of the main physical parameters to pay attention to.

Yeah, 100%. As well as, you know, getting up off the floor or standing on one leg balance is thought to correlate with brain health. I mean, I'm not sure how many of these tests are being used clinically, but certainly, you know, I mean, walking is something that we're literally engineered as a species to do. You know, that's the way that we're able to move about the world and procure food. So any change to somebody's walking pattern is going to raise eyebrows of any healthcare professional. But for me, I wasn't a healthcare professional. I was just a guy concerned about his mom. And I had the ability, thanks to my sort of atypical career, that at a certain point I decided to step in and accompany my mom to doctor's appointments. And we began in New York City, which is where, you know, my mom lives. But ultimately, when we couldn't find answers in any of the neighboring hospitals by my mom's house, we cast a wider net, ultimately taking us to the Cleveland Clinic. And the Cleveland Clinic is known for taking on complex medical cases. What they do is they kind of assemble a team around a patient. You know, everybody from an endocrinologist to, you know, neurologist to, I mean, you name it, they basically, you know, they're sort of like the place you go when, you know, all else fails. And on the other hand, it's thought to be a cathedral to modern medicine. So we went there and ben there for the first time. My mom was diagnosed with a neurodegenerative disease. She was prescribed Drugs for both Parkinson's disease and Alzheimer's disease. And when I tell you that was one of the worst weeks of my life, I mean, I'm a pretty chill guy, but I had a panic attack when I began googling those drugs and realizing that not only are they of highly limited efficacy, but they have no disease modifying capacity.

Well, what's, by the way, an example for people who don't know what type of drugs you get placed on with Alzheimer's. You know, I guess one that I'm familiar with are, you know, ampakenes that a lot of biohackers will use as a smart drug as well. But what. What were some of the drugs that were recommended to her?

Yeah, so, I mean, the most. The most common one is a drug called Aricept or donepezil, which. Or donepezole. I don't know. I mean, I've heard doctors pronounce it a myriad of different ways, but essentially what it is is it helps increased levels of acetylcholine, which is a neurotransmitter involved in learning and memory at the synapse. The problem in Alzheimer's disease is that the neurons that produce acetylcholine begin to slowly die. There's widespread neuronal dysfunction in Alzheimer's disease, and so these drugs sort of act like chemical band aids to try to increase the availability of that neurotransmitter at the synapse in hopes of it sort of improving cognitive function. So some biohackers will take, actually Aricept, but, you know, I'm of the opinion, and I know, you know, I'm pretty sure that you are, too, that there's no such thing as a biological free lunch. So I'm always hesitant, not when you're.

You're. I mean, and a lot of people get a crash after they use something like that just due to constant depletion of choline and acetylcholine levels. You know, anytime you're dumping an acetylcholinesterase inhibitor like that into your body. Yeah, you're right. There's no biological free lunch. And I know that donepezil has some other side effects that go along with it, but. Yeah, it's a convenient bandaid, I guess, for the Cleveland Clinic.

Yeah, I mean, and the other drug was essentially a replacement for dopamine because my mom had those movement symptoms that I was talking about, you know, the change to her gait, which was indicative of some kind of Parkinsonian complex. And so in Parkinson's disease, A group of neurons in a region of the brain called the substantia nigra begin to die off. And by the time you show your first symptom of Parkinson's disease. Parkinson's disease, half of the dopaminergic neurons in that part of the brain are already dead. So again, talking about, you know, a biochemical band aid, you're basically trying to replace dopamine by these neurons that are slowly dying but have already significantly perished by the, you know, at the point of being prescribed a drug like this. And also, what I think these doctors neglect to mention is that if the drugs don't work, a patient really shouldn't be on them because they're pro oxidants. You know, there's like these sort of double edged swords that are present everywhere in biology. Like the fact that oxygen, you know, we simultaneously need it for life, right? We need to breathe. But oxygen is an oxidant and it ages things, it makes things go bad. Like a sliced apple that you leave out on the counter, right? Well, the same thing with these neurotransmitters like serotonin, dopamine, acetylcholine. We need them for the proper functioning of our brain cells. Right? But having too much lingering at the synapse actually acts like a pro oxidant. It's one of the reasons why the drug mdma, otherwise known as ecstasy, is so dangerous to your brain cells because it causes a flood of serotonin into the synapse, which literally burns away the dendrites, which serve as a sort of physical correlates of memory.

Wait, can you say that again? Because a lot of people are super interested in mdma, even as like a, like a frequent microdose right now, by the way, ecstasy, for those of you who aren't familiar with it.

Yeah. So MDMA is, you know, it's a, it's a, it's a street drug, but it's actually also got some medical merit. It's being studied as a potential therapeutic for post traumatic stress syndrome. And look for people with clinical problems like ptsd. I, you know, when all else fails, I would not deprive them of the potential of seeing some kind of therapeutic benefit from these drugs. But I'm talking about most people using them recreationally. Again, there's no such thing as a biological free lunch. And when you break the regulatory dam that governs serotonin release at the synaptic cleft, well, you're basically causing a whole, or leaving the door open for a whole host of problems. That's why many people feel depressed the day after, you know, using a drug like mdma, but over the long term, it literally can cause brain damage. I've actually become, and not to go on too much of a tangent, but I've become somewhat interested in the research on psilocybin mushrooms because unlike mdma, which again breaks the regulatory dam and floods the synapse with your own serotonin, psilocybin actually acts like a serotonin agonist, activating the same receptors, but not really tinkering too much with your body's own serotonin release. So, I mean, that's kind of how I understand the difference in those two compounds.

That's interesting, especially when you, when you consider that MDMA was synthesized, you know, psilocybin is, you can get, you know, some DMT analogs and synthetic psilocybin derivatives, you know, off of laboratory chemical websites, and they work pretty similarly to psilocybin. Although the effects, I've toyed around with a few of these, the effects seem to last much longer, which probably means that they are indeed affecting serotonin receptors even more than say, naturally based psilocybin from, let's say a mushroom grown out of a cow patty. But MDMA is, it's chemically synthesized. And I would be interested to see if some of the same risks are inherent with something like microdosing with lsd, for example. But when it comes to exhaustion of some of the neurotransmitters, what you're saying is that similar to some of these Alzheimer's drugs, you risk some of the same issues, like a serotonin desensitized sensitivity to serotonin or to dopamine, for example.

Yeah, I mean, so that'si mean, that's one of the problems is that, you know, you can cause a downregulation of the receptors that literally bob up to the surface of the receiving neuron. Those receptors can actually become downregulated when you force too much neurotransmitter into that cleft. It's one of the reasons why dopamine stimulating drugs can be so addictive because, you know, you essentially create a dependency, a tolerance to dopamine. The same, same thing happens with the dopamine replacement drug in Parkinson's disease. Actually, it's very interesting. So when you flood the brain with synthetic dopamine, which comes in the form of a drug for Parkinson's patients called Sinemet, there's a downregulation of the dopamine receptor. It's sort of like Insulin resistance, you become tolerant to dopamine. So this leads to less receptors on the surface of the receiving neuron and you need to take more of the drug to have the same effect. What happens over time? Actually, this is a very strange side effect of Parkinson's drugs. Some Parkinson's patients actually start to display risky behavior, like they begin to gamble maybe a little bit more or engage in, you know, more risky sexual activity, which is very strange to think about a Parkinson's patient, you know, becoming a, you know, a sex fiend. But, but nonetheless, it's super interesting. That's why. And one of the things I talk about in the book is the absence of these neurotransmitters making the receptor become more upregulated as a means of sort of resensitizing your brain to various things. I know you talk about coffee and getting off coffee for a week here and there to sort of resensitize your brain maybe to adenosine receptors, right? So it's really the same mechanism throughout biology that's really elegantly and beautifully reappropriated. You know, the same thing occurs to insulin. You know, you repeatedly pound insulin receptors with insulin. You're going to become insulin resistant or tolerant to insulin. So the same thing happens in the brain with our, with our various neurotransmitters, especially when we pharmacologically tinker with them.

Now you actually get into this a little bit in the book. And by the way, we're completely ruining the Burning man experience for a lot of listeners right now. Anyways, though, you get into a very interesting perspective that you have. And I want to return to your mom here in a second, but you talk about dopamine and I believe you refer to it as like abstinence from hedonism in the book. Can you describe a little bit more what you mean by abstinence from hedonism? And if there is a way for someone to like weave together an intelligent use of something like plant based medicines or any of these other things that would cause potential exhaustion of dopamine or serotonin.

Well, I mean, that's what I say in the book, is that absence makes the dopamine receptor grow fonder. And really what I'm talking about is the fact that we all as human beings experience something called hedonic adaptation. You know, this is very easily illustrated. If you've ever sort of desired something and then gotten what you've desired, whether it's a girl that you have a crush on or a guy that you have a Crush on or a car that you really want. You know, the fantasy is always a lot more powerful than actually having and spending continuous time around the object that you desire.

So almost like a chemical version of a Familiarity breeds contempt.

Exactly, exactly. You know, a car that you've always wanted, for example, once that car has been sitting in your driveway for six months. I mean, you don't have the same level of, you know, reward, the same sensation of reward that you had. Maybe the first couple of weeks that you had that car and driving it was full of novelty. So what I advocate in the book is sort of taking a moment every once in a while to step off the hedonic treadmill and to allow your brain really to resensitize the things that make you happy. Because we can become tolerant to this stuff. I mean, a lot of people experience that with hyper palatable foods that I talk a lot about the fact that our food supply has become rife with foods that push our brains to a bliss point beyond which self control is completely impossible. It's sort of like, you know, the culinary equivalent of pornography. Pornography. Actual pornography does the same thing. You know, it's so extreme. It's like not something that could ever be replicated with. I mean, you know, on average, in a typical sense, with normal human relationship. And so what it does is it kind of short circuits our brain's reward system.

Right. When from an ancestral standpoint, would we have been surrounded by dozens or hundreds or even thousands of beautiful women who we could basically, you know, for lack of a better word, and. And do so over and over again? Yeah, there's a definite, definite effect on dopamine. There's a great website, by the way, have you been to yourbrainonporn.com I have.

Not, but I'm gonna check it out.

It lays all this out wonderfully. I would say that any person who wants to know more about what porn does to your brain is pretty dramatic, pretty shocking really. Anyways, though, so we got from your mom into porn and dopamine. But let's go back to what happened. So she left the Cleveland Clinic, she got prescribed these medications for Parkinson's and Alzheimer's. You started to dig deep into these drugs and figure out they probably weren't really the best thing for your mom to be taking based on some of the stuff we just mentioned. So what'd you do?

Yeah, I mean, I began to wonder why. And one of the most shocking things that I learned when I began my investigation is that changes begin in the brain decades before the first symptom when talking about the most common form of dementia, which is Alzheimer's disease. And so I realized that this is a decades long process that was probably sort of simmering in my mom's brain before the emergence of symptoms.

And.

And it became really clear to me that this was something that, you know, there might be some kind of lifestyle intervention that I could use to help my mom. But it became kind of simultaneously a mission for me to try to understand, as best I could, what I could do to help prevent this from ever happening to my own brain. Because I had this new. This newly discovered risk factor, the fact that my mom had dementia. So when you have a family member with a condition, I mean, that's essentially a risk factor for you to develop the same condition. And, you know, having a lifelong passion, as I mentioned, for health and nutrition, that's sort of where I began. But also, Ben, at the same time as my mom was succumbing to the ravages of this condition, there was. There was this strange overlap where my mom's mom, my grandmother, was alive at the same time, and she was 96 when she died. But up until her death, you know, she was cognitively sharp. My grandma did not have dementia. So I intuitively had the sense that there had to have been something that shifted in between my grandmother's generation and my mom's generation that pulled the trigger, so to speak, on my mom developing this condition and my grandmother being relatively safeguarded against it. And if you look at our environment, I mean, obviously a lot has changed, right? We have iPhones. You know, we are. We have cars. Our lifestyles are dramatically different. But I would say that the most profound change has occurred to our food supply. And so I began looking there. I began looking at the foods and how they contribute to a person's overall metabolic health and how that might contribute to conditions like Alzheimer's disease and Parkinson's disease. And I did this despite the fact that my mom was not formally diagnosed with Alzheimer's disease. She was diagnosed with a much more rare form of dementia. But nonetheless, I kind of assumed that what is good for the brain is good for the brain.

What do you mean? A much more rare form of dementia?

So she has something that kind of feels like having Alzheimer's disease and Parkinson's disease at the same time.

Is there a name for that?

Yeah, it's called Lewy Body Dementia, and it's like 1% of dementia cases. Wow. Yeah.

I've never heard of that.

Yeah. There's virtually no research on it, but it's a form of Parkinsonism. So it's actually got a lot in common with Parkinson's disease. It's known as a synucleinopathy, which means that in Alzheimer's disease. Alzheimer's disease is characterized in part by an aggregation of a form of plaque in the brain called amyloid beta. In Parkinson's disease, there's also an accumulation of amyloid beta. But the central plaque in Parkinson's disease is a little bit different. It's called alpha synuclein and alpha synuclein. It's thought actually that what causes that protein to clump and aggregate in the brains of these patients might actually begin in the gut. It's very interesting research, but Lewy body dementia. So these plaques with alpha synuclein, the plaques that they form are called Lewy bodies. So Lewy bodies are present in Parkinson's disease, but Lewy body dementia is different than Parkinson's disease because Parkinson's disease is usually, at least not until the later stages, a dementia. It's a movement disorder. So Lewy body dementia is different because at the onset, my mom displayed both symptoms of a movement disorder and cognitive decline, which is usually atypical. You can look at the most well known patient or public figure with Parkinson's disease is Michael J. Fox, and he clearly doesn't have dementia. He goes on talk shows, he has movement symptoms. But Parkinson's disease usually is not dementia until the later stages, at which point it becomes Parkinson's disease dementia. Lewy body dementia is a variant where you get the dementia and you get the Parkinson's at the same time. It's very tragic.

So at that point, what did you do?

Well, I began looking at all of the risk factors at play when it comes to Alzheimer's disease and Parkinson's disease. But, you know, the fact that Alzheimer's disease is the most common form of dementia by far means that there's going to be a lot more research about it on PubMed. And so, you know, when looking for dietary interventions that relate to Parkinson's disease and Lewy body dementia, you're grasping at straws. So for better or worse, you know, I went for Alzheimer's disease and I just became fixated on understanding the risk factors, both the non modifiable risk factors, like genes. You know, we can talk about the ApoE4 allele. I'm a big, I'm very interested in the ApoE4 allele and the nutrigenomics surrounding that. But also I started looking at the modifiable risk factors Everything from, you know, diet to metabolic health to education to, you name it. And I learned that if you have type 2 diabetes, your risk for developing Alzheimer's disease increases anywhere between two and four fold. And if you look to parts of the world where their food supply has not been industrialized, but the genetic risk factor for developing Alzheimer's disease is present, like in Ibadan, Nigeria, you see that the most well defined Alzheimer's risk gene there has little to no association with actually developing Alzheimer's disease. So I was like, the food supply really is probably playing a very significant role in terms of our overall increased risk of developing this condition here in the US and so I began looking at our food supply and I realized that we're eating 60% by calories, ultra processed packaged foods. When I was growing up, my mom was terrified of healthy natural fats. You know, she was brought about in a time where saturated fats were demonized. And, you know, I grew up consuming foods like margarine and corn oil. My mom was always afraid of eating eggs. I never saw her eat any red meat. The only kinds of protein that she ate were, you know, chicken breasts and turkey breasts because they were, you know, full of protein. But actually they're, you know, as a food, chicken breast is pretty nutrient poor. Other than the fact that it's got a lot of protein in it. That's pretty much all it has in it.

And so that's, that's why I drench my chicken in olive oil and eat the skin and chew the ends off the bones like a, like a whole rotisserie chicken. That's how I eat chicken. If I'm gonna eat it.

That's exactly what I do. That's exactly what I do. I believe we have a biological imperative to not be wasteful and whole. Animal consumption, I think, benefits our health as much as it benefits the earth. I agree.

And even organ meat and awful aside like kidney and heart and liver, I. If I have guests over to my home and we're having either like my bone in ribeye or a rotisserie chicken or, you know, beer can chicken off the grill. I am well known for basically going, now this might sound offensive, but I'll just say it anyways. Going Helen Keller style and walking around the table, grabbing people's bones that they haven't eaten and just basically drenching them in olive oil and salt on my plate and finishing people's bones, chewing the ends off and, and digging my teeth into the bone of the ribeye because I'm such A believer in the fact that lean meat is pretty low down on the totem pole when it comes to getting all the nutrients out of an animal based source of protein.

You are a beast. Ben Greenfield. Yeah, I completely agree. I mean, when we're eating, you know, connective tissue and ligaments and collagen and, you know, organ meats, and we're getting that collagen, collagen is really high in an amino acid called glycine, which actually helps our bodies, some animal models show, better metabolize methionine, which is more abundant in muscle meat. So, I mean, I think it's all about balance. And by sticking only to muscle meat, I think we're doing our bodies a disservice.

Now, your mom didn't do that, obviously, as you've alluded to. But before we return back to that, I don't want to neglect this population you were talking about that carries these alleles that would increase the risk for Alzheimer's. I assume you're talking about the apoe, the apolipoprotein E gene. Can you describe a little bit more about why it is that someone with that particular genetic factor would have an increased risk of Alzheimer's? And in addition, what they found or what has been noted in these populations who carry that genotype but don't show Alzheimer's progression?

Yeah, so I mean, I looked at studies with Nigerians that live in a certain part of Nigeria called Ibadan, where they've done some really interesting epidemiology there, looking at the ApoE4 allele frequency. And they see that it mirrors pretty much that of here in the United States. And what they found was here in the US it's well known that carrying one copy of the allele increases your risk for developing Alzheimer's disease between two and four fold. And having two copies increases your risk anywhere between 10 and 14 fold. And this is relative risk. Again, this is not a determinant gene. It's not like having early onset familial Alzheimer's disease, which is a very rare and niche variant of. It's sort of a mutation that determines whether or not you're going to develop Alzheimer's. But most people, when we talk about Alzheimer's disease, the vast majority of people are going to develop what's called late onset or sporadic Alzheimer's disease. And that's a gene that's not baked into your genome. It's more influenced by genes, probably a multitude of genes, genes that we have yet to even identify, but the most well defined of them is called the APOE4 allele. And just to sort of illustrate that for you, if you have genes that put you at higher risk for cardiovascular disease, that's also going to increase your risk for developing Alzheimer's disease.

I carry both, by the way. So this is a topic near and dear to my heart. I'm apoe4.3 4 and also carry some of those cardiovascular risk disease genes. As a matter of fact, I have a doctor who I think my podcast interview with him is probably going to come out after this podcast interview. But I've been working with him on my genes, the genes of both myself and my boys, and making some pretty dramatic shifts in everything from saturated fat consumption to the type of nutrients that I'm consuming and even a little bit more robust management of some of the things we're going to talk about on today's show based on the fact that I am Apoe 3.

4.

And so I have to go out of my way to learn a lot more about this stuff. And frankly, so do a lot of other people.

Is that a new finding for you, being 3.4, or is that something you've known about for a while?

It's something that I had noted on my 23andMe results, but it's one of those things where you need a medical practitioner to highlight the importance of potential risk of that for you before it really drives the. Drives the point home. So while I was aware of it, having a doctor say, Ben, you really need to pay attention to, for example, coconut oil and butter consumption versus your monounsaturated fat consumption a lot more dramatically. And I know that we'll talk more about saturated fats in a little bit and how to know how many to eat. I don't want to shove them all under the bus, but yeah, I mean, I've, for example, stepped back dramatically on my intake of saturated fats.

Yeah, I mean, look, we're at the very tip of the iceberg in terms of understanding, you know, personalized nutrition to a T. But I've at this point spent a lot of time with all of the leading researchers in the dementia prevention space, and not one of them is recommending to me to consume more saturated fat. I'll just, you know, put it to you that way. And I'm a big believer in the fact that everybody's different. There's no such thing as a one size fits all diet. And while certain people, I'm sure, can better metabolize an excessive amount of saturated fat, when it comes to making a widespread recommendation you know, there's no evidence to say for anybody that butter is going to dramatically or even, you know, in any significant way improve brain function or brain health. Whereas, you know, one thing that I talk about all the time on my, in my book, on my Instagram, wherever, is that the only oil for which there exists a strong supportive body of evidence to say it's going to improve your health is really extra virgin olive oil. I mean, irrespective of what genes you have. We can look to population studies which are imperfect, but you know, we know that extra virgin olive oil is a staple of the Mediterranean dietary pattern. And research out of Rush University led by Martha Claire Morris has shown that adherence to a Mediterranean style diet which uses extra virgin olive oil exclusively. I'm not talking about coconut oil or butter or even avocado oil. If you adhere to that diet strongly, you can achieve a 65% risk reduction for developing Alzheimer's disease and dementia. So I mean, I remember that in.

Your book there was a specific molecule that you talked about in the book that's present in olive oil. It was like. Was it oleox oleocanthal, something like that? Like a phenol in olive oil?

Yeah. Yes, it's a powerful anti inflammatory. In fact, I call extra virgin olive oil nature's Advil. It's a very powerful, you know, they've shown it to be as anti inflammatory as low dose ibuprofen, which is Advil. And so that's one of the. No kidding.

I didn't know they'd compared it to Advil in clinical research.

Yeah, I mean not, you know, branded Advil, but the generic, you know, chemical which Advil is at its, at its core is ibuprofen.

I was gonna say don't, don't cost me my ibuprofen sponsorship for this episode, please.

Yeah, so I mean, so I mean that's population level. We can look to randomized control trials. There was the predimed trial that was recently reanalyzed. I'm sure you talked about that, but the results were the same.

I should note, by the way, I mean, you mentioned olive oil. I've seen a little bit of research on fish oil seeming to appear to help a little bit with Apoe 4 carriers. The other thing would be when we talk about coconut oil and MCT oil, I know some people might point out the fact that, that you see in a lot of books and I even think there are some studies that look at Alzheimer's and oral dosing of medium chain triglycerides. MCT oil or MCT from coconuts and show those to be effective. But even those seem to be. In those studies, the participants seem to be deriving the benefits from the ketone body beta hydroxybutyrate, meaning that you could probably get some of those same benefits with ketone esters, ketone salts, or shocker fasting, like an intermittent fasting protocol. So even high dose MCT oil is something that might not be necessary in my opinion, at least for management of Alzheimer's.

Yeah. Although I'm a little bit more, I guess the term, it's a stock market term, but bullish. I'm a little more bullish on MCT oil. I think it's. You're right. I mean, I think it's probably better to produce ketones as nature intended for free in your liver. As a result of consuming a low carb diet or occasionally fasting or even intermittent fasting, most people wake up in a mild state of ketosis. But ketones are not just an alternate fuel that the brain will happily use. And this is, by the way, this is important because one of the potential Suspects in why APOE 4s have a higher risk of developing Alzheimer's disease is that evident in their brains from a very young age is sort of a reduced ability to create ATP from glucose. Right. And this occurs typically in most people, regardless of the gene, as they get older. And it's accelerated by things like type 2 diabetes and obesity. But the brain's ability to use ketones as a fuel source is undeterred by these things. So that's. It's believed that ketones sort of serve as an energetic life raft for a brain that maybe isn't doing as well on glucose. But aside from that, aside from the fact that ketones are a powerful fuel for the brain, I think what's most interesting and what's come to light recently in the research is the fact that ketones also serve as a signaling molecule in the brain. That more than just allowing the brain to sort of keep the lights on, the brain upregulates production of certain endogenous antioxidants like glutathione when ketones become available. So this is super cool. And this is one of the reasons why, I think, you know, if, if you're staying within your calories and it's not, you know, affecting your body composition, like, and you can potentially have a supply of ketones going up to the brain over the course of the day, even if you're in a non ketotic state, meaning you're like in a fed state. I think that's probably not going to be a bad thing. That's my hypothesis. And we actually don't know because typically throughout our evolutionary history, the body would never have ketones available when glucose was also available. Ketones would only start to become produced once food would cease to be available. Now, only as of the past, I don't know, two years, are we able to, as humans, have an elevated level of blood sugar as well as ketones. Right. Because we have these incredible supplements. So nobody knows what the long term effects of having both elevated at the same time are. But as a potential signaling molecule, I think, I don't know. I'm cautiously optimistic.

Yeah, I think that the argument that our ancestors would never have experienced high blood levels of glucose and ketones is actually a little bit flawed for two reasons. The first is that organ meats, particularly liver, and I was talking with Dominique d' Agostino about this, this contains naturally high levels of beta hydroxybutyrate. So if you are returning back to organ meats, eating organ meats, technically you are assuming that you're getting some amount of gluconeogenesis from the protein or maybe consuming something else along with the liver. You are actually elevating ketones from just oral consumption of them along with glucose simultaneously.

And that's interesting.

The other factor happened to me just this morning. I had a cup of coffee, coffee, which we know mobilizes liver glycogen and steps up blood glucose, even if you're in a fasted state. And then I did a workout, which is also a notorious way to increase blood glucose again because you mobilize muscle glycogen and liver glycogen even in the absence of consuming glucose. And so this morning I'm wearing a continuous blood glucose monitor. Right now I had a blood glucose of 117. And then I went downstairs and I have this little device called a level that measures your ketones. And my ketones were at about 3.8. So I simultaneously had blood glucose at 117 ketones of 3.8. And I'm walking around hyper ketotic and technically hyperglycemic, but not because I ate a crap ton of MCT oil and then washed it down with a sweet potato.

That's very interesting. Yeah, I didn't realize that you can eat ketones by eating organ meats like liver, but yeah, I would wonder the relative levels of each and how transient they are and whatnot. But, but, but, yeah, nonetheless, I am, I'm Pretty, you know, I'm pretty gung ho.

We're doing a great job rabbit holing here away from those, those darn Nigerians that you were talking about. Let's, let's go back to that. So, so these folks have the APOE genotype. It's not expressed. It, it appears to not be expressed because of their diet.

Yeah, because they're eating a less industrialized diet. I mean, they are eating about a third less carbohydrates overall, dramatically, radically less sugar. You know, there's other lifestyle factors at play too. Again, it's, you know, epidemiological research like this, it's kind of hard to tease out causation because all you can really identify are correlates. But Nonetheless, there, the ApoE4 allele has little to no association with Alzheimer's disease. So what that suggests, which is very, very interesting, is that if you live in the United States and you have an increased genetic risk of developing Alzheimer's disease due to the presence of an ApoE4 allele in your gene, you might simply move to Ibadan, Nigeria and see that risk abolished. And that, to me is pretty fascinating. And what it tells me is that we're doing something here in the US and increasingly abroad because, you know, chronic diseases is slowly becoming our number one export that seems to really be pulling the trigger on gene expression when it, you know, as it pertains to Alzheimer's disease.

Hmm, interesting. And that' sthat kind of brings us full circle to this idea of saturated fat consumption. I'd love to address that next. And then, of course, you know, I know that we'll come back to your mom and some of the steps that you took with her, but regarding saturated fat, can we talk about that for a second just so we don't leave people hanging? Because there's a lot of people consuming saturated fat. You talk about this idea in the book that a high fat diet could damage the brain. Can you get into that? Because there are a lot of people who are doing kind of like this modified ketosis Atkins carnivorous diet approach that does have, especially relative to monounsaturated Mediterranean based fats like the extra virgin olive oils and the fish oils that we were talking about. It's a little bit low in those and pretty high in some of these saturated fats. Can you get into, into how a saturated fat diet or a high fat diet could damage the brain? Because there are books out there about, there's like, what's the book about? The gal who used coconut oil to heal her husband's onset of dementia and Alzheimer's. You know what I'm talking about?

Yeah, that's Mary Newport. I actually cite that exact case study in my book. It's very, very interesting. She's become a good friend of mine.

Okay, talk about that for a second. That this whole her and this idea of all high fat diet in the brain.

Well, so Mary Newport is a Florida based neonatologist whose husband developed Alzheimer's disease. And seven years into the disease, Mary discovered an ad, or as a press release rather, for a new medical grade food that was being approved or going for approval from the fda. And what it was going to essentially do is supply energy to the metabolically ailing Alzheimer's disease brain. So as we talked about, you know, people that have genetic risk, they develop, you know, a reduced ability ATP from glucose. And ultimately in Alzheimer's disease, brain's ability to create ATP from glucose is diminished by about 50%. So it's one of the reasons why they're now referring to Alzheimer's disease as a form of diabetes of the brain. It essentially is starving for energy. And so Mary saw this medical grade food that was promising to basically supplement brain energy using fat, using this fraction of coconut oil called a medium chain triglyceride, that becomes instantly converted by the liver into beta hydroxybutyrate, which the brain will happily use as a fuel source. But Mary, rather than wait for this drug to get approved, this food product to be approved by the fda. Her background in neonatology helped her to realize that medium chain triglycerides are routinely fed to newborns, neonates. They help babies that are born prematurely put on weight. And also breast milk, natural breast made human breast milk is rich in medium chain triglycerides. And a newborn baby actually spends quite a bit of time in ketone. So she put two and two together and realized that these same fats could be found in coconut oil, although to a lower, you know, to a lesser concentration, and began giving her husband just pure coconut oil, putting it, you know, in whatever food that she could, his morning oatmeal, feeding it to him by the spoonful. And she noticed that his cognition improved dramatically. You know, and this is an anecdote, so I just want to be really clear that anecdotes are not the same thing as having a robust data pool and studying in a randomized control trial. But nonetheless, Mary believes that feeding her husband coconut oil really helped to improve his cognition. And in my book Genius Foods, I actually show these cognitive tests, these drawings that Mary had her husband do that really do seem to illustrate an improvement in cognitive function. It could have been a practice effect, but. But nonetheless, she reports that on the day that she skipped giving her husband coconut oil, she saw a decline in his cognitive ability. So this is a case report that she's since published and kind of went viral on the Internet. I certainly became aware of her work very early on in the journey with my mother. But her, her hypothesis has since been validated by a lot of the research that we seem to be getting published by the day in regards to ketones. So, I mean, she, it doesn't seem that she was wrong, Ben. And so how does that jive with.

The idea of a high fat diet being damaging for the brain? Because that's a high fat diet, right?

Yeah. So. No, well, what I talk about in the book is the fact that the high fat diet, as it's studied in animal models, is usually a combination of high fat and high sugar. And that usually, without fail, leads to accelerated brain decay and cognitive impairment in these animal models. Okay. When it comes to the kinds of fat that we need to be eating to support healthy brain function, there's a lot of misconceptions out there. And there's no doubt a lot of the sort of push to consume more fat comes from the fact that the keto diet and the paleo diet have become so trendy as of late. And so I've actually never been on the bandwagon to endorse eating lots and lots and lots of added oils and fats because, you know, for one, we in the fitness community have been saying for a long time, don't consume, don't drink your calories. Right. And we're usually talking about sugar in that regard. But I mean, the same thing I think holds true for fat. And when it comes to the types of fats that we're eating, there's a big difference biologically in how we respond to saturated fats versus monounsaturated fats and polyunsaturated. The only fat that really seems to be healthy to be consumed liberally is not butter, it's not even fish oil, but it's extra virgin olive oil. It's monounsaturated fat, which is found in the fat of wild salmon, it's found in the fat of grass fed beef, and it's found predominantly in extra virgin olive oil. That's the only fat that animal research and population randomized controlled trials show is good to be consumed liberally. We can look at, look to studies that show benefit for fats like fish oil. But again, I mean, you have to realize that when we're talking about getting more fish oil in your diet, we're talking about trace amounts of fish oil compared to.

It sounds to me like what you're saying is that a high fat diet should be a high fat diet that is high in monounsaturated Mediterranean based fats, has some amount of saturated fat fats present. But especially if you carry this, for example, the APOE 44 or even the APOE 34 is skewed more towards monounsaturated fats and away from saturated fats and that it should include a high dose of things like extra virgin olive oil as opposed to the type of high fat diet that we see indeed causing brain damage in some of these studies, which is essentially like a slurry of sugar and lard and soybean oil that they're feeding rodent models.

Yeah, absolutely. Particularly if you carry the ApoE4 allele, I would say we really want to focus on monounsaturated fat. But you know, even if you don't carry the ApoE4 allele, again in animal studies, it really seems to be the case that in terms of its effect on the liver inflammation in the body, monounsaturated fat really is the one fat. Oleic acid is the one fat that was that we really want to lean on as being a staple dietary oil. And even that being said, I'm not a big fan of lots and lots of added fats. Again, it can easily add a lot of calories to the diet, but in terms of nutrient density, extracts of fat are not quite as nutrient dense as say a cruciferous vegetable or a piece of grass fed ribeye or a piece of wild salmon.

Yeah. What I've found, based on some of the digging I've done in literature, after really getting a little bit more interested in this kind of after that doc talked to me about my Apoe 3. Four issues, is that saturated fat consumption should really only comprise like 5 to 10% of your total daily intake of fat as opposed to, you know, upwards of like 20 to 30%, sometimes more that a lot of these, you know, ketogenic or high fat diet enthusiasts are consuming.

Yeah, I mean, I haven't really come to a conclusion in terms of the exact percentage. So in my book I say, you know, if it's, if the fat is found in whole foods, like if it's the fat naturally found in grass fed beef, for example, which you know, contrary to popular Belief is actually not that high in saturated fat. It's got a much lower percentage of saturated fat compared to grain fed beef. Then you're a. Okay. You know, I think the benefits of eating those foods outweigh the risk. But then when it comes to consuming, you know, copious amounts of coconut oil or putting butter in and on everything there, I think it's probably wise to sort of hedge your bets.

By the way, thank you for saying copious before I did. For once on a podcast, I was not the first person to say copious. For those of you who get on me for using the word copious, Max said it first. I should mention, by the way, because this happened to me the other day. I was at a spartan race in Colorado a few days ago and I checked into my little condo and I was fortunate enough to have a little kitchenette. And I had swung by Whole Foods on my way in and bought one of these rotisserie chickens. Yes, I know there's some cold expeller pressed canola oil on the chicken. It's not perfect, but also I'm not orthorexic anyways, though. So I had a bed of cold vegetables and this chicken and decided I was gonna toss in the oven and broil it to kind of heat it up a little bit and get it nice and crispy. And I wandered down into the village because this spartan race was at a ski resort. I walked into this Italian restaurant because I wanted something other than just cold vegetables and rotisserie chicken. I wanted olive oil to. To just douse all over these vegetables before I had them. And I asked them for extra virgin olive oil and they said, well, we have it, but it's cut half and half with canola oil. Kate Shanahan, in her book Deep Nutrition, harps on this about how even five star Napa Valley restaurants are now cutting half and half their extra virgin olive oil with canola oil. And you'll know, of course, that this has been done or that your extra virgin olive oil is really not packed with the flavanols and polyphenols and all of the, all the goodies that you've alluded to, Max, because it's either clear or it's, you know, it's very transparent. It's just kind of this pale yellow color instead of the dark green color with little flakes and specks floating in it. And it doesn't have that kind of spicy flavor that I believe some of that. Remind me again, oleocanthal.

Is that oleocanthal?

Yeah, that Oleocanthal gives it. I mean, you want your extra virgin olive oil to be kind of lip smackingly spicy. And if it's not, it's probably not real extra virgin olive oil. I'll link to an article. By the way, if you're listening in, go to BenGreenfieldFitness.com GeniusFoods because I have a whole article that I'll link to on kind of like this, this whole scam in the extra virgin olive oil industry. But just please know before you rush out and just grab your giant Costco brand plastic bottle of extra Virginia extra virgin unquote olive oil. Not all olive oil is created equal. I did want to talk about vegetable oil a little bit more though, Max, because you harp on it quite a bit for obvious reasons that we've kind of talked about a little bit in the book. But when it comes to omega 6 fatty acids, I'm concerned because it seems as though a lot of people are getting rid of those excessively in their diet. How do you approach this idea of omega 6 fatty acids?

Yeah, I mean, I think, you know, I don't think. I know omega 6 fatty acids are vital to life, but today we over consume them by an order of magnitude at least. And you know, the brain requires a tremendous amount of omega 3 fatty acids, but it also requires omega 6 fatty acids acids. It's got an equal proportion of DHA fat and something called arachidonic acid which our bodies can create when we consume something called linoleic acid, which is found in abundance in grain and seed oils like canola oil, corn oil, soybean oil. But we also get arachidonic acid naturally in meat products and things like that. Today we're over consuming Austria oils and, and that is not without consequence, Ben, because these oils are industrially manufactured and chemically disfigured. 100 years ago they made up virtually zero percent of our caloric intake. Today they make up about 10%. Because today we have the chemistry labs and the machinery required to create them. But what happens is that most of them, if not all of them, undergo a process called. Well, even before we get to this deodorization process, which is probably the most nefarious of all of the industrial steps required to create these oils. Usually they're extracted from these foods like corn and soybeans using harsh chemical solvents and heat. As a kid I would even look at a stock of corn and wonder how they'd get the oil from it because to me it seemed like a pretty non oily Food. But food scientists are pretty smart. They're paid a lot of money, and they found that you can actually use chemicals and solvents to get oil from these products. And then you put them through a number of industrial steps, ultimately deodorizing them so that they have no flavor. I mean, corn oil doesn't taste or smell like corn. And manufacturers love this. It allows them to use this oil in everything from mayonnaises to mayos to salad dressings to granola bars. They're used to fry nuts in. They're used to fry fried dried foods in, and they're used to coat dried fruits to keep them from sticking together in the. In the dried foods bin. But the problem is this step, this geodonization step.

My wonderful plantains that I love to purchase at the Whole Foods bulk food section, they put palm oil on them. And again, I'm not orthorexic. If I got nothing else to eat, I'll swing into Whole Foods and have my macadamia nuts with my little plantains in there as my trail mix. But, yeah, you're right. I think a lot of people, though, are aware of that. But what I'm more curious about is this idea that when you cut out too many Omega 6s, and even when you do that and you step up, like your fish oil, a lot of people, and I do this as well, but I eat a lot of these, what would be called parent essential oils in combination with it, a lot of people megadose with something we talked about earlier, like fish oil. And that can actually replace this fat in the mitochondrial membrane called cardiolipin. And when that happens, you don't actually get proper cellular metabolism occurring. You can actually cause mitochondrial damage by limiting omega 6s excessively while consuming a lot of omega 3s. It's one of those issues where you can go too far in the opposite direction. So I think there's some Omega 6 superstars out there that people really should be eating, like gamma linoleic acid or conjugated linoleic acid, you know, from things like hemp seeds and primrose oil and black currant oil and, you know, cla. You can get that in supplement form. Pomegranates have a lot of it. But I think, you know, what I wanted to kind of harp on, because I don't want to send people the message to just cut out all omega 6s. You actually need more omega 6s than you do omega 3s. Yeah.

Or like a comparable ratio. I think it's pulling hairs over, you know, really Trying to match them one to one. But if you, if you end up eating whole properly produced foods, you're gonna end up meeting that ratio without stressing about it at the end of the day. I mean, the ratio of omega 6 fats to omega 3 fats found in grass fed beef identically mirrors that ratio. The healthy ratio found in the human brain.

Is that, is that a 4 to 1?

It's, I believe it's about a, it's a, it's either a one to one or a two to one. Okay, probably a two to one.

Yeah, I've seen, I've seen mixed data. You know, like the fish oil I consume is a one to one, you know, and I've seen it as high as a 4 to 1, not much higher than that. When it comes. We're talking about, by the way, that the omega 6 to omega 3 fatty acid ratio, for those of you listening in. But I think ultimately we should, should clarify that not all omega 6 fatty acids are bad and many are actually necessary. And if you're not including those and you're consuming a whole bunch of say, fish oil, it could actually do some damage to the mitochondria in my opinion. There's a book about this. I don't know if you've read this one, it's kind of new, Max, but it's called Radical metabolism by somebody actually lives a few miles from me. Ann Louis, Luis Gittleman. Have you heard of this one before?

No, I haven't.

Okay. Yeah, you should check it out. Sheshe gets pretty far into these parent essential oils and omega 6 fatty acids. That's probably why it's on my mind right now. But yeah, I just wanted to mention that Omega 6s could definitely be something that are good for you in a certain amount.

Yeah, I mean, it's a good reason toto really kind of take a step back and not be extremist in your views on, on these compounds. And you know how complex our biology is. I mean you could even argue that not all trans fats are bad. I mean, look at conjugated linolenic acid found in grass fed beef. You know, it's studied as being a potential cancer fighter and it's a naturally occurring trans fat. So.

Yeah, and kind of similar to that, you talk about this in the book hdl, right? A lot of people are on this quest to get their horror HDL as high as freaking possible. And I was actually at the ancestral health symposium and there was this guy that gave a presentation about lean mass. What do you call lean mass hyper responders. I think it was lean mass hyper responders who have extremely high amounts of HDL with low amounts of triglycerides due to their physical activity, endurance, et cetera. And maybe that's a population. I don't know if we need to go down that rabbit hole right now for whom very high levels of HDL might not be harmful. But you get into HDL in your book and talk about why high HDL in some cases could not be favorable. Can you talk about that a little bit?

Yeah. Well, extremely high HDL can be a risk factor for certain things. I mean, in general, it's considered that having high hdl, and, you know, for the general population, high HDL and low triglycerides is generally cardiovascularly favorable lipoprotein profile, or lipid profile, rather. But hdl. I think there's been numerous efforts to try to artificially raise hdl, and the outcomes in terms of cardiovascular disease prevention has been somewhat less favorable than expected. I was even looking at a study before we hopped on the call where they've been injecting a newly synthetic, creative form of HDL into patients with heart disease to see if it helps clear up their already clogged arteries. And it wasn't really that effective. Drugs that have raised HDL have not been effective in terms of preventing cardiovascular disease. So I think the reality is a lot more complicated than, you know, we've been led to believe. And, you know, you know, you know this. Your audience is savvy. Like, you know, HDL is not necessarily just the good HDL as we've been led to believe, the same way that LDL is not just the bad cholesterol, the that we've been led to believe. When it comes to HDL cholesterol, the latest thinking is that it's really more about quality over quantity and that we want our HDL particles to be functional. And when we say functional, we're talking at least partly about an ability to pick up cholesterol from the far reaches of the body, delivered to these lipoproteins by immune cells called macrophages, and return that cholesterol to the liver, where it can be recycled. This is called cholesterol efflux capacity. And I talk about this a little bit in the book Genius Foods. But interestingly, one way to boost the functional ability of HDL particles is to practice fasting. So intermittent fasting, for a number of reasons, is one of the aspects of my protocol. And it's not rocket science. I don't really labor over the amount of hours that people should spend fasting. I just basically recommend to not eat for one to two to three hours after you wake up and to not eat for two to three hours before bed. It's as simple as that.

So what you're talking about with HDL is basically this idea that your HDL can scavenge cholesterol from, for example, inflamed areas or damage from arterial plaques, bring it back to the liver. And what you're saying is that there is a way to make that more functional so you don't just have high hdl, which could just be a sign that you've got a lot of inflammation, but instead that HDL is actually doing its job properly. And one of the ways to increase the amount of functional HDL is via an intermittent fasting protocol.

Yeah, well, I mean, I've seen limited research on, you know, because they don't even have a clinically validated test for the functional capacity of hdl. They're not testing for that in clinics. So just to be clear, there's not a whole lot of research out there, but fasting for 24 hours has been shown to improve that. I don't know if they looked specifically at shorter windows, but you could look at other research like what's being put out by Valter Longo, Satchin Panda. And it seems that shorter fasts are able to improve lipid profiles in subjects.

So especially in conjunction with high intake of plant matter, fiber from plant matter seems to have a profound impact on hdl. Not necessarily the giant bowl of oatmeal for breakfast, but a lot my own diet. I would fall into the category of lean mass hyper responder. And I'll link to a helpful article for those of you who want to read a little bit more about lean mass hyper responders and HDL to triglyceride ratios. Because that whole piece is fascinating. I wish I could remember the name of the guy who wrote the article on it, but I'll hunt it down and put it in the shownotes for everyone listening@BenGreenfieldFitness.com GeniusFoods the idea though, is that your HDL to triglyceride ratio is extremely important. And the high intake of wild plant matter, the intermittent fasting, et cetera, would be one way to actually improve that ratio.

Yeah, definitely. I mean, it all comes down to really allowing the liver to properly recycle these particles. And that's, I think, really what, you know, is what's going to help improve the functional capacity of these HDL particles. But also it's what's going to help improve the, you know, the pattern of LDL lipoproteins circulating in your blood. You know, and we can talk about the different between large and buoyant LDL particles compared to small and dense LDL particles, but it comes down to allowing the liver, which creates these particles, to also be able to reabsorb them and recycle them. And one of the ways that saturated fat is able to increase levels of both LDL and HDL is by reducing the amount of LDL receptors on the liver. One of the many reasons why, for most people, I don't advocate for an excessive saturated fat consumption, whereas monounsaturated fat seems to reduce inflammation on the liver, help the liver purge itself of stored fat, and ease the burden on the liver, so to speak, so that it can more effectively do its job. Job, which is recycling these lipoproteins among. Among other things.

Yeah. And by the way, to clarify, I think what the. What the research on high HDL was was people who had cardiovascular incidents or high levels of CRP inflammation after having a heart attack or. Or some kind of like a myocardial infarction, they actually processed high HDL differently, and it actually increased risk of mortality in people with cardiovascular issues. So I think probably the problem there was that poor heart function came before the high HDL or the high HDL was elevated in response to inflammation. And so in some cases, it could be the fact that heart disease is producing the high levels of hdl. And so if you have extremely high levels of HDL and like, cardiovascular risk factors or maybe a genetic predisposition to cardiovascular problems, you should go have your heart checked out and test your levels of C reaction active protein. Or if you just get a basic blood panel and you have high HSCRP but also high hdl, it could be a sign that your high HDL isn't from you eating the healthiest diet on the planet, but could instead be a response to inflammation.

Exactly. A symptom and not a cause, which would be my hypothesis, Right?

Yeah, exactly. Now, I know that we have limited time, but I wanted to make sure that I covered another thing that you talked about about, because I know a lot of people are doing this. I already touched on it briefly. But this whole idea of tracking blood glucose. You have a recommendation that goes beyond just looking at your blood glucose values. I've talked about on the show. You know, the idea that Alzheimer's is often referred to as type 3 diabetes due to high blood glucose causing some of these beta amyloid plaques and neural inflammation. But when it comes to tracking blood glucose, I think the one that you talk about is Homa IR in the book. Can you discuss that a little bit and why you'd want to track something like that?

Yeah. So the Homa IR is a very important biomarker to measure, and it's essentially calculated using two biomarkers. It's calculated using your fasting glucose and your fasting insulin. Basically, what you do is you take your fasting glucose, which is usually going to be in milligrams per deciliter, multiply that by your first fasting insulin, and you divide that by the number 405, and what the resulting number is going to give you is a measure of your insulin sensitivity or conversely, your insulin resistance. And this number answers, it asks and answers a very simple question. Okay, how much insulin does your pancreas need to pump out to keep your fasting blood sugar at its current level? That's a very simple way of answering that question. And, and, you know, it takes into account your fasting insulin, which is very infrequently tested in the clinic. But chronically elevated insulin can precede chronically elevated blood sugar by, I don't know, a decade. You know, this is something discovered by Joseph Kraft, the late Joseph Kraft. So, yeah, chronically elevated blood sugar is actually a lagging marker of chronically elevated insulin, which can take years before insulin resistance develops. But chronically elevated insulin is not going to be good for your health. And so we can look to this HOMA ir and all things considered, having a lower HOMA IR is better. A lower HOMA IR is going to tell you basically that you are more insulin sensitive. And this is important because having higher insulin sensitivity correlates with a number of things that we want to happen, right, where it's going to lead to better cognitive function, better metabolic health, a greater ability to dispose of glucose, and ultimately, it's going to create reduced risk for any number of chronic diseases because, you know, insulin resistance is considered sort of a hallmark of modern chronic, non communicable disease.

So if somebody has gotten a blood test, just a basic blood panel, and they know what their fasting glucose was, and they also know what their fasting insulin was, they can just calculate this themselves. It's fasting glucose. Then you multiply that by fasting insulin and you divide it by 405, and you want. You want the result to be under one. Ideally, yeah.

I mean, normal is generally. And I say normal in sort of air quotes because it's anything under than 2, 2. But generally speaking, you really want your homa ir to be optimal. And I would say that that's under one.

Is that the one that can be used to predict Alzheimer's, or do you actually need to test something else to predict whether or not you're going to get Alzheimer's? Because you touched on that briefly a couple minutes ago. But is that what you would track, or is there a different thing to track for prediction of Alzheimer's?

I don't believe that there's a validated connection between homa IR and Alzheimer's disease, but homa IR is a measure of insulin resistance or sensitivity, and insulin resistance is the Hallmark of type 2 diabetes. And once you've progressed to type 2 diabetes, your risk for developing Alzheimer's disease increases two to four fold. And all told, chronically elevated insulin might account for 40% of Alzheimer's cases. So that's a statistic published in the Journal of Alzheimer's Disease. And so, all things considered, you really want to make sure that your insulin is low. I mean, that's the inverse of chronically elevated insulin is having a nice healthy fasting insulin level, a nice healthy fasting blood sugar. And if you have those two things, your homa IR is likely going to be under one.

What about testing something like insulin receptor substrate?

That's a very good question. So there's a blood test that was able to determine over 10 years with 100% accuracy whether not a person was going to develop Alzheimer's disease. And that was looking at a protein called IRS1, which is thought to correlate tightly with brain insulin sensitivity. That has still not really made it to routine clinical practice in terms of measuring that. I don't know if it's expensive or what they found in that small trial was replicated, but. But what it does tell you is that keeping the brain insulin sensitive and metabolically healthy really should be goal number one when it comes to preventing conditions like Alzheimer's disease and dementia.

That's not a blood test. I could just go to direct labs and order this insulin substrate.

I haven't seen any lab that's doing it, so I don't believe.

So at this point, just pay attention to your homa iron.

Well, I would say in terms of biomarkers, yeah, you want to look at your Homa IR, you want to look at your CRP, which is one measure of systemic inflammation, your hemoglobin A1C. It's a pretty validated marker of your three month average blood sugar. So you want to make sure that that's low. And then homocysteine is another marker that I would say is very important. Again, you want that to be lower. All things considered, having elevated homocysteine is a risk factor for cardiovascular disease and Alzheimer's disease. If any of those are elevated or higher than they should be, then you should see your physician and you should discuss that with them. You can also read Genius Foods and I talk about all these different markers and what you can do to push them into a more favorable direction.

Yeah. Also test for an MTHFR mutation if you have the homocysteine. Homocysteine issues, because a lot of times you'll get folic acid and that can get converted. You know, if you're taking some multivitamin with a bunch of synthetic folic acid in it, that can get converted into homocysteine too. I've seen people have that cluster of like, high homocysteine, high folic acid, high circulating levels of vitamin B, and it seems to be because they've got an MTHFR issue that's jacking up the homocysteine because they're just dumping a bunch of, you know, like vitamin 4 to 5 substances and multivitamins with folic acid down their throat, thinking that's good for them, when in fact it kind of creates that inflammatory firestorm. So, yeah, I mean, we're establishing a few reasons in this podcast. I think that everybody should go out and just do a simple salivary genetic test to start to dig into this stuff, especially people who are doing things like multivitamins, lots of saturated fat, butter and coconut oil. I mean, there's some things you should look at before you. You jump into the diet. That seems to be working for one person. That probably isn't doing your brain any favors if you carry any of these risk factors.

Yeah, exactly. Well said. I think everybody should get a look under the hood every once in a while. And I mean that both in terms of what's going on with the biomarkers that we just talked about, but also your genes. I think people should know. I don't think that there's any reason to be afraid. I feel very empowered by the information that I've been able to glean from the literature, and, and if I were sort of coaching an APOE 4 carrier, I would say, look, there's no reason to be afraid. You can just kind of change your diet. And the research strongly supports that. We can't guarantee with 100% certainty that you're not going to develop this condition. We just don't have all the answers yet. But nonetheless, we do have agency when it comes to our cognitive health and our cognitive function. And, you know, fear is just one thing that I think is not going to help the situation. I think it's better to be empowered so that we can make choices and let that sort of guide the decisions that we make moment to moment. When it comes to our physical exercise, which is very important, we didn't even get into that, but that's like. That's a subject for a whole other episode diet. The research really does support that. We do have a say, and. And I'm optimistic.

Yeah, yeah. You just need to do more of that pec deck that you and I were doing at the gym. It really comes down to that.

I'm still sore, Ben. I'm still sore.

Yeah, that's all right. You're swole, too. What happened with your mom eventually, like, coming full circle. What shook out with everything that you were putting into researching this for your mom?

I mean, that's kind of the hardest question for me to answer because my mom is doing all right, but I wouldn't say that she's doing great. It's really hard. It's been a major stress on my family, and sometimes I'm around my mom and I see what the disease has done to her, and it makes me want to cry. She is not really the same person. Her quality of life has been diminished greatly. And I. When I first began learning all of this stuff about nutrition and ketogenic diets, oh, my God. I mean, I remember every time I'd go to her apartment, it was like coming down the mountaintop with the teachings from a higher power, trying to really kind of get her to adhere to this rigorous dietary protocol. But ultimately, I would go to her house and I would see an open bag of chips or, you know, like, roles or something like that, and I didn't want to. I didn't want it to affect me emotionally because I would get upset, at least initially. And the last thing I would ever want my mom to do would be to feel shame about, you know, having a craving and wanting to satiate that craving and have, like, a little blip of a dopamine hit, you know, despite this terrible disease that really is robbing her of. Of so much. And so she's. Yeah, I mean, it's really, really hard. And it also keeps me, you know, like, to borrow a term from that news network, it Keeps me honest. Like, I, you know, I see a lot in the wellness industry and, you know, claims that are unsubstantiated about reversing dementia and Alzheimer's disease and things like that. And, you know, I mean, if I could give my mom a pill tomorrow or put her on a diet tomorrow that would reverse her disease, I would do it, but I just don't see that as happening. I think, you know, getting a normal, healthy person to adhere to a ketogenic diet is hard enough. Right. But, like, getting somebody with dementia, and especially a person with dementia who's cared for by caregivers who are completely uneducated, to adhere to such a rigorous dietary protocol when their brains are actually crying out for sugar and things that are anything, anything but ketogenic, it's like a major, major stress. In fact, there was a recent trial published on patients with mild to moderate Alzheimer's disease where they actually showed an improvement when on a ketogenic diet. But what they found was that patients with moderate Alzheimer's disease, the fallout from the intervention was just so significant, such a high percentage, because it was such a stress on both the patient and the caregiver. So at this point, I love my mom to death, and I just. I'm trying to do whatever I can, but it's hard. And she's also on a number of these pharmaceutical drugs still. And finding good medical care is so difficult. I still see. I mean, at this point, I know a million doctors, many of which are great, but still, I would say most doctors don't really give patients the time. And also doctors have limited tools when it comes to conditions like dementia. We know more about space than we know about our own brains. And so I just have become so steadfast in my passion for getting the message of prevention out to younger people, that being around my mom really motivates me, and I just want her to have the best quality of life that she can at this point.

Yeah. Well, the silver lining is that it led to you writing this book. And we really didn't even touch on a lot of stuff I wanted to ask you. I mean, gaba, glutamate ratios, you get into that and how to manage that. You talk about alcohol and how to minimize the damaging effects of alcohol, when to drink, what to combine it with. You even talk about cholesterol and the fact that high fat diets don't seem to have much of an impact on cholesterol and that your body produces its own. I mean, there's so much stuff in this book we didn't even. We didn't even scratch the surface of. So I'll put a link to your book of course in the show notes. I do recommend this everybody. It's called Genius Foods. Super easy to find. Grab it. My copy is admittedly a little dog eared, but as you can probably sense from this podcast, Max knows his stuff. He has a passion for researching this. He's also. I can attest to this kind of living it. He's a healthy guy and we have a blast together when we happen to be at the same health conference or able to chat together. You just happen to be able to be a fly on the wall for today's conversation. But ultimately I would take a deeper dive into his book for sure. So I'm going to put that as well as links to everything that we talked about from like the article about Lean Mass Hyper responder that we didn't get a chance to dig into to yourbrainonporn.com to simplify link to go grab yourself a 23andMe test. I'll put everything over there at BenGreenfieldFitness.com GeniusFoods BenGreenfieldFitness.com geniusfoods Max, thanks for giving your time. Thanks for writing this book and for continuing to do the work that you do.

Dude, my pleasure man. And thank you so much for having me on. This is an awesome chat and I look forward to the next time we get to work out together again.

It'll be New York. I'll be out there speaking at David Boulay's Chef and the Doctor. For those of you listening in, great chance to hear me talk about food while you're stuffing your gaping maw with really good food. It's called the chef and the Doctor series. I think November 14th I'll be speaking in New York, but I'll be there a few days, Max. So we'll hang out and maybe hook up at Equinox or something and throw down some pecans deck.

Yeah, sounds great.

All right. Well folks, thanks for listening in again. BenGreenfieldFitness.com Genius Foods is the link. The book is Genius Foods Become Smarter, happier and more productive while protecting your brain for life. I'm Ben Greenfield along with Max Lugavere signing out from BenGreenfieldFitness.com have an amazing week.

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