Paul Saladino challenges modern dietary dogma by exposing plant toxins like phytoalexins—linked to thyroid dysfunction and autoimmune flares—while citing WWII experiments proving 10mg vitamin C/day prevents scurvy. His ancestral carnivore-ish diet (meat, organs, honey) avoids metabolic risks tied to vegetable oils and linoleic acid, which he argues drive obesity and diabetes despite rising meat consumption. Grass-fed bison from regenerative farms like Rome Ranch offer cleaner fat and bioavailable nutrients (e.g., creatine), contrasting with grain-fed beef laced with glyphosate and feminizing pesticides. Saladino’s data—high LDL without plaque—undercuts the lipid hypothesis, urging metabolic health over blanket cholesterol fears, but faces societal resistance despite ancestral and clinical evidence. [Automatically generated summary]
Listen, man, I've been telling everybody that I eat mostly meat, and they look at me like I'm going to die.
And it's kind of funny.
And I've had these conversations with people, and they were like, oh, well, if you eat too much meat...
Jamie, can we get more water?
Let's only have one water out here.
I've been telling these people that I eat only meat, and they're like, well, if you eat too much meat, it causes colon cancer, it causes this, it causes that.
And one of the things that I say, and it's a talking point that I actually stole from you, is that most plants are inedible, but almost all animals are edible.
And when you say that to them, they look at you like, oh shit.
If you just go out and eat random plants, you'll get sick as fuck.
That's real.
So when I tell people I eat mostly meat, they look at me like you're doing something really stupid.
I remember there was a story about a guy in a nursing home and he had went out and picked mushrooms for the people in the nursing home and cooked them up and they all died.
Because he fucked up.
Probably this older guy couldn't see or maybe just forgot what's edible or maybe he was just losing his mind.
But the point is, most of these things you see are not edible.
And if you think about it from the perspective of a plant, it makes more sense.
But we never do that anthropomorphization.
We never think about that.
But as I was learning about this and thinking about carnivore diets and animal-based diets, I had to learn a lot of stuff myself.
I was trained as a physician.
I wasn't trained as an anthropologist.
And I took ecology in college.
When you look at what we know about the timeline of life on Earth, 500 plus million years of plant and animal co-evolution.
And there's a lot of people who have speculated this, that essentially plants evolve, animals evolve, animals start eating plants, plants evolve defenses, animals evolve defenses against the defenses.
And there's a whole series of enzymatic systems in our liver, the phase one and phase two detoxification systems, they're called cytochrome P450 and other reactionary systems in our liver that are meant to detoxify things.
And a lot of people speculate, and I think this is really reasonable, that the majority of the reason we have those is so that we could eat plants from time to time so we didn't starve during our evolution.
But there's a real interesting interaction here.
This is warfare.
This is an arms race that's 400 million years old between plants and animals.
And so what was so interesting for me as I got deeper and deeper into this idea around, can humans exist?
Should humans exist?
Will humans thrive on a completely animal-based diet?
You start to realize, wait a minute, why are we imagining that plants are benign?
They're beautiful, they're fun to look at, but they are rooted in the ground.
They can't run away from us.
What's their defense?
Well, if you're out in the desert, a cacti's got a thorn, or a rose has a thorn, a spine.
But most of them just have plant defense chemicals, and that's not even conjecture.
That's just known botanical science that plants make chemicals, broadly called phytoalexins, That are meant to dissuade animals, insects, fungi from over-consuming them.
And so my fear is that we've assumed that plants are good for us.
And we see everything with these plant compounds through the lens of these are good for us.
How can we prove they're good for us?
There's a whole different part of the story.
What if we think about it from a plant's perspective?
What if these plant chemicals are not good for us?
And we're misinterpreting the research, and I can talk about why I think we are.
And maybe the plants are just making these chemicals to say, hey, if you eat a lot of me, you're not gonna feel good.
I'm gonna affect your thyroid, I'm gonna affect your androgens, your sex hormones, or whatever.
I'm gonna make you have diarrhea or nausea, or I'm gonna kill you.
And we've just been thinking, more plants, more plants, more plants, when it's like, wait a minute, why are we eating plants in the first place?
Like where your body responds to these effects that these plants are producing, and it actually, the response by your body is good.
The same way the response from a sauna is good.
Your body really doesn't belong in 180 degree temperature, but when you put it in 180 degree temperature, It develops these heat shock proteins, and it's actually good.
It's good for you to do that for short periods of time.
Is that possible with plants?
I know Dr. Rhonda Patrick is really into broccoli sprouts, and I think for that very particular reason.
Yeah, so this is really interesting, and if you think about it differently, it starts to make more sense, I believe, or there's a whole different paradigm, a whole different lens through which we can view this.
So, as I was writing my book, I came up with these terms environmental hormesis and molecular hormesis.
Molecular hormesis is broadly termed xenohormesis by some people.
Xeno is this Latin term that means alien or foreign.
So when you think about these, in common parlance, people lump together exercise, ketosis, sunlight, sauna with plant compounds.
But I think that's not accurate.
I don't think we should be doing that.
I think we have environmental hormesis and molecular hormesis, and they're different things.
So I won't debate that plants can be beneficial as medicine, but to use them as food presupposes that molecular hormesis is good for us, and I'll tell you why I don't think it is.
So when you go in the sauna, or when you are in ketosis, or when you're in the sun, or when you exercise, you do generate reactive oxygen species, superoxide radicals, and they activate a system in your body called the NRF2 system.
I can pull up a picture of it in a second.
And that turns on genes that are involved in the antioxidant response to manage these free radicals.
Life is this elegant dance of electron movement and protons too and other functional groups in chemistry.
But the movement of electrons is oxidation and reduction with the loss of electrons being oxidation, the gain of electrons being reduction.
And so when we think about oxidative stress, we're talking about molecules pulling electrons from other molecules, creating free radicals, which broadly means that there are unpaired electrons.
Now, these are very reactive molecules that can then create things like lipid peroxides or, you know, free radicals within proteins, which change the conformation of the protein.
And we know these can be damaging for humans.
One of the reasons that cigarette smoking is bad for us is because it creates a ton of free radicals, lots of oxidative stress.
But a little bit of oxidative stress, or just the right amount, the Goldilocks amount, is necessary for life.
We don't want to get rid of all of the oxidative radicals in our body.
They're critical signaling molecules at the level of the mitochondria.
So this whole movement toward antioxidants and more antioxidant chemicals is eventually, if we snuff out all of the oxidative radicals or all the reactive oxygen species in the human body, we'll be dead.
We need these for signaling.
So a little bit of oxidative stress is good.
Too much, stressful, creates problems.
Not enough, stressful, creates problems.
It's definitely a Goldilocks thing.
So when you are in the sauna or you are in the sunlight or you exercise, you will create oxidative stress.
That oxidative stress turns on NRF2. This is essentially a transcription factor that translocates to the nucleus, turns on genes involved in the antioxidant response, things like glutathione peroxidase, thioredoxin, things like this.
They manage those free radicals.
And that's just, it's kind of clean, right?
You have an input to the system, it turns on a gene.
Molecular hormesis is a little different.
It's like going to the pharmacy and taking a medicine.
But what we never get with plants is the package insert, quote-unquote, that comes with medications in the pharmacy.
If you go to the pharmacy and you get a drug, lisinoprol, metoprolol, a statin drug, even if you get ibuprofen or naproxen and leave at the pharmacy, on the bottle, there's a list of all the side effects.
When we use exogenous molecules for humans, we know that they don't really play well with our biochemistry.
They're going to do one thing which may be an intended effect, but then they're going to have other effects elsewhere which could be damaging.
And invariably we see this with medications we take.
We know that beta blockers can affect glucose tolerance and they can affect We have sympathetic signaling in the human body with the nervous system, and we know that lisinopril and drugs like this which affect the kidneys can have problems with electrolyte balance or other things.
They can affect the lungs because they're affecting the way that angiotensin-converting enzyme works in the lungs.
They have side effects.
And so my concern is that we're conflating the two, and we're forgetting about the side effects that are associated with molecular hormesis.
I think that there certainly are studies with molecules like sulforaphane, which is this isothiocyanate compound from broccoli, that show that it also triggers NRF2. It triggers this antioxidant response system.
But what we aren't told about much is the other side effects of sulforaphane, the so-called package insert that sulforaphane has.
And when you look at that, there's a large amount of evidence that this whole class of molecules, isothiocyanates, Actually have many negative effects in the body.
And when you think about it from a plant's perspective, sulforaphane is pretty clearly a toxin.
It's a booby trap.
So one of the things I like to ask people is how much sulforaphane is in broccoli seeds?
And the answer is zero until you chew them.
There's no sulforaphane in broccoli or kale or kohlrabi or any of these brassica vegetables until you chew them.
There's a precursor molecule called glucoraphanin, which is a glucosinolate.
And it's like a booby trap.
It's like superglue.
You get two things combining.
So you get glucoraphanin is the precursor molecule.
There's an enzyme called myrosinase in a separate compartment of the cell.
When you chew the cell and you break the cell wall, they combine.
And then out comes sulforaphane.
So it's a booby trap.
It's like, if you're gonna eat me, I'm gonna make this molecule.
It's gonna affect you.
It's gonna be a pro-oxidant, right?
Because if you look at the chemistry of sulforaphane, it actually is a pro-oxidant, meaning it's pulling electrons from other molecules.
It's not actually coming into our body and acting as an antioxidant.
It's turning on our antioxidant defense system, but it's also doing other negative things in the human body.
In the case of isothiocyanates, it's actually been shown to damage DNA, which is a process called clastigenesis, and it inhibits iodine absorption at the level of the thyroid.
And there are other molecules like this that are also found in these type of foods, the brassicate family of foods.
Things like goitrin or allele isothiocyanate.
They're all isothiocyanates.
So they're widely known to affect iodine chemistry at the level of the thyroid.
Have you ever seen people with the big necks in Africa, like the goiters?
There's an endemic goiter.
You get this huge neck.
That's hypothyroidism because they're consuming lots of foods that are goitrogenic foods, lots of foods that have similarly isothiocyanate compounds that are inhibiting the absorption or at least the utilization of iodine at the level of the thyroid.
So it's working against the thyroid.
So the intent of plants is very clear here.
It's saying, if you eat too much of me, I'm going to affect your thyroid negatively, and that's going to affect every other hormonal system in your body.
So yes, sulforaphane can be beneficial because it turns on our antioxidant response system, but it also has many side effects which are ignored.
And we see this pattern over and over and over, and this is what was fascinating.
We see this pattern over and over and over with plant molecules.
And then if you look at these two, people might say, well, is the risk worth the benefit?
And I would argue it's not.
Or I would argue the benefit is not worth the risk because you can get your NRF2 system turned on without those molecules because you can do environmental hormesis.
You can go in the sauna, you can exercise, you can fast, you can be in ketosis.
There's really good studies in cold water swimmers in Berlin And they show that cold water exposure.
So they go and they swim in cold water for like an hour.
And they'll show that their glutathione level goes down, meaning that their oxidized level of glutathione goes up, their reduced level of glutathione goes down.
They're using their endogenous antioxidant molecule, one of them, which is glutathione, To mitigate these newly produced oxidative radicals these free radicals in the human body produced by cold water swimming and then the next day They'll see their glutathione is a little bit above normal.
That's hormesis.
That's environmental hormesis So my argument is can we really say that plant molecules give us a net benefit?
I don't think we can There's lots of interesting studies here that would argue that we don't really get a net benefit from plant molecules It's kind of a redundant effect.
We can get This NRF2 system, this antioxidant response system turned on without them, and then we're getting all of the downstream negative side effects of these plant molecules.
Have there been any independent studies that show people taking like broccoli sprouts and then doing it for a prolonged period of time, measuring their system, and then doing environmental hormesis and seeing if they measure up?
Well, there's actually studies that show they have two groups of people, and I can pull these up if you want.
There's studies that compare people that eat essentially no vegetables or low fruits and vegetables to high fruits and vegetables.
And they'll compare them at 4, 8, or 12 weeks.
And at the end, they see no differences in the oxidative stress markers, the inflammatory markers, markers of DNA damage.
So it's pretty shaky ground to say that invariably all the studies with fruits and vegetables show that they provide this benefit.
In the short term, sulforaphane can create more antioxidant response.
You can get more glutathione.
But if you take it out a little bit of time, it doesn't look like there's any difference between people who are eating things like broccoli or gerlusalum artichokes or carrots or cabbage or any of these other vegetables compared to a group that eats none of them.
So there's these fruit and vegetable intervention studies which don't show any differences between these people.
So all the people that are thinking that they're doing a good thing for their system by taking these vegetables and fruits that your body has this hermetic response, you can have the exact same response from cold plunge, from sauna, from exercise?
Yeah, because if you look at the amount of vitamin C, they say there that between the 70 milligram group and the 10 milligram group, there was no difference in clinical outcomes.
The prevailing thinking is that 10 milligrams is not enough for optimal health, but we don't actually know.
There are roles of vitamin C beyond the formation of collagen, which is the main thing that gets broken when we see scurvy, or at least that's the physical manifestations.
You get bleeding gums, your teeth fall out.
This is all collagenous tissue.
The connective tissue in the human body starts to break down because you can't hydroxylate proline residues on the collagen molecule.
But when you look at it beyond that, there's actually some pretty good studies.
I'll see if I can find one.
I've definitely got one in here that shows that if you look at people eating, they did another experiment with excess fruits and vegetables.
And they had one group that had small amounts of fruits and vegetables.
And now we're going to skip up to 70 milligrams.
So it's a little bit more than 10. There's no experiments with like long-term 10 milligrams of vitamin C per day.
But there's an experiment that compares 70 milligrams of vitamin C per day from low fruits and vegetables to 270 milligrams of vitamin C from fruits and vegetables, and there were no clinical differences in those outcomes in those people.
So one group has low fruits and vegetables, one group has high fruits and vegetables.
Well, I think that if you're thinking about things in terms of oxidative stress, that happens pretty quickly.
You would definitely, I think, begin to see increased DNA damage.
We measure it with this marker called 8-hydroxy-2-deoxyguanosine, lipid peroxides, inflammation.
I think you would see it.
You start to see it pretty quickly when you get lower levels of vitamin C. The higher vitamin C group with more fruits and vegetables certainly had a higher level of vitamin C in their blood, but they didn't have any differences in terms of those markers.
So if you go to the vitamin C folder, Jamie, and then you go to the vitamin C from an evolutionary perspective study...
You'll see a list of all the interventional studies with vitamin C. Scroll down to the table two.
So one more table down.
That one.
So you'll see these are interventional studies with vitamin C and there's an RCT there for the common cold.
It's a meta-analysis, actually, which 11,306 participants and there was no effect on the incidence of the common cold.
So this gets into the interesting conversation about epidemiology, and I know you know about this, the way that epidemiology is so misleading for us.
And if you look at the association of vitamin C in the blood, there's an association with better outcomes.
But when we do interventional studies, we don't see it.
And in this table, you can see no effect on mortality, no effect on the incidence of the common cold, no effect on cardiovascular events, and essentially no decrease in systolic blood pressure with an intervention.
No effect on the incidences of the common cold, but what about once someone has a cold?
That's like when emergency and all these different vitamin C supplements, this is what they're always claiming, is that taking it while you have the cold is what's going to reduce the duration of the disease.
Concluded that vitamin C supplementation has no effect on the incidence of the common cold.
Or if you have a baseline of unhealth, something that's been super relevant with the current COVID conversation.
If you have a baseline of ill health or baseline of metabolic dysfunction, sometimes synonymous with insulin resistance, per a given vitamin C intake, there's lower levels of vitamin C in the body.
So if you look at animal foods, like if you eat nose to tail, if you're eating a couple ounces of liver per day and some meat per day and other organs, you can get pretty close to 70 milligrams of vitamin C a day.
Which is basically the RDA.
I think the RDA might be 70 or 90 milligrams of vitamin C.
I recently was hanging out with Steve Rinella, and he was telling me, historically, the trappers, like these fur trappers, maybe in the 1800s.
At some point along the way, we lost this ancestral knowledge that eating organs is so important and that all indigenous cultures do it and they savor the organs really above all other things and they distribute them among the tribe and these trappers went out and they started to just not, they started to get sick from just eating the muscle meat and they had to start incorporating organs in their diet.
It was a historical reference.
I'm not sure where he read it, but yeah, if you look at the way that indigenous cultures do this and you look at the way that other animals do this as well, they don't waste anything.
Particularly we have talked about it many times the podcast wolves the alpha wolf will eat the liver and the other wolves have to stand by and there's a crazy documentary about a guy who lived with wolves and One of the ways he tricked these wolves and then thinking that he was the alpha Was he would have an animal and he would put a liver in the animal so they would bring a carcass and he would be growling at them while he ate the liver and they were like wow I guess this guy's the fucking boss he's eating the liver and If you eat liver, you get to be an alpha male or an alpha female.
Well, it was weird that he knew, and that this is just the wolves know in their pack mentality that the alpha is the one that gets the most nutritious piece of the animal.
Yeah, so he wrote The Fat of the Land, Not by Bread Alone.
He had quotes.
I think I have a quote from him here.
Let's see, I think it's in the Anthropology.
So he would say that the...
Actually, it's in the nose-to-tail folder, Jamie, if you're looking for that.
There's a screenshot there.
So he would say that...
meat of any kind is in great demand it is interesting to note the following are the favorite cuts the brisket of the beef with the fat and the cartilages so these indigenous cultures in the in the arctic would they would favor things with fat and connective tissue the skin and subcutaneous fat of the warthog pigskin hogs head and brains and And number four is the liver of any animal.
I know you had the guys from Black Rifle on and they were saying that when they were taking the desiccated organ supplements they had a rush of energy but I kind of have this thing that I like to do with people where I have them eat raw liver and it's really cool to see how it turns their brain on.
The baseline nutrition depends, you know, will determine how much of a buzz they get but Of course, there's always food contamination issues.
I would say it can't be that bad, but then you hear about, like, the people in Iceland that eat that pickled shark that Anthony Bourdain told me was the single most disgusting thing he's ever eaten in his life.
I think that in the tribe, so there's an interesting tribe in Africa called the New Air tribe, and liver is so sacred that they couldn't even touch it with human hands.
I don't know how they got it from the animal to people's mouths, but a lot of cultures eat it raw.
They'll just cut it up and eat it raw.
I think that the idea is you lose a little bit of nutrients when you cook it.
Not much, but you lose a little bit.
So I've always been fascinated by...
This is such a nutrient-rich organ.
How much of it can I actually preserve in terms of nutrients?
And do I feel differently when I eat it raw?
And there's a lot of interesting nutrients in liver that aren't well represented in the muscle meat, which we were talking about.
So muscle meat's a great source of B12 and zinc and iron and other things.
So in the nose-to-tail folder, Jamie, there's a graphic from my book that compares...
Yeah, I wonder if they do anything to the grains to make them overeat it.
Because there are lots of studies in rodents.
Sometimes you can use rodents that are genetically predisposed to become obese, but if you alter the food, and we know this with humans, you can alter food in some ways to make it more palatable and to kind of short-circuit the satiety mechanisms.
The way I saw it, it was like there was a pipe in the center of the room.
Force-feeding ducks at Hudson Valley Fogwall.
Go up that.
Feeding ducks for Fogwall.
I think this is probably one where they...
Yeah, see, it's weird because you're grabbing the duck.
They're not going to be into that no matter what you do.
their mouth it just seems gross yeah it is what here's what's weird about it is that any grosser than things that are legal you know because there's a lot of stuff that's legal that we do to animals like when do we decide what's legal and what's not legal because factory farming should be fucking completely illegal And it's legal in California.
You can get factory-fed animals and you can buy them left and right.
What you can't get is foie gras anymore.
And I'm like, well, listen, guys.
You're not making any sense.
Like, this is one small moment of this duck's day where they're feeding him.
And they're shoving a tube in his mouth and overfeeding him.
The life of a pig that you eat for bacon is a terrible, tortured life.
And you're okay with that.
You're just not okay with this fucking duck.
Getting extra grain pumped down its mouth.
Meanwhile, they're just living a normal life other than that.
There's a lot of corn and soy subsidies that are supported by it, and it's really unfortunate.
But there's a lot of really interesting discussion about the sustainability of grass-fed, grass-finished meat, and this regenerative agriculture concept.
Like, could you still have jack-in-the-box if you had grass-fed, grass-finished meat?
I think we can both agree that grass-fed, grass-finished meat is healthier to consume.
But the disagreement comes, like Bourdain, again, rest his soul, would say he prefers grain-fed cows because he finds the meat to be more delicious and tender.
He liked it better as a chef.
And, you know, that's a culinary choice.
Like, he, as an artist creating food, he preferred an animal that was, you know, like, people like wagyu.
You know, they like that kind of, I think that's, that's a fucking dying animal, man.
I mean, if you look at the way that cattle are factory farmed, the reason they have all that intramuscular fat is because they are less metabolically healthy than their grass-fed, grass-finished cohort.
The sustainability or the scalability argument is so important to consider.
So when I think about this, I think about it from a couple of perspectives.
There's the land use perspective, but there's also just the actual mathematics of it that 99-ish percentage of cows that we eat that are grain finished had 85% of their life on grass.
They're not raised from calves in the factory farm.
So then I think, wait a minute, we're already raising all of our cattle on grass for 85% of their lives.
We're just sending them to factory farms at the end.
And I think it's a consumer-driven thing.
It's people who want that type of meat or they're not familiar with the gamey flavor or texture, or they want it to be intramuscular fat.
They want it to have more marbling.
And then the other aspect is the actual land use.
And then when you think about how much land is used to grow corn and soy, and then if we get rid of all the corn and soy that goes to animals and feed lots, we can graze cattle there.
And then there's actually, I believe it's called the Conservation Reserve Program.
The federal government pays farmers to let their lands lay fallow for decades.
There's hundreds of thousands of acres in the United States that are not being farmed because they were monocropped to basic, they were monocropped so badly that they had no nutrients, they can't grow plants on it.
So what I think what everyone is missing, well, not the people in the regenerative agriculture space, not you, but I think that the mainstream is missing the fact that in order to regenerate land, in order to make land healthy, you put animals on the land.
That's why the center of the country where there were millions of bison and elk and antelope and deer and pronghorn had the richest soil anywhere until we monocropped it.
And then we deplete the nutrients.
It's just a sink.
We're just pulling nutrients out.
But when you talk to the folks at White Oak Pastures in Georgia or other regenerative farms and you look at the soil, it's incredible that when animals live on the soil in an ecosystem, It puts nutrients back into the soil.
The soil is like the color of coffee grounds.
So I was in Georgia recently at Bluffton at White Oak doing photographs for a cookbook I'm writing.
And Will Harris, who's a colleague of Joel Salatin, I know you've had Joel on the podcast.
Love him.
Yeah.
And so Will has two jars in one of the churches on his property in Bluffton.
And one jar is soil from his farm.
And it's the color of coffee grounds.
It's like 5% soil carbon.
The other jar is from 25 yards away on his neighbor's pasture, growing cotton or soy.
It's like the color of this wood table.
It's light brown.
They're completely different.
And if you look at the soil content of carbon, it's 0.5%.
So you have 10x the amount of carbon in the soil when it's farmed regeneratively.
They've been doing regenerative agriculture there for 20 years.
And you can see this steady increase in the amount of soil carbon.
Well, it just completely makes sense because manure is fertilizer.
Animals eat the grass.
They make manure.
The manure is fertilizer.
Worms and bugs live under the manure.
There's an entire ecosystem that evolves from Around these animals living the way they've lived for hundreds of thousands if not millions of years it makes sense that it all works together synergistically to feed the soil and to provide nutrients for the very animals and those animals will die on that land and they will rot they will provide even more fertilizer and then other animals will live off of them and live in that area and they too will die and they will Shit all over the place and piss all over the place and they will feed the
soil.
And this is a system.
And we fucked that system up by growing corn.
We fucked that system up by growing, you know, a million acres of soybeans.
Well, it seems like we thought it was a great idea during World War I and World War II because they needed food.
The reason why all this subsidies of farmers happened is not that the agriculture business is evil and the government is in bed with them.
What happened was during the First and Second World War, there was a need for surplus food.
There was a need for food because back then there was a very real concern for supplies for troops, for supplies for the United States.
I mean, we were at war.
I mean, a crazy war that I don't think today in our 2020 version of war, which always happens in some remote, faraway land, and it's always a domination by the United States.
I don't think we really understand the desperate and terrifying times when they were, you know, asking people to donate metal and rubber.
I mean, it was a crazy time.
And the government stepped in and said, we are going to pay farmers To grow corn.
We need food.
And so they subsidized these farmers to grow all this food.
Now it's become a different animal because now they're subsidizing people to grow corn that is mostly in a lot of...
Like I have a friend who has a farm and they grow it for livestock.
They have a huge area that they grow corn.
And it's all, by the way, Monsanto corn, right?
They're spraying that fucking Roundup on it, which is, you know, glyphosate is terrible for you.
And I had a podcast about that recently, about environmental chemicals and how bad they are for you and then how that stuff actually can be in the meat and can, in turn, get into your system and provide you with all sorts of problems.
And this is why there's subsidizing of farmers.
I mean, it's also because we need farmers.
We need to keep them healthy and healthy.
This is just not the way to do it, though.
If we could just get people off the tit of corn, get people off the tit of these monocrop agriculture, we would be a healthier country.
If we can have these giant areas where people can grow all kinds of things, like polyphase farms, the way Joel Salatin runs things.
He moves all of his animals around.
He lets all of his pigs, they live like wild pigs.
They just eat acorns and nuts and all these different things and he supplements them sometimes and he has incredible soil like the other farm you're describing and incredibly healthy animals.
But if you look at the ground and you look at a square foot of the ground at Rome Ranch, you can see that on the pastures that the bison are in, maybe only 30 or 40% of that earth is growing grass.
But you know that in the future, if you move it out 20 years like White Oak Pastures has done, When I was in Georgia, every millimeter of that ground is growing grass.
It's like thick grass, right?
And that's feeding the cattle in a much more rich way.
And so that's what regenerative agriculture is about.
Well, we go out there with Katie and Taylor, who own the farm and take care of it, and there's people out there who work with a bison, and they know which animals are more aggressive.
They ate a little bit of berries here and there, but most of what their diet was was meat.
And there was a benefit to that in terms of the way they could travel, because they could go without food longer than people that were mostly carbohydrate-based.
The carbohydrate-based guys, like the soldiers, would crash and the Comanches could keep going because their body would just go into ketosis and they would live off fat.
It was a natural shift back and forth between eating meat and eating fat and eating organs to not eating for a while.
And so few humans in 2020 have gone for more than 18 hours without eating food.
Very few of us in how many decades we've lived or have utilized the fat burning systems in our body.
You know, you can use glucose or fructose or sugars.
You can use carbohydrates.
And you can do glycolysis.
But there's a whole other system where you can either use fat that's coming in or use fat from your body in beta-oxidation and ketones, move the fat, basically, precursor molecules around your body.
And when we get adapted to that, we have this extra engine.
We have two engines.
We're both hybrid and gas.
But if we go long enough without ever using the hybrid fat-burning engine, we kind of lose it.
It's kind of interesting today that there are a lot of people that are interested in intermittent fasting or having a very specific feeding window, and they are seeing benefits of that.
I was reading some article recently that was saying a study shows that there's no weight loss benefit to intermittent fasting.
And I'm like, who made that fucking study?
And who are you studying?
Everybody that I know that's done it has lost weight.
What are you talking about?
What is that study about?
And why would someone be even interested in promoting that?
Were they intermittent fasting with standard American diet food?
I think it's pretty clear.
There's a lot of compelling data in both, at least in animal models, and I believe in human models too, that having a feeding window and having time when your body shifts from We're good to go.
Amp kinase at a very broad level, when you have more of this ketogenic physiology, when you exhaust the glycogen in your liver, you turn on these autophagy mechanisms.
You do the cellular housecleaning, and that's beneficial for humans.
Damaged cells and damaged proteins within cells and damaged mitochondria.
So within the cell, there are these, quote, powerhouse factories, which are probably ancient bacteria, you know, billions of years ago that combined with a single-celled organism and we became eukaryotic with a membrane-bound nucleus and a membrane-bound organelle called mitochondria, which produces ATP for the body.
And so Within the body, there are all these organelles within our cells, and some of them, the job of that organelle is to basically be the trash compactor.
Old proteins are ubiquinated and they're moved to the organelles that recycle them.
And so you do this cellular housecleaning, and it seems to happen more when you're in this state of ketosis or when you're not...
Using the glucose from, or when you're not in sort of an anabolic physiology.
And so you can see that with our ancestors, we would have switched back and forth.
We wouldn't have been successful in hunts every day.
We would have had some hunts that were successful and some gathering sessions which were successful and others which weren't.
And when they're not successful, you're fasting.
And so that's a beneficial thing.
I mean, I think that that intermittent cellular housecleaning is an ancestral pattern that we would do well to espouse, to mirror.
So your body doesn't have any food to digest, so it's like, look, let's do some cleaning up.
We got a bunch of junk laying around the attic.
Let's sweep it up.
But if we're doing the standard American thing, which is to eat constantly and snack throughout the day, and then can't wait to have dinner, and then can't wait to have breakfast, and can't wait to have lunch, and Your body never really gets a break.
I mean, it would be so interesting to look at the Western population or the American population and see how many of them actually exhaust liver glycogen overnight, how many people actually wake up with ketones in their blood.
I think it would be a fraction.
I think the majority of people never get rid of their liver glycogen, never actually flip.
To be fair, I actually don't think we should always be in ketosis either.
I think that that can present some challenges to the human physiology and that intermittent, you know, inclusion of carbohydrates can be beneficial for humans.
And this is a cycle, it's a circle, like many things are in our life and our ancestors.
In spite of the fact that they favored meat and organs, they certainly would have had carbohydrates from time to time when they were available.
So that's this balance.
I think that personally, when the people I've worked with and in the reading that I've done, everything I've learned, it works better to be cyclic ketosis rather than persistent ketosis all the time.
Though ketogenic physiology, I think, is intrinsic to humans.
It's beneficial, super healthy, and a lot of people find massive benefits from it.
Well, ketosis, particularly for people that have epilepsy, and for SEALs that work on those rebreathers, they found that being in ketosis can keep them from having seizures, which is really kind of fascinating as well.
there are tribes that's what we see and it's so interesting to me that they have a preference for animal foods a lot of them will eat tubers occasionally there's actually a pretty cool study I think you'll find it in the anthropology folder Jamie or it's termed Hadza fallback foods it's the fourth one there and this is such a cool study I really want to go spend time with the Hadza next year.
Because I first got interested in the carnivore diet because of autoimmunity.
And the way that, just the hypothesis, could some of these plant toxins that we were kind of talking about earlier, could these be triggering immunologic reactions in humans?
And we know they do.
Gluten is a plant lectin, and it certainly triggers an immunologic reaction in the small intestine.
Could that model be at play on a bigger scale for people with vitiligo?
I had eczema and asthma, which is an autoimmune condition.
What about autoimmune thyroid disease?
What about psychiatric illness, which I believe is autoimmune as well?
So I have not had any flares of eczema since I've been eating a carnivore or carnivore-ish diet for the last two years, except one time when I reincorporated some plants back in my diet in an experiment with squash.
And there are, I mean, squash is one of the foods that I would think is fairly ancestrally consistent and fairly less offensive to humans because in the book, I don't, the book is not meant to convince everyone to stop eating all plants.
The book is really meant to do a couple things.
It's meant to help people understand that animal meat and organs are the foods that we've been eating throughout our evolution.
They're wrongly vilified today, and we can talk about why with the epidemiology.
And they should be a part of any, they're an integral part of any healthy human diet.
And then I created kind of a spectrum of plant toxicity, thinking about hunter-gatherer tribes and which parts of plants they favor and which parts of plants they discard.
And then thirdly, I think it's important to understand what we talked about, processed vegetable oils and processed sugars, hugely bad for humans.
But I'm really interested in carnivore and carnivore-ish type diets so that the most number of people can benefit.
So for about a year and three quarters, I had just meat and organs and fat.
And I was in ketosis all the time, depending how much protein I had.
And then I had some thoughts about, well, what does my blood sugar look like when I do this?
I got a CGM. I got one of these continuous glucose monitors.
And I started incorporating carbohydrates first as an experiment.
And what I noticed was that with sort of these less toxic carbohydrates, or what I think of as more ancestrally consistent sources of carbohydrates, I felt even better.
The eczema didn't come back with honey.
I had occasional fruit.
I found that I couldn't overeat fruit.
I couldn't, if I ate too much fruit, I felt bloated and kind of just farty and didn't feel good.
Fruit seems to have this built-in mechanism where we can only eat so much of it.
Honey is, you know, I can eat a moderate amount and feel just fine, but the inclusion of those carbohydrates actually made me feel a little better.
I slept a little better.
With long-term ketosis for myself and what I've observed for some people, perhaps not all, with long-term ketosis, electrolyte deficiencies a lot of times develop.
People get cramps, they get palpitations.
And we know that when ketogenic physiology happens, our body partitions electrolytes differently than Sodium, you know, sodium retention in the kidneys different.
And then when sodium becomes a little bit funky, our body wastes a little magnesium, a little potassium.
And so that started to kind of make sense to me.
I thought, oh, maybe it doesn't have to be as dogmatic as full meat and organs.
Maybe we can, you know, maybe more people would benefit if we think about this more like our ancestors, right?
More like the Hadza, eating berries, or boobab, or baobab, and then honey occasionally.
And you can always look at your blood sugar with a CGM or other metrics.
What was fascinating, and I actually have all my blood work, if you want to see it, or any of my continuous glucose monitor readings, but you can see, this is all in the lab work or the blood work folder, Jamie.
And there at the bottom, there's those three images of my blood sugar, and there's a few other ones.
But you can see that with honey and mead and organs, don't really have much of a change in the blood sugar at all.
It's pretty mild most of the time, and it stays very consistent.
But if you look at the literature on honey, there's studies.
So when I first thought about honey, I thought this is going to cause dental cavities.
And I'm good friends with a periodontist.
Incidentally, a periodontist who has an advanced leukemia, who's on a carnivore diet and doing really well- But he was pointing me to a bunch of evidence that honey's been used to treat oral candida.
It actually can have activity against cariogenic bacteria in the mouth.
B-A-O-B-O-B. So you see, the black bar is how many people like honey, right?
And the next bar is meat, and then Baobob, berries, and tubers.
So both males and females, they don't really like tubers a whole lot.
They'll dig them as a fallback food.
And actually, the title of this paper is Hadza Fallback Foods.
But at the end of the paper, they say there's this observed behavior that if there's a lot of meat in the camp, the women will stop digging tubers for two to three days.
Baobab is this tree in Tanzania that has this fruit.
I've never had it, but it has this kind of dry fruit pulp on the outside of the seeds.
Maybe you can find a picture of Baobab, Jamie, but...
For folks that are just listening, they're really fat and wide, and then the top, they have these tiny little branches.
Jamie, go to the left side, the left of the other images that you were looking at, and go drop down into the lower right-hand corner of that one, the bulbous one.
But if you look at tooth decay in the Hadza, there's some interesting findings.
The women, actually, that eat indigenous ancestrally don't really have significant tooth decay.
The men have higher rates of tooth decay, and we don't know whether that's because they're eating more honey or because they also smoke tobacco and marijuana.
And tobacco and marijuana are certainly associated with dental cavities or periodontitis.
So there's been some concern about that.
But at least in myself, I haven't seen anything.
And I've actually talked to a number of dentists who have said, no, honey is protective in the mouth, which goes against everything we think.
But there are studies that look at the pH of the mouth.
So I'm not a dentist.
I'm a medical doctor.
But when I've been educated by dentists, Tooth decay appears to happen when the pH of the mouth drops.
When we eat sugar or something that's fermentable or in the setting probably of fat-soluble vitamin deficiency, the pH of the mouth drops and the cariogenic bacteria are able to thrive.
Well, if you look at the pH of the mouth when you eat honey, it drops and then it rebounds more quickly.
So it's interesting.
Is there something in the honey that prevents that?
It's certainly an ancestrally consistent food.
If you look at where honey is available in the world, it's eaten everywhere it's available.
And fructose and glucose have different biochemistry.
In glucose biochemistry, there's a stopgap.
There's a rate-limiting enzyme called phosphofructokinase, meaning that if you try and overeat glucose, your body's gonna put the brakes on it and not do glycolysis, which is the process by which you turn glucose that you're eating into energy, right?
There's no break on fructose.
So fructose bypasses phosphofructokinase and can essentially move down the shared glycolytic pathway into the formation of the glycerol backbone and triglycerides, which are essentially fats, without any breaks.
So the problem is not high fructose corn syrup itself.
It's that you can eat it without stopping, right?
That you can get massive amounts of it and they're calorically bereft.
So if you were to eat, if you, if I were to give you, if you look at isocaloric studies of fructose, there's no evidence that they, that fructose increases uric acid or blood pressure or weight gain.
Isocaloric.
But when anything with high fructose corn syrup is going to be so enticing, is going to short surrogate your satiety mechanisms so much that you're just going to overeat it in a way that fruit doesn't do, right?
That's another thing that I noticed about doing the carnivore diet for that one month was that satiety, when you're only eating meat, you don't eat as much.
You just don't.
It's not just an elimination diet, but in many ways, you're reducing calories just because you're just not as hungry.
And you eat to satisfaction, but overall the calorie consumption is much less than if you were eating it along with like macaroni and cheese or, you know, cream corn or bread or all these other things.
You would keep eating.
Like if you have a steak and you only eat this 18 ounce ribeye, you will...
You're only going to eat a certain amount.
I mean, maybe you'll eat the whole thing, but maybe you'll get like three quarters of the way and you'll be like, I'm good.
But if you've got mashed potatoes and gravy and bread, you'll just keep fucking eating.
And it's weird.
It's weird.
Your body just wants to stuff more stuff into your mouth.
There are different satiety mechanisms, I think, happening at the level of the hypothalamus in the brain when you're just eating protein and fat versus protein and fat and carbohydrates.
And there's nuance there as well.
There's some really interesting evidence that polyunsaturated fatty acids probably hijack these satiety mechanisms as well.
And that linoleic acid specifically and other omega-6s can have negative consequences at the level of the brain and you don't get that satiety response to turn off.
But, yeah, I agree with you.
Every once in a while on strict carnivore diets, people can't eat enough because of this.
And they do benefit from including some carbohydrates in their diet.
And I think, you know, our ancestors have done that occasionally.
But, again...
I do think that for humans to thrive, we should not fear meat and organs, and you make that the center of your diet.
And like you're saying, I think that there is a benefit to a carnivore-ish diet.
Just like you, how many people are going to eat just meat and organs for their whole life?
Some, a devoted few, and they're definitely going to benefit.
But I think that the number is 10 to 20 to 100x who might benefit from understanding that meat and organs are valuable, incorrectly vilified, and that there's a spectrum of plant toxicity.
And that expands it.
Because when I tell people that I eat meat and organs and fat, they look at me really funny.
But if I tell them that occasionally I eat an avocado or some raspberries or some blueberries or some honey...
The gears start turning.
They're like, maybe I could do that.
And it starts to look like, I would say, a reimagined version of a paleolithic diet.
Because that's what we're essentially asking.
What is the species-appropriate human diet?
What is the genetic congruence between our environment and our genetics in 2020?
I believe we're really still programmed to eat like Our ancestors, and that we still thrive doing this.
But it can be a little bit more broad for people than just a strict carnivore diet for those that will espouse that.
If I say, hey, what about avocado?
So in the book, in chapter 12, I talk about this spectrum of plant toxicity.
And if you think about it from a plant's perspective, There are parts of a plant that it wants you to eat, usually, like the fruit, and a lot of parts of the plant that it doesn't want you to eat.
So if you chew the seeds, that's where this, you were talking about these negative compounds that only happen when you chew certain seeds, like apple seeds.
So all the stone fruits, peaches, plums, even almonds, they have this cyanogenic glycoside, amygdalin, and they're toxic, like apricot kernels.
The FDA, I think, had to step in, or the USDA had to step in and have manufacturers remove apricot kernels from trail mix.
There was a big, there was a big fervor about the Hunza a couple of years ago, maybe a decade ago, And there was this widely promulgated false notion that they were having this longevity benefit from this amygdalin in the apricot kernels.
And it was really potentially dangerous for humans.
So they ended up with these apricot kernels, the apricot seed in trail mix.
And the USDA or the FDA had to step in and say, no, no, no, you can't do that.
That has a toxic compound.
And almonds were very toxic and we kind of bred it out of them.
So a lot of the foods we eat today are sort of, we're stripping the toxins away from the plants, but the intentions were clear.
One of those goofy vegan doctors who looks like shit was on this podcast and he was talking about how he got really, really sick because he picked these berries.
He's locked into this world and applauded and that's where he gets his love from.
And if you leave that world by God, I've seen people do it and they get attacked in the most vicious and horrific ways.
When their body is falling apart and they incorporate salmon and all of a sudden they start getting erections and they start feeling better, people will attack them.
I understand where these people are coming from in terms of them not wanting to do harm.
I understand it.
I see their perspective.
But the vicious ways they attack people that leave that...
I'm going to call it a cult because it's kind of like a cult.
But there was a point in time where if I was queasy, the texture of that, when I was chewing on it, if I was of a weaker constitution, we might have had an issue.
So in the evolution folder, Jamie, I don't know if the study will be great to pull up, but there's a study in there, the vegetarian ERP brain study.
So they've done studies with vegetarians and vegans and omnivores looking at the EEG. So looking at the electroencephalogram and looking at the way the brain responds at a neocortical and a more basic level.
And so the bottom thing there is kind of a complex statement, but you see what they say.
The findings suggest that vegetarians' aversion toward non-vegetarian food prevails at the subjective level.
And it's consistent with personal beliefs.
But at the neural level, the intrinsic motivational salience of animal food remains.
So that means that in the deeper brain, they still crave meat.
We're exercising more, smoking less, rates of cancer are the same.
We drink essentially the same amount of alcohol.
And that's where the story gets to be really interesting.
And none of this is causal.
None of this is, you know, interventional studies.
These are just kind of detective work.
So look at the 10.18.41, Jamie.
That's diabetes prevalence.
It tells the exact same story.
It's just, it's scary.
So something is going on.
And we kind of have to say, we kind of have to be, as a medical community, we have to be honest and say, look at diabetes.
That's formally diagnosed diabetes with hemoglobin A1c and fasting glucose.
Like, these are people who are very far on the spectrum of metabolic dysfunction.
Again, it's skyrocketed.
And so what's going on here?
And so now, Jamie, if you go to 10.16.56, that was the first one you brought up.
We can look, and this is detective work, but we can start to make inferences, or guesses at least, based on trends and calories from major food groups.
This is actually a pretty cool graphic.
So the top line there, the green one, is grains.
It goes up a little bit, but since 1995 it's gone down.
You can even look at sugars and sweeteners.
Again, they go up a little bit, but in the last 20 years, they've gone down.
And the consumption of meat has gone up, so we'll consider meat as a probable driver.
But look at that red line in the middle.
You see what that line is?
That's vegetable oil, man.
And then if you dig into that meat as a driver, this is the 10.18.34, Jamie.
Look at the total meat consumption by type.
That one.
So what are we eating more of?
It's not red meat, the type that's getting vilified.
We're eating more chicken.
So you might say, oh, red meat is driving the problem.
And you can see soybean is the main one, but canola, sunflower, cottonseed, peanut, and other.
This is completely evolutionarily inconsistent.
This is completely dis-synchronous with our evolution.
We would never have been grinding soybeans up into oil.
We didn't have the ability to do this.
And then you can get into all of the reasons this might be doing this, but, you know, as I kind of dug into this, it gets a little bit deep in the weeds, but at a molecular level, these polyunsaturated fats, they act differently in our body, and we don't fully have this figured out.
But at the level of our mitochondria, it does look like these polyunsaturated fats, this linoleic acid-rich vegetable oil, is signaling things differently.
And I think there's a lot of compelling evidence to suggest that linoleic acid is driving adipocyte hypertrophy, meaning fat cells are getting bigger.
And fat cells can do two things.
They can get bigger or they can divide.
When fat cells get big and they don't divide, they eventually start leaking out inflammatory mediators, leaking out free fatty acids.
And so what you see is you start to see this interesting set of data that points to the fact that maybe all these excess linoleic acid is driving our fat cells to get really big, but isn't allowing them to divide the way they're supposed to.
You can imagine evolutionarily that as winter is coming, we might have had a few more seeds, which are foods in nature that have linoleic acid, but nothing like our consumption today.
So maybe it was advantageous to get a little bit more linoleic acid when things might be scarce in the winter in northerly climes.
Maybe there's an evolutionary mechanism here, but the potential is that every single day, all of us in the Western world, if we're eating excess vegetable oils, excess polyunsaturated fats, specifically linoleic acid, we are driving a signal to our adipocytes that winter is coming.
Get fat.
Stay fat.
Whoa.
So it's just this evolutionary inconsistency, and it's not rocket science.
It's like, wait a minute, just stop eating those oils and really stop consuming animals fed corn and soy, especially pigs and monogastric animals like chickens.
Ruminants are unique.
Because they have a rumen, ruminants can take polyunsaturated fats and make them into saturated fats.
Humans can't do this.
Monogastric animals, humans, chickens...
Pigs, they can't do that.
Any polyunsaturated fat you give a pig is ending up in its fat.
Any polyunsaturated fat that you or I eat is ending up in our fat tissue.
We need a small amount, but there's an evolutionary amount that I think has always been seen.
If we look at cultures of indigenous people, they all have two to three percent of their calories as linoleic acid.
You look at how much- What is the source of that usually?
Usually animal fat.
There's about 1.6 to 1.8% animal fat in a grass-fed cow.
And to be fair, in a grain-fed cow, it's not a whole lot more.
There's about 2% linoleic acid in the fat of a ruminant animal, a deer, a cow, a bison.
But if you look at chicken, they're up at 23, 24%.
Pork, 15 to 16% because they're fed corn and soy.
Like you said earlier, if you let a pig, like if you're out hunting hogs, that hog is gonna have a fat, you know, maybe 5 to 6% linoleic acid.
And you can totally, it totally changes.
You know, chickens, the same research has been done showing that chickens in the wild, I don't know what a wild chicken looks like, but like wild flightless birds, their fat looks different than when they're fed corn and soy.
Not surprisingly, because monogastric animals, chickens, turkey, duck, pork, you know, pigs, humans, we store the polyunsaturated fat.
So I think this is a really interesting hypothesis.
We don't have enough data to say this, but man, it's so compelling.
And, you know, the other side of the equation is certainly high fructose corn syrup is not helping anything.
But I think it's important for people to understand that that might not be the only villain.
And that a lot of people might get rid of the sugar but then continue eating processed food or hummus with canola oil or, you know, chips from the store that are cooked in soybean oil and not understand it.
And this could be driving a lot of the disease that we're seeing in a really subtle way.
Oh, okay, 1967 review of sugar, fat, and heart disease.
The studies used in the review were handpicked by the Sugar Group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat.
So that scared everybody and got everybody to eat margarine.
So you think about, you still save some if you dehydrate at 140, but in a freeze dryer they lower the pressure and then they pull out the water at a low pressure.
It's essentially sublimation where you can go from solid to gas without going through liquid.
So you preserve as much as possible, like a pretty good amount stays in there.
The capsules are amazing because you can just take them and they're portable.
Maybe if people really want the powder, we'd make it.
But I think the capsules are better for people and it's portable and it's easy and you can condense an ounce of organ into a reasonable amount of pills.
It's real food, so there's no additives or preservatives or anything in there.
So it doesn't get that.
You'd have to take six to eight pills to get an ounce of organs, but that's a good amount of organs.
Yeah, they're all grass-fed, grass-finished animals from New Zealand, and we're actually working really hard to develop a regenerative chain in the U.S. Really?
I like to do intermittent fasting, but I like to do it earlier in the day.
So I like to eat my dinner, quote, at 3 or 4 o'clock.
And I eat breakfast at 8 or 9. So I've got like an 18-hour eating window, 16 to 18-hour eating window most days.
Why do you do it that way?
Because I think there's some evidence, or at least, I think there's a little bit of evidence, at least in diabetics, and then personally I've experienced better sleep when I finish eating dinner earlier.
Melatonin and insulin do have a little bit of a contradictory effect.
You know, if you eat late at night, is the insulin spike going to affect your body's ability to release melatonin from the hypothalamus and actually initiate sleep?
It's like, are you supposed to be eating right before you go to sleep?
I'm not sure.
I just thought, ah, it's easier to sleep if I eat earlier in the day.
And I'll just go out probably three or four times a day and do pull-ups, do some kettlebell swings, hit the punching bag for 10 or 15 minutes multiple times.
If I do multiple, if I do like a big exercise, it could be any time.
2017, they did a study where they strapped heart rate monitors on 200 or so, 198 different Hadza men and women, and tracked them to see what their cardiovascular fitness was.
It's kind of that low-level activity throughout the day.
It just feels good for your brain, too.
And I'll be at home working, writing, or answering emails or something, and I don't want to do that for three hours.
I want to do it for 45 minutes or an hour, get up, do some pull-ups, go outside, breathe some air, go see the natural world, go outside barefoot, and move around.
Cardiovascular disease and heart attacks, the difference between the rate of cardiovascular disease and heart attacks today versus, like, the early 1900s.
It would be essentially the same reflection on the graph.
It would be an up angle that you would not want to skate, you know?
And again, it's the question, what is driving this?
What is driving this?
Because we were eating more saturated fat in 1900. We were eating way more saturated fat in 1800 or 1840. And the only oils we used were animal fats, which are not entirely saturated.
They're about half mono and half saturated.
Half mono and saturated, half saturated.
With a very small amount of polyunsaturated.
So to say that it's saturated fat driving this doesn't make a whole lot of sense.
Again, this is just correlation, but there's not even a correlation there.
The correlation is with vegetable oil.
And if you get into this research, it's complex, but it's pretty darn striking.
If you look at linoleic acid, and you look at the molecule, it's polyunsaturated.
So it's a long-chain carbon.
And polyunsaturation means it has double bonds between the carbons.
And those double bonds can be oxidized.
Remember we talked about oxidation earlier and this formation of lipid peroxides?
Well, those molecules, polyunsaturated fats and even monounsaturated fat, any unsaturation point in a carbon skeleton molecule like a long-chain fatty acid is going to make it susceptible to oxidation.
And then lipid peroxides, which are lipids that have had an electron stolen from that double bond, Then those are more susceptible, those are more reactive with other lipids, and they create these lipid peroxide reactions.
And then you're getting oxidative stress from the lipids.
And if you look at, we should back up for a moment.
This goes back to what we were talking about earlier.
One of the reasons saturated fat has been thought of as bad for so long is because it raises LDL. But if LDL is not de novo causing atherosclerosis, then we have a whole different equation.
Well, let's get into that because this is one of the big questions that I got when I told people I was going to eat an animal-only diet for a month.
They're like, what about your cholesterol?
What are you going to do about your...
And I'll be like, ugh...
And I try to tell them that dietary cholesterol does not raise cholesterol in your blood lipids and they just glaze over and they're like, well, you know, you're taking in a lot of cholesterol.
And it's just most people don't have the time to research this or to get into the weeds and to try to shift their perception about what cholesterol is.
About the benefits of cholesterol, the necessity of cholesterol for the human diet, for production of hormones.
So LDL is low density lipoprotein and it's formed from VLDL after it becomes IDL, which is intermediate density lipoprotein.
So when you eat fat in your diet, it is generally in triglyceride form, which is packaged into molecules called chylomicrons, which move from the intestines to the liver.
In the liver, cholesterol, which is actually a steroid backbone molecule, is packaged with triglycerides into a VLDL, a very low density lipoprotein particle.
It's like a bus.
It moves triglycerides and cholesterol around the body because they're nutrients, because they're essential for human life, because like you said, hormones are made from a cholesterol backbone.
And if you did not have cholesterol, you would be very sick and die.
There's a genetic condition called Smith-Lemley-Opitz syndrome, which is a mutation in one of the enzymes that makes cholesterol.
It's pretty far down in the pathway.
But a lot of these kids die in utero.
Those that are born have severe retardation, both mental and physical.
They're extremely resistant.
They're extremely susceptible to infections and they have a lot of problems with sleep and diabetes and other issues because they don't make cholesterol.
They have extremely low LDL because they can't make cholesterol in the liver and probably in peripheral tissues either.
And so the way we treat these kids is with egg yolks.
We just give them tons and tons of dietary cholesterol in hopes that that will be some sort of a supplement that they can use to make LDL As their LDL goes up they do better.
They're never going to have a normal life but there are so many studies that point to The value of low-density lipoprotein and if we just think about it evolutionarily Why would nature why would evolution have designed a particle?
That kills us within our body that at the same time defends us from infection and So there are good studies in animal models that show that if you knock out the LDL receptor in mice and rats, the levels of LDL in the blood drop a lot.
And those mice and rats are protected against infections.
So they can infuse bacteria, gram-negative bacteria, into those rats, and the higher levels of LDL are protective in those studies.
And the same thing has been true in human.
You can look for this correlation, so this is epidemiology.
At some point, we should definitely talk about why epidemiology can be so misleading.
But higher levels of cholesterol are correlated with lower admission to the hospital for infectious complications.
And we definitely see in animal models, and essentially with humans, with the Smith-Lemley-Opitz genetic model, That lower levels of cholesterol predispose to infection because LDL, lower levels of serum cholesterol, meaning low-density lip protein, predispose to infection because that low-density lip protein particle is part of the immune system.
And so is HDL. So HDL is high-density lip protein.
It leaves the liver as kind of an empty bus.
LDL leaves the liver as VLDL, a full bus, drops off people along the way, becomes a less full bus.
VLDL becomes LDL. HDL is an empty bus.
It goes along the body picking things up and then returning to the liver.
But HDL and LDL both have roles in the immune system.
So why do we think that a molecule, a lipoprotein particle that serves an indispensable role in human biochemistry or at least human physiology is killing us?
At a very high level, they would say, HDL's good, LDL's bad.
You want less LDL, and you want more HDL. Why would they say that?
Because there's something called the lipid hypothesis.
And the lipid hypothesis is that, essentially, in a concentration-dependent manner, LDL ends up in the arterial wall.
Okay, this is the lipid hypothesis.
I disagree with this.
I think it's an incomplete hypothesis.
And so they would say, if you have more LDL, It's just gonna kind of leak into your arterial wall because it naturally gets taken up, and as more LDL ends up in your artery wall, you get more atherosclerosis and more plaque.
It's a lot of epidemiology, Mendelian randomizations, and genome-wide association studies.
So this is really interesting.
We should dig into this.
So if you look at basic epidemiology, so let's just think about epidemiology.
You've talked about this on the show before, but I want to define this for people.
So epidemiology is essentially an observational study.
There's no experiment done.
They're giving people surveys, and they're either following them moving forward, prospective, or they're looking back at what they've done in the past, a retrospective study.
And so epidemiology can generate correlations, but we cannot draw causative inference from that data.
We can have a correlation, which we then test with an interventional study.
LDL is kind of tough to test with an interventional study, but there's some really cool stuff here that starts to break it down.
If you look at overall cohorts of people, so if you look at the Framingham study, for instance, and you look at LDL on the x-axis and incidence of cardiovascular disease on the y-axis, I actually have two graphs of this that I'll show you that'll make it really helpful to break it down.
So if you look at those two, and you don't do anything to, this is in the lipids and CVD folder, Jamie.
You see that CAC LDL only graphic.
So, if you look at this, this is the basic data from Framingham, okay?
This is correlation, this is epidemiology.
Increasing risk of cardiovascular disease on the y-axis, LDL on the x-axis, okay?
So, it's things like this that make people say, oh yeah, LDL, it's probably causing atherosclerosis, which is the formation of plaque within the arterial wall.
But go to the other one, Jamie.
CACLDLHDL. So this is the exact same data stratified by a third variable.
And this is what is never considered with LDL, in my opinion.
The lipid hypothesis is flawed because it's incomplete.
It misses the third variable or fourth variable.
In this stratification, we've looked at HDL. We've looked at the, quote, good cholesterol, which we really don't know a whole lot about, probably an immune participant.
But HDL levels do correlate with metabolic health, synonymous with insulin resistance.
So what can we say about these people?
This is the exact same data that I split into four lines here.
Those with the lowest level of HDL are the most metabolically unhealthy.
These are the most obese, the most likely to have diabetes, the most likely to have insulin resistance.
You can see they have a pretty good risk Relative risk of cardiovascular disease as LDL increases.
But look at the bottom.
Look at the people who are most insulin sensitive.
There's essentially no correlation, or the correlation is massively different between people with a high HDL, good metabolic health, and LDL increasing.
But what if you just have high LDL and low HDL? Then you probably have diabetes, and in that case you have, then you're in trouble.
So the issue is not LDL, it's low HDL. Well, the issue, low HDL is reflective of an underlying pathology, which is metabolic dysfunction and or insulin resistance.
The issue is insulin resistance metabolic dysfunction.
So we're using HDL level as a proxy for metabolic health here.
Of LDL to HDL? I actually, it's tricky because there's a whole group of people now, right?
So I have a good friend, Dave Feldman, who's doing, he's an engineer, super smart guy.
He's doing a lot of really cool work on this and they're actually about to start a study with lean mass hyper responders.
Within the space, the carnivore ketogenic space, there are people who begin eating this way and they see their LDL go up significantly.
So some people don't see LDL rise, but I did.
I have a pretty high, quote, LDL. And so within the space, there's a lot of people with high LDLs who look like me.
Pretty fit, active, don't have chest pain, don't believe I have cardiovascular disease.
We can talk about my blood work and what I've done to confirm that But there's a whole group of people called lean mass hyper responders and dave's hypothesis Which I agree with completely is that elevated LDL alone is too simplistic a metric Mainstream medicine gets hyper focused on LDL or more specifically apob Which is a proxy again for the number of LDL particles?
That's too simplistic because I think there's context here and And the context is that I don't believe there's sufficient evidence to say that high LDL in somebody that's metabolically healthy is the same as high LDL in somebody that's metabolically unhealthy.
There's a third variable.
We have to think about multiple variables because there's a context.
And it makes sense, right?
There are other things that are like this.
Uric acid is a good example, too.
Incidentally, both LDL and uric acid rise when humans fast.
So if you stop eating, your LDL is going to go up.
And that's been demonstrated multiple times in studies.
Fasting raises LDL. They've even shown this in hibernating bears.
Hibernating bears have a rise in LDL, but they don't develop atherosclerosis over the course of their hibernation period.
There's actually a screenshot at the bottom in the lipid CBD folder, Jamie, and I'll pull up.
There's another study here with the hibernating bear study.
It's pretty fascinating.
The bear's athero hibernation.
And so we see this over and over in humans that fasting raises LDL, fasting raises uric acid, but fasting, people who fast, people who do ketogenic diets, they don't get gout.
They don't get atherosclerosis in quite the same way, or at least that's the hypothesis.
Certainly bears don't, and we observe it.
It seems strange that fasting would raise LDL. It does until you think about LDL as a nutrient carrier.
So Dave is developing something called a lipid energy model, and I want to give him all credit for this.
I've actually got a set of slides that will probably make it clear when I talk about it.
But Dave's hypothesis is that if you are burning mostly fat as energy, and even somebody that eats some carbohydrates can be burning mostly fat as energy, You are going to be moving more LDL in your blood to move that fat around.
And we certainly know that interventions can do that.
And it makes sense.
When you fast, you're depleting liver glycogen, your ketones are going up, and you are burning fat.
You're not burning as much glucose.
You're burning more fat.
Your free fatty acids are gonna go up.
Your LDL is gonna go up.
And so you kind of scratch your head there, at least I did, and looked at this and thought, Are you telling me that in something that would happen routinely for humans, fasting like we talked about, intermittent fasting, unsuccessful hunts, that's killing us in a way?
That's causing atherosclerosis?
That doesn't make any sense.
And it certainly doesn't happen in bears and other hibernating mammals.
So LDL will rise in response to fasting.
LDL seems to rise in response to what we choose to burn as our primary fuel.
We're still kind of trying to figure this out.
He just texted me this morning.
He's like, I've got all this really great data.
He's almost ready to share it.
It's super interesting stuff.
But the whole idea of what LDL is doing in the human body, I think, has been misconstrued and misunderstood.
Again, the lipid hypothesis would say the more LDL, the more atherosclerosis.
Well, if that's the case, and it's kind of tied into that model, is the notion that LDL must cause atherosclerosis de novo, or in and of itself.
Because if more LDL equals atherosclerosis, then LDL is causing atherosclerosis.
I don't think anyone who subscribes to the lipid energy model is going to debate that.
But if LDL causes atherosclerosis de novo, why don't we get atherosclerosis in veins?
Why do we only get atherosclerosis in arteries?
There's the same amount of LDL throughout our body.
Veins and arteries are a contiguous system.
And so why are we developing plaque in arteries but not veins?
We never see plaque in veins unless they are transplanted into the arterial system.
So there's clearly more things going on.
And in the case of arteries versus veins, the prevailing hypothesis is that it's endothelial damage.
So the inside of a blood vessel is the endothelium.
And something has to damage the endothelium for this to happen, it seems.
And higher pressure systems, the arteries, seem to damage the endothelium and this network of glycoproteins on the surface of the endothelium called the glycocalyx.
And that doesn't happen in veins.
They're lower pressure.
At least this is one hypothesis.
But for LDL to cause atherosclerosis in and of itself, it just doesn't seem to be, it doesn't seem to work.
And studies like that with Framingham make me think, there's a third variable.
So if you look at the general population, sure, you might see a correlation between LDL and cardiovascular disease, but if you look at it a little more precisely or a little more carefully, you start to separate out those who are metabolically healthy, which granted is the minority, from those who are metabolically unwell.
If the majority of people in our society are metabolically unwell, of course it looks like there's a correlation.
But what about this group over here, you and me, who are metabolically healthy, if our LDL goes up, is that gonna cause atherosclerosis?
I think the evidence for that is paltry at best and is not there.
And I think that we are eating a diet that we believe to be ancestrally consistent.
Why would that kill us, right?
And so one of the things that I've done, so I have an elevated LDL. I will freely admit that.
So the LDL has been above 300. For 300 milligrams per deciliter, which is essentially a density measure, for all two years that I have done a carnivore diet.
Before that, I don't have familial hypercholesterolemia, though.
But my LDL is as high as people with homozygous...
No, but then they'll say, and they'll say, great, and they say, doc, I feel good.
And they say, oh, wait, but your LDL's too high.
You gotta change anything.
And then they won't tell me anything.
And they'll say, oh, I'm eating meat.
And they go, oh, you gotta change that.
Whatever you did that cured your diabetes, caused all this weight loss, that's bad for you because your LDL has gone high because we have this myopic LDL-centric perspective that excludes the contextual variables.
So before I went to medical school, I was actually a physician assistant and I worked in cardiology for four years.
And I think it's a lot of what we are taught in medicine is all we know, right?
We're taught this is the model.
And if you look at it, there is evidence, there is correlational evidence that shows the lower the LDL, The lower the incidence of heart disease, but it misses the context.
And if you start to put in the contextual variables, the model breaks down.
And so I think it's just, it's been parroted over and over and over.
And the prevailing thinking is just, this is what it is, this is what it is.
But there certainly are cardiologists.
I've had three or four cardiologists on my podcast that don't subscribe to this model.
And there's a lot of them out there.
A lot of my friends and colleagues in the medical world are skeptical of this model.
So I'll finish my story because I talked about my super high LDL. Before we get to that, these doctors that don't prescribe to that model, it seems to me that if you're going to step outside the mainstream, it's kind of a precarious route.
And would they be hesitant to do so if you're dealing with non-metabolically healthy people?
So would they make the distinction like, hey, I'm looking at you, Paul, you look very fit, you're lean, you exercise, you look great.
Your LDL is high, your HDL is high, but all the other biomarkers are excellent.
Or would they look at a guy who's fat, who doesn't have a good diet, who's not metabolically healthy, but who also has high LDL? Would they treat them differently?
Because these cardiologists are savvy enough to understand context.
So if you go to a cardiologist and they don't check fasting insulin or hemoglobin A1C or put a continuous glucose monitor on you, they're missing the context.
And so these are just laboratory markers that give you a sense of your metabolic health.
And so absolutely, these colleagues of mine would treat those people completely differently because it's context, right?
The way that I've talked about it in the past is just this analogy.
If you have dry wood for the winter in your garage, it's not just going to spark a fire, right?
Dry wood can be good.
You can build things with it.
You can build a house with dry wood.
LDL can be good in the absence of metabolic dysfunction.
It's the fact that in the setting of metabolic dysfunction, the LDL, and this is just my hypothesis, right?
I don't think anyone knows this.
The LDL perhaps gets retained.
So LDL is a lipoprotein.
I think it moves in and out of the endothelium into the subendothelial space freely.
And there's something about, there's potentially something about the LDL moving into that subendothelial space getting retained in that subendothelial space.
So if you were to take a blood vessel and cut it, you know, lengthwise and look down at like a tube, there's multiple layers.
Look, I got more foam here.
So distracting for Joe.
You know, there's multiple layers, right?
The innermost layer, if the blood's in here, the innermost layer is the endothelium.
And below that is the intima and then the submucosal layer and the adventitia.
And just below the endothelium are immune cells called macrophages.
And what appears to happen with atherosclerosis is that the LDL particles get retained in there for some reason, and the macrophages kind of pick them up.
They eat them.
They endocytose them.
They phagocytose them.
And so they kind of eat these LDL particles, potentially as, you know, they're trying to take care of something that could be problematic, and then they become foam cells.
They get full of more and more lipid, and that's the beginning of a fatty streak.
And again, this is very high-level basic stuff.
It's a little more complex.
But there's something going on, I think, at the level of that subentima, that subendothelial space, that these macrophages are not responding properly to LDL, or the LDL looks damaged.
And so now you start to get into ideas of oxidized LDL versus native LDL. And what causes LDL to oxidize?
Well, there's good evidence that excess linoleic acid in the diet might be doing it.
Excess oxidative stress might be doing it.
Or, at the level of the macrophage, when you have metabolic dysfunction, it's broadly disordered insulin signaling.
So what you're saying about LDL and HDL, is this something that you've ever debated with a cardiologist that follows the mainstream ideas of what is good or bad about HDL and HDL or LDL? There's a family doc who's going to come on my podcast soon that I'm planning to debate about it.
All LDLs not created equal, and even mainstream lipidologists.
So I recently heard a podcast between two folks who are pretty prominent in the lipid community, and even they were admitting, and they're proponents, I believe they are proponents, I don't want to put words in their mouth, of the lipid hypothesis.
And even they were admitting that the quality of the LDL particle matters.
And as soon as you introduce quality of the LDL particle, you introduce that third variable.
And what determines the quality of the LDL particle?
It's the context.
It's our overall metabolic health as humans.
And we should not be looking at lab markers or metrics in isolation as humans.
I know that cardiologists are intelligent and well-meaning, but I fear that within the medical establishment, we're just myopically looking at LDL. And I worked in cardiology for four years as a physician assistant before I went back to medical school and did my residency and all this stuff.
So we're very LDL-centric, and it's becoming more and more ensconced.
It's just all about lowering ApoB, which essentially means lowering LDL. And I just don't think that's the right thing for people.
If someone is not willing to make dietary lifestyle change, yes, you probably should lower ApoB.
But if we are telling people the full truth, in my opinion, it is, hey, your lifestyle is causing this.
And here's how you should eat.
Now, the problem there is that the mainstream medical establishment is so hung up on the fact that saturated fat raises LDL that they can't possibly recommend the animal foods that people should be eating.
So they don't even know what to tell people.
They'll tell people to eat more vegetable oil, which is the wrong thing.
And there are some really good studies.
The Minnesota Coronary Experiment and the Sydney Diet Heart Study were pretty fantastic studies.
I've got them both in the notes here if you want to see them.
Chris Ramsden, who is the investigator on both of those, or at least the second publication of both of these, is a national hero, in my opinion.
In the Minnesota coronary experiment, they were randomized.
It's a randomized interventional trial.
And it's a blinded trial where they had one group that was higher saturated fat and one group that was higher polyunsaturated fat.
And the polyunsaturated fat diet clearly did worse, clearly did worse.
More heart disease, more death, more cancer.
That's the other thing about polyunsaturated fat is there are a lot of signals for increased cancer.
The Citi Diet Heart showed exactly the same thing.
More polyunsaturated fat, more death, more cardiovascular disease, more cancer.
So there's some interventional studies that are pretty hard to ignore, just putting them head to head, and yet, because we are so myopic, because we are so focused on LDL, and we don't think about context or metabolic health, how could a physician recommend TALLO? Well, just breaking down all the shit that you've said in this podcast is giving people a headache right now.
And I'll tell you, so it's with a CAC, so it's a coronary artery calcium score.
It's a CT scan of the heart.
It's not a perfect test, but it's a pretty darn good test.
So Dave and his colleagues are doing a study where they're going to do CTA, which is CT coronary angiogram.
And I'm going to try and be a part of that study as well.
They're going to take people who are lean mass hyper responders.
They just got all the funding for it, I think.
And they're going to do CT coronary angiogram one year apart.
So what's interesting here, Joe, is that for kids with familial hypercholesterolemia, now again, granted, they're disordered lipid metabolism, disordered lipid metabolism.
They're not healthy lipid metabolism, right?
So they don't look quite like me.
They have a high LDL, but their LDL metabolism doesn't work properly.
They develop atherosclerosis within the first few years of their life, okay?
And they have LDL levels that are equivalent to mine.
Now, I've had an LDL above 300 for more than two years.
I also have a family history of early heart disease and of primary relative.
My dad had a heart attack when he was 43. So I'm 43. My dad had a heart attack when he was 43. So I have risk factors for coronary artery disease.
Oh, I mean, he was an internist, so he was not sleeping well, he was not eating well, he didn't think about this at all, he didn't know.
And that's what's so ironic, is my dad is such a role model for me, you know?
Amazing guy.
He was texting me, all excited I was coming on the podcast today, and he's such an amazing guy, and he meant so well for his patients, but I just don't think that mainstream medicine thought about this contextual stuff.
He's not, but he did wear a CGM, and I think he's going to try and move his diet in the right direction when he sees what his postprandial after eating blood sugars are.
It's getting better and better, but I saw a part of his dietary recall from the folks at NutriSense, which is the company that does the CGM, And it was, he was eating grass-fed meat, he takes the desiccated organ supplements, and he's eating some white rice, and I think he had like some banana bread.
And the thing I keep trying to get him to stop is eating glucerna, or vegetable oil.
Because he's eating these weight loss shakes that have soybean oil in them.
And, you know, he hasn't shared with me his CGM and I want to be respectful.
And if he will share with me his continuous glucose monitoring, we can look at his metabolic health.
Because I'm not going to order blood work for my dad.
But I can look at his continuous glucose monitor.
Like, this is the kind of stuff that really tells you about your metabolic health.
There's no way to lie with a continuous glucose monitor.
And so I think that he has some room to improve, but it's slow.
He helped me edit the book.
I think he was so proud when I wrote the book and just so excited that I was thinking this way.
It was so interesting to have this traditionally trained father, this internist, read my book and go, whoa, that's kind of interesting, Paul.
I mean, he's reading the chapter on lipids going, this isn't what I learned.
Maybe there's more I should be thinking about.
So we've had a lot of conversations.
And I mean, one of the reasons, the whole reason I think about this stuff, Joe, is because I want people that I care about to be around and I want to be able to share that with other people so that they can experience their life better.
So there's physiologic changes in the human gut that happen when you stop fiber abruptly.
So we don't know entirely, but I think that the most compelling theory that I've heard or been able to come up with is it has to do with bile salts.
And, you know, we talked about the bile earlier in the gallbladder and, you know, putting it on liver.
So your bile is in your liver on your right upper quadrant.
And when you eat meat or fat, your bile contracts.
There's hormones, choleocystokinin.
You release bile.
Bile is a combination of cholesterol, bile salts, bilirubin.
And bile salts are supposed to be reabsorbed in your small intestine.
So, you know, you have this stomach, a duodenum, a jejunum, an ileum, which is your small intestine.
Then you have the ileocecal valve and the large intestine.
The large intestine is like the colon, right?
And the colon goes up and over and down.
And so if bile acids end up in the colon, they are cathartic, meaning they will cause diarrhea.
And so I think that for the majority of people, if they are going to do a transition from a fiber-full diet to a zero fiber or a lower fiber diet, you want to do it slowly.
Because I think that in the small intestine, the small intestine needs to catch up and reabsorb these bile acids.
If the bile acids move through the ileocecal valve into the colon, they'll cause diarrhea.
And so your body takes time.
And so I think what happened in your case, because I was following it closely, I was texting Mark Bell.
So when I work with people and they get the diarrhea, I have them add back avocado or something with a little bit of fiber to help because the fiber will bind up the bile acids a little bit.
But in your case, it sounded like what happened was something adjusted and it eventually stopped.
And my suspicion is that the small intestine eventually catches up and says, hey, there's more bile acids.
The common perception of fiber is that it's essential, that it cleans out your body, and that to live without fiber you're going to get constipated, you're going to have all these problems.
If you actually look at the medical literature, There's no evidence that fiber improves constipation.
So fiber can give you bigger poops, but there's good meta-analysis.
There's interventional studies that show that fiber doesn't relieve the other symptoms of constipation, which are pain, difficulty with passage, bleeding.
Constipation sucks.
Nobody wants that.
But fiber will give you bigger poops that are usually more painful to pass.
And fiber also causes a ton of gas and bloating for people.
There's a really fascinating study from 2012. It's an interventional study with fiber.
And they had three groups of people.
I think it's 60 people.
They divided them into three groups of 20. And they all had idiopathic constipation.
Well, when I was drinking kale shakes for a while, I was drinking kale shakes in the morning, and it had a similar effect to the carnivore diet in the first two weeks.
Like, it just, woo!
It opened up the canyon and lubed up the old water slide, and things were just flying out of me.
Well, I think it was also, I was doing it with MCT oil, and I was adding fruits and all sorts of other stuff to the kale shakes, but I thought I was doing the right thing, and I was feeling pretty good while I was doing it, but absolutely not as good as I did when I went to the carnivore diet.
I think I was getting this burst of carbohydrates and sugars and nutrients, and also I was thinking because The poop was coming out so easy and quickly.
My friend C.T. Fletcher, he is a power lifter and he had a terrible diet at one point in time and wound up having heart disease and it runs in his family and he had to get a heart transplant.
Yeah and so now he has a heart transplant and he has a new heart and he's exercising again and he's gone completely plant-based and he thinks it's a good thing for his health and for his body and you know he used to be a guy who ate a lot of cheeseburgers and McDonald's shakes and stuff and just wasn't really eating that healthy and now just kind of completely changed his diet and I don't have the knowledge to tell him that that's not the way to make your heart healthy.
If you are very careful about supplementation and you think about creatine and carnitine and choline and vitamin K2 and B12 and bioavailable proteins, I mean, you could sustain yourself on a vegan diet in my opinion.
But I would also encourage him not to ignore the evidence on polyunsaturated fatty acids and to be sure that with his transplanted heart, that he's carefully watching it and looking at the right metrics and really looking at the right measures, which may give him some indication of atherosclerosis that he's carefully watching it and looking at the right metrics
So if somebody were to do a vegan diet with no vegetable oils, they might be able to do okay given they were getting enough calories, enough protein, enough of these nutrients, and we're supplementing with the right things.
But I fear that a lot of vegans are going to think, canola oil, that's great, that's vegan, or soybean oil, that's great.
Or they're going to eat these plant-based garbage burgers, which are full of this vegetable oil.
But if you could get him to just completely objectively learn and not disrespect his choice to become plant-based, what would you say would be the optimal thing for someone to do?
Having recovered from heart failure and a heart transplant, what would you recommend?
So eat meat and organs as a center of your diet from well-raised animals.
Rome Ranch, White Oak Pastures, Polyface Farms.
Don't fear the organ meats.
Don't fear red meat.
I really think...
I mean, there's tons of stuff in the book about why this information's bad.
Know which plants are the most toxic.
Eliminate the most toxic plants.
And eliminate vegetable oils and processed sugars like the plague.
And I think if you do that, you're going to thrive.
And I think you're going to feel really good.
Now...
We're at a crossroads, Joe.
The mainstream medical establishment doesn't agree with this and I'm fully ready and I think this is gonna become my life's work.
It's really exciting to be in this pace and say, hey, I think these ideas are wrong and they need to be refined and I think that more people will benefit if we refine these ideas.
I think people are suffering.
Because of incorrect information foist upon us for the last 70 years by the mainstream medical establishment.
I think that as humans, it's okay to be a part of the cycle of life and death, and we will all die, and we will all go back to the earth.
At some point, these atoms that I am renting will return to the earth.
And so I think that it's okay to take life respectfully in a hunted way.
But if more people did this, and this is not necessarily scalable in 2020, but I think if more people did this, it's like a sacrament.
And I don't mean that in any sacrilegious way, but it was just like, it was one of the most clarifying things I've ever done to remind me, be a good person.
Here is the universal bounty to you.
And I hope this doesn't sound too woo-woo, but it was my personal experience.
Like, here is the universal bounty to you in this moment.
Like, you better be a good person because you are so fortunate to have this nutritious food here.
It's just very striking.
I think it would change.
And that's completely different than the vegan ideation that we're being harmful to animals or we're being disrespectful.
It was like, wow.
It was almost like that animal gave me the gift, like, be a better human.
Well, I had this thought before I started hunting that I was either going to become a vegetarian or was going to become a hunter.
I had seen a lot of those documentaries and those videos online about factory farming and it's appalling.
It's disgusting.
It makes you sad.
It makes you sickened.
I was trying to figure out what can I do?
Would I be capable of killing an animal?
I never killed an animal before.
And then after I did, I went hunting with Steve Rinella on his television show.
I shot a mule deer.
We ate it over a fire.
And I said right away, I'm doing this from now on.
This is what I'm doing.
Because it resonated.
It made sense.
It felt good.
It was a very difficult thing to do.
It took days and days of hiking many, many miles in the mountains.
To find a mule deer and to shoot it and then to haul it out of there and then to cut it up and eat it or cook it and eat it.
It's a weird word, spiritual, but it is a spiritual experience because it connected you with the life that sustains you.
Like you were there.
I looked at that animal when I squeezed that trigger off and watched it drop.
And then when we were cutting it and hauling it out and eating the liver and eating the heart and cooking meat over the fire, immediately it all made sense to me.
I was like, okay, this feels so much different than buying meat in a store.
When I take a piece of elk meat, I shot an elk last week.
In Utah, when I take a piece of elk meat two weeks ago and I put that on the Traeger, I season it and I put it there and I cook it and then I'm eating it and I'm feeding it to my family, I have a connection to that meat.
I looked in the eyes of that elk when I released that arrow.
I watched it drop 15 seconds later.
I felt the relief, I felt the happiness and I felt the gratitude that this animal is going to be how I get my meat.
And hundreds of pounds of meat, I'm going to give it to my friends.
To your tribe.
Yeah, I love it.
I love all of it about.
And the people that I've met through this pursuit have been some of the best people I've ever met in my life.
Some of the nicest, most disciplined, most warm, friendly, loving people.
They're not animal haters.
They're not cruel people.
They're people who understand where their food comes from.
And it's a different connection to food the hunters have a different idea of life and death and the average person who's shielded by it Who's using their credit card to pay for a supermarket hitman to make cheeseburgers for them?
And that's that's not the way to go and I know that it's not sustainable for everybody to do it like you said in 2020 but there's a lot of things that everybody Not everybody becomes a black belt in jiu-jitsu.
Not everybody becomes a race car driver.
Not everybody becomes a doctor.
It's fucking hard to do.
There's a lot of shit that's hard to do.
I'm not saying you have to do it, but for a person who chooses to have a connection, it is available for you.
But the price of entry is difficult.
It's hard to learn how to do it properly.
It's really hard to learn how to do it with a bow.
It requires a lot of physical exertion.
There's a lot of workouts that I do all throughout the year, specifically my cardio workouts, that I'm doing so that I have endurance in the mountains.
That's why I do it, because I've been exhausted trying to make it up a hill, especially my friend Cam Haynes, hunting with that fucking guy, just trying to follow him, just trying to walk behind him, forget about running.
I'm doing it because I understand that come the moment of truth, you have to be at your best.
It's not easy.
But if you don't want to do that, you can get meat from sustainable farms.
You can get meat from places like Polyface Farms, ButcherBox, which is a great company that's one of the sponsors of my podcast.
All their meat is grass-fed, grass-finished from sustainable places that are ethically raised animals.
You can get that food.
You can get it the right way.
You don't have to hunt it.
But if you want to hunt it, that's available too.
Most people are not going to have the time or even the desire to do it.
But it can be done.
But I don't like that argument where people say, well, it's not sustainable for everybody.
Well, neither is most things that are hard to do.
Most things that are hard to do, you're not going to do.
Most people are not going to win the CrossFit Games.
Does that mean we should stop the CrossFit Games?
Well, it's not sustainable.
Most people can't do it.
Does that mean we should stop marathons?
Because most people aren't going to run a marathon.
There's hard things to do that are very rewarding.
And most of those things come with There's an immense satisfaction in completing them.
And this is where hunting is different than any other source of gathering food.
Because it's a discipline.
It's in many ways an athletic pursuit.
And then it also sustains you and sustains your family.
And like you said, every time you eat, you have a story.
You remember.
Every time you eat that elk that you got with a bow, you're probably going to remember that time in the wilderness.
And think about if that was all the food you ate.
Every food had a story like that.
How are you going to live your life in a different way?
And so one of the things that's been so interesting for me recently is realizing that the carnivore diet and thinking about animal-based diets was just a stepping stone.
It was kind of the entree to think about a broader concept about the way that we as humans have forgotten.
That there's this broad amnesia, and I've thought about this and kind of called it the remembering, Just this idea that it's about more than the way we eat.
It's about the way we live on the earth, being in nature and doing things like hunting and getting back to these roots.
This, to me, is what gets me really excited that we're starting to think about the way our ancestors ate in an ancestrally consistent diet, but we also need to think about We're good to go.
That was 2012. I've been in 100% for the last eight years.
I think about it all day long, especially now that I've become a bow hunter.
It's funny, I was with my friend John Dudley and we were at a UFC fight.
John was in the crowd right behind me.
It was a big fight about to go on.
And I said, this is what I'm thinking.
I was thinking about archery.
That's what I was thinking.
I was pulling a bow back.
Anytime something's boring to me, I think about archery.
If someone's talking about something I'm not really interested in, I'll listen.
But in the back of my head, I'm thinking about centering my pin, centering the bubble, drawing back, pulling with the scapula.
Getting a surprise release.
It's a massive obsession.
And there's a different spiritual connection to bow hunting, I think, because it is so difficult and it is so physical.
It requires this being in the moment in a way that nothing else does because there's so many moving parts that you have to align correctly in order to execute.
What people don't understand what we're talking about is it's hard in the moment of truth when you're anticipating the shot to not flinch or move.
And with archery, it is so important that the shot goes off I'll say this for most people because there are a lot of people that are extremely good archers that don't do it this way, but they have practiced their way by pulling the trigger and consciously pulling the trigger, what they call a command release.
They've practiced it for so long they could pull it off.
My friend Cam Haynes is one of those people.
My friend Remy Warren, he's another one of those people.
There's great archers.
There's a guy named Tim Gillingham.
He's one of the best archers on earth.
He wins world championships and he pulls the trigger.
He has a finger trigger and he pulls it and he beats everybody.
He's very well celebrated as one of the best archers in the world.
But for the most part, for most people, you're better off having a surprise release.
You're better off taking the idea of the shot going off and you just go through the motions of getting it to go off, but you really have no idea when it's going to go off.
But it's hard to do with the thumb thing.
Really, a lot of people cheat.
They pretend they're doing that, like, yeah, I'm getting a surprise release and I'm watching my pitch.
My elk in Utah this year was very unusual in that I had to run to get to the waterhole before the elk did.
I was in a patch of trees and I was hidden and I heard the elk screaming and we knew there was a waterhole here and he was trotting down.
I tried a couple spots, but there was no clean path to shoot through the trees.
And I managed to do it quickly and quietly enough so that he didn't see me moving and I was hiding behind trees.
But I knew I had to get all the way to the waterhole before him.
So I had to run and I had to jump over logs.
So there's these downed trees.
I'd hop on top of these trees and jump over them.
So I ran about, you know, 50, 60 yards until I got to this spot where he was.
I really had a sprint.
And then I had to calm myself down, and I looked at him.
I ranged him, and I had the bow in my hands.
He looks up at me, and I drew back as he was looking at me.
Because I'm in full camo, with gloves, face mask, headgear, full Sitka gear.
He was like, what the fuck is that?
And then...
I probably had a second before he realized what I was, before he was going to bolt, and I released the arrow right at that moment.
So it was intense, and it was super adrenaline-packed, because I knew I had to run, too.
So there was all this, like, he's at the waterhole, I range him, he steps away from the waterhole, and then he looks up, and as he's looking up, I'm just drawn back.
And I think I had a second or two before he was like, oh, that's a fucking person, man, dressed up like a tree.
But it was so, it was so, it was a moment where if I hadn't prepared properly, I would have never been able to pull it off.
If I wasn't physically in shape, I would have never been able to run there and have my heart rate drop down.
If I wasn't confident enough in my shooting that I shot so many thousands and thousands and thousands of arrows, I wouldn't have been able to execute because it was a weird shot too.
It's such a cool thing to have the story wrapped up in all of it.
It's so rich.
It's such a different experience than we get as humans.
As soon as I think about the irony of 2020 or even the last century that we've put ourselves in digital worlds to work on computers indoors to make fake numbers in a bank account or green pieces of paper that allow us to go hike and do the things that we were doing in our whole life.
I mean, whether it's the oxygen that you get from them or whether it's just a signal to your body that this is a natural way to exist, to be in wilderness, in nature.
It feels good for you.
Like to just be walking through and just seeing it, it enriches your soul.
There's something about looking at mountains and trees and like a stream that it's this crazy natural beauty, this natural artwork.
That your senses react to this in this incredibly pleasing way.
Like, wow!
Like, I remember we came over this ridge, and there's a creek below us, and there's this beautiful green hill, and there's a mountain behind it, and I heard this bull elk on the hill above it screaming, brrrr!
And I'm looking at this and I'm like, this is gorgeous.
It's so pretty.
Like everything about it just made my whole body just feel good.
Like a drug.
Like a happy drug.
Cell phone didn't work.
You know, there's no signal out there.
It's just peaceful.
Just peaceful.
Just nature the way it was for who knows how many hundreds of thousands of years before people ever even came here.
There's a connection that we have to this wild world that we evolved through that we don't, we're just, we're like neutered.
When we're out here with the concrete and we're looking at buildings and it's, you know, the way we live and there's a lot of great benefits to living in cities and all that stuff.
But there's something about it when you're in a car, you're just, you know, sitting at a desk, you're muted.
And I think that in some ways, I suspect that it's built into our consciousness, just like that ERP study that I showed you with meat.
And I think there have been similar EEG studies with nature scenery that ultimately we're animals.
And we try to pretend that we're not.
And I think that we're trying to become the best animal that we can be, the most ethical, kind, empathetic animal.
But we still, I think that we would do well to consider the fact that if we discard everywhere we've come from, We may end up in a position that's pretty miserable for humans.
If we discard wilderness, if we discard what I believe are the most ancestrally consistent foods, if we discard the patterns of human interaction, we're just going to go further down.
My fear is that this is inevitable and that what we are going to become is some sort of a symbiotic thing where we're part...
We're going to be a cyborg.
We're going to be part electronics.
We're going to be more immersed in the electronic world than even we are now.
And that this trend of becoming addicted to your phones and constantly online and all these different things that we all see with people, that this is just a step in this...
Inevitable process.
But right now we're not there.
So right now that is not enriching to us.
It doesn't feel good.
This might be what a person is a thousand years from now.
It might be out of our control.
It might be just the way of entropy, the way the world works, the way of innovation, the way of just the evolution of the biological thing that is a human being.
It might inevitably move in that direction.
But it's not that way right now.
And if you live that way right now, you'll be miserable.
You'll be depressed.
You'll be disconnected.
And that's why you see all these people that are living online most of the time on Twitter just fucking arguing and throwing shit at each other like insane patients.
They're like people in a mental institution.
And they really are mentally unwell.
They're in a depressed, crazy, agitated state most of the day arguing with people.
I would imagine, I don't know what the number is, but maybe 40% of all interactions on Twitter are people yelling at each other.
I wanted to, before we get going, I wanted to talk about the benefits of, when you talk about grass-fed, grass-finished meat, what is the nutritional benefit of that over, in terms of essential fatty acids and nutrient content, over animals that are fed grain?
You know, the persistent organic pollutants, the dioxins.
So you've got to imagine that cows eating good grass are going to have less of that in their fat.
It's in the soil, so the longer a farm has not been using those, the better.
But the cleaner the cow, it's going to have less of that in its fat.
Less of this, less glyphosate.
Glyphosate's water-soluble, so it'll probably be in the muscle.
Atrazine is fat-soluble.
But this is the kind of stuff that's never been really looked at.
So grass-feeding is not as much about the increased nutrient content.
Grass-fed, grass-finished, or grain-finished, they're both nutrient-rich, but the grass-finished is going to have less of the bad stuff in the meat and less of the bad stuff in the fat, in my opinion.
And it's also a thousand times more ethical and part of an ecosystem, which is the only way humans are going to persist on this planet.
I mean, certainly you can imagine there's going to be more carotenoids from the grass if the cow is finished on grass versus the grains, which are not going to be...
You see that with salmon.
You know, they have to give salmon these coloring pills if they're farm-raised to get them to make the flesh not...
It would be super interesting to do some studies on that.
You know, to take the elk meat that you've hunted, to put it through like gas chromatography, mass spec, do some analyses and look at it compared to like grass-fed beef or something.
See if it's like excess carnitine or maybe some more choline or carnosine or something.
I'm sure there's something in there that makes it special.
So acetylcholine is a neurotransmitter, and I think alpha brain has huperzine A, which is an acetylcholinesterase inhibitor, and that allows more acetylcholine in the synapse.
So if you increase acetylcholine in the synapse, it can be a nootropic.
Absolutely.
But choline is a precursor for acetylcholine and phosphatidylcholine, which is the phospholipid that makes up all the cells of our body and the myelin sheath on neurons.
And again, really, really, really hard to get an optimal amount of choline without eating animals.
So Jamie, in the folder nutrients, there's one called creatine-enhanced veggie.
There have been interventional studies on vegans, and they give them 20 grams of creatine for five days, which is a loading dose, and they get smarter.
But I think if you're eating a pound of meat per day plus, you're probably not going to get a whole lot of performance benefits supplementing with creatine.
If you go to the evolution folder, Jamie, there's a brain size change graphic that's pretty cool.
So, this is a graphic from my book and you can look at the size of the human brain Based on the cranial vault size.
And this is fascinating.
And there's a lot of theories as to why this happened, but some of the most compelling, in my opinion, are around the advent of hunting in humans.
And when you had Bill von Hippel on, so you can see here, this is millions of years on the x-axis and the size of the human brain on the y-axis.
You have the primate ancestors, Australopithecus, Homo habilis, Homo erectus, fire, and then Neanderthals, and then Homo sapiens.
So something really clearly, this is another Tony Hawk skate ramp, right?
What the heck happened there?
Something happened.
I think the most compelling ideas are right there that I labeled in the graph, that around two million years ago, we see the occurrence of stone tools, these bifacial tools, these Acheulean tools, and evidence for hunting, cut marks on animals, bones, and evidence for mass animal graves.
So this is really cool.
I would postulate that humans becoming hunters, becoming hunters made us human.
Steve Rinella is doing the happy dance right now because he's right.
Hunting animals made us human by providing indispensable nutrients like creatine that were prime releasers or allowed our brains to grow in this special way.
His brother Dennis makes a very compelling argument for it as well because his brother Dennis is a scientist and he goes deep into the actual physical changes to the brain and to synapses and to the body's ability to produce language that occur while under the influence of psilocybin.
Well, it could be they were happening at the same time.
I mean, this is also, they think that it might have made people better hunters because psilocybin, particularly in low doses, increases visual acuity and probably makes you more creative too.
Makes you figure out how to hunt better and maybe responsible for the development of tools and other forms of creativity that benefited human beings to evolve and become better hunters.
I want to do it again, but I think about it set in setting and kind of respectfully.
The first time I did it was a few years ago.
And so I'd never done it before in my life.
So it's only within the first few years that I tried it, the last few years.
But my experience was profound.
And I don't doubt any of that with what I experienced.
It was clarity.
I felt so at home in the natural world.
It was incredible.
And I was out hiking in Seattle where I was doing my residency.
And I was with a friend.
And we were by a lake.
And it was just me in the wilderness.
I was by myself.
I had a different connection with trees and plants and it felt so different.
It was just like a door opened to this experience.
It was like a whole different, unique thing.
And I was with a friend.
He had to go back.
He was on call and I said, just leave me here.
I never wanted to leave.
I felt so at home in the wilderness.
And so, you know, I hope that it's probably controversial, maybe not in 2020 for a mainstream physician to say I've used psilocybin, you know?
I don't think so anymore.
It's now being used in trials for PTSD. John Hopkins, yeah.
I mean, it's incredibly powerful, which actually gets to an important point that I should make about plants, which is that I don't want anyone to think that I'm against plants as medicine.
I think there are many plant compounds that are very valuable for humans.
Medical marijuana, psilocybin, clearly impactful for humans.
But there's a real dividing line between that and using plants as food or using plants to make you better every day.
So we should just say that.
But yeah, I mean, my experience with psilocybin was profound, and I think that it's something that I hope more trials will happen with, with the FDA.
You know, I was reading about it.
I knew they were doing studies at Hopkins and they were doing studies at NYU. And I thought, I almost felt irresponsible as a physician not knowing what this experience was like.
I wanted to turn off the default mode network.
I wanted to see what it was like without ego.
And it was an incredible experience.
So having had that experience, I don't doubt it.
When I was at White Oak Pastures a couple weeks ago, I was walking through a pasture with cow pies and there were psilocybe cyanosis growing.
It just makes sense that they would try it, right?
I mean, they flip over cow patties.
If you watch primates, they do it to get bugs and grubs and all that.
It makes sense they would try the mushrooms, and if they did try it and started tripping and found it to be incredibly euphoric and enjoyable, I would imagine they would consume it quite a bit.
What Terence McKenna's research shows is that it corresponds with a climate change and a decreasing of the rainforest and it's rescinding into grasslands, and that that would also increase the number of ruminants and these cattle, these undulates that were leaving these piles of shit, and then these mushrooms would grow on them.