How and why Insulin Resistance drives chronic disease with Dr Isabella Cooper

I would say in my field of research is a bit of a frustration on my side because there's

only this focus on glucose, the starchy part or the sugary part of carbohydrate and not

focusing on things that can trigger insulin receptors without affecting your blood glucose

and without elevating your insulin.

So you can actually stay perfectly in ketosis and still not have health benefits that you

would expect to see when you're in ketosis.

So I'm absolutely delighted today to be speaking to a dear friend as well as somebody I work

within this place.

I'll explain how I know Isabella and in a minute, but first of all, I just want to go

through your bio because I want people to understand that we like talking to experts

on this show.

You know, if there's a few people who work in a particular field, we like talking to

the one who really is the expert in this field and we're doing that today.

So you're a biochemistry medical pathology scientist and ketogenic specialist whose research

focuses on aging biology, hyper-installanemia, ketogenic science and chronic diseases including

cancer, Alzheimer's, cardiovascular, endocrine and autoimmune conditions.

So that's your kind of area of research, your PhD with which I'm pretty familiar because

I've known you for a while, established the first comprehensive characterization of metabolic

endocrine, lipidemic, LDL responses and extracellular, vesicle phenotypes in long-term ketosis

and across distinct metabolic states in crossover clinical trials.

We're going to come onto the PhD study as well.

You've also published a diagnostic grading scale for metabolic phenotypes and have formerly

classified hyper-installanemia osteophragilitis in the MDPI medical dictionary.

So you have left your legacy in a number of ways already.

You're a member of a few organizations, the Royal Society of Biology, Endocrine Society,

Biome Chemical Society, Physiological Society and Associate Fellow of the Higher Education

Academy.

You've got a BSC on's in biochemistry, which is why you're my go-to on all things biochemistry

with also medical physiology, advanced cancer biology, endocrineology, immunology, neurology,

receiving multiple awards for scientific and teaching excellence, including Faculty of

Science and Technology Awards, UK Biochemical Society Award and Multiple Deans List Honours.

And you're also on the Scientific Advisory Board of the European Keto Live Centre.

That is one hell of a bio, especially for someone so young.

Right, you're going to realise there's going to be some big words in this, but I'm going

to say that every time Isabella uses a word that I can't pronounce, which for a few

there, I'm going to put my hand up and then she's going to put it into lay language

hopefully.

Much more interesting is how I know you.

We met at a conference many years ago, I think it's about a decade ago now and we've met

up at quite a few conferences since and you've just become a friend and we're in chat

groups together with various interests, whether that's nutrition health or just sort of

general freedom, dare I say, things that we're interested in in terms of sort of human rights

and civil rights and what it is to be a human being in this world.

But perhaps the most intimate thing that I can share is, a number of people know that

I went through a major, major, major lawsuit against associated newspapers limited with

Dr Malcolm Kendrick, which spanned quite a few years, started in 2019 and we had a trial

in 2023 in the summer and we had a verdict then in the summer of 2024 and for the trial

which was almost two weeks up in London at the High Court, which is where Prince Harry

and Elton John and all those famous people are now.

It's such a famous set of steps if you go and Google the High Court or look at defamation

cases in the UK.

And Andy and I stayed with you during that trial and honestly you kept us sane because

it was the most stressful thing I've ever done in my whole life.

I mean it was also incredibly exhilarating and exciting and entertaining and mind blowing

and all the rest of it and you just looked after us all that time and you packed us off

with a keto breakfast and a keto lunch and a keto dinner.

You are an amazing cook by the way, as well as a brilliant biochemist and all that kind

of thing.

And honestly I can never thank you enough for that because that was just my biggest

hour of need and you were there for us and just thank you for that.

But you're a very, very dear friend and you're also brilliant.

And we're going to talk today about some areas that interest a lot of people, which is

going to be things like keto diets, keto genesis, hyperinsulinemia, but having described

your field, can you give us the background to how you got into it because I think it's

a really interesting story.

Yeah, I mean, I guess it's a load of past things from my childhood to now, but ultimately

I would say the biggest push was becoming a mother, you know, I mean the moment you're

pregnant as a woman, the first thing you're thinking is, what am I putting in my body

that's affecting my developing child?

And you know, I was at that time living in LA and so you would hear a lot about endocrine

disruptors that are in plastics, in plastic bottles of the water and, you know, being half

Chinese, things that you eat that are also going to affect the group of the baby, affect

your hormones.

And then even to the point that after I had my first child, it's a very special diet

that you have afterwards that affects what's in your breast milk, affects your hormones

and recovery after pregnancy.

And then making the choices of what foods do I give to my child, what's most nutritious

and nutritious doesn't mean it just contains what the body needs.

It also doesn't contain harmful things or things that are subtracting negatively from

the body.

So you can't just look at a food and just think, well, it's rich in iron, if it's got

other molecules that are actually keylating iron out of your body, let's say.

So these sort of things and that's very much in Chinese culture as well.

And you know, but that went further, it went further into using nappies at birth, you

know, I was really in tears of the chemical exposure, again, the endocrine exposures to

developing children and developing babies.

And so, you know, I potty trained my daughters from birth and there's a lot of great research

in that about how using nappies can really affect them negatively in their endocrine system.

So anyway, you know, that was always an interest of mine.

I was always reading scientific literature and I ultimately wanted to be able to test things

for myself, you know, to really, you know, and you can do some things at home to solve,

but I really sort of got deeper and deeper into it.

And, you know, as I age, not only was there a learning of what our children are supposed

to that can make them hyperactive and, you know, distracted and had huge mood swings,

all of these sort of things.

At the same time, my parents and their generation were aging and you could start to see these

common diseases that are always occurring.

And, you know, there's many, many things that can positively, negatively affect our

health, but ultimately food is the biggest one, really is the biggest one.

And, you know, in Chinese culture, the moment you're unwell, the first thing that's recommended

is to fast.

And so, you know, it's curious why would you fast?

And the next thing you do after fasting is drink bone broth, meat, heavy, fatty, heavy

meat, bone broth, and so to understand why is this?

And, yeah, so I just sort of got really interested in that and I was heavily reading into the scientific

literature and ultimately I recognize when I, as I was reading nutrition science, it's

like, well, I don't know enough.

I need to know more at the biochemistry level because it's very easy to fool yourself,

convince yourself of things and look for the literature that satisfies your own belief

system, things like that.

And I just wanted to be able to go down to the one plus one equals two, you know, two for

two equals four, and really sort of go further down to see, you know, to understand how

studies are conducted, how they're constructed, because often research can produce results

that are, you know, positive to the hypothesis of what the scientists are suggesting, but

that's because they've actually built into the design of the study, their own bias, without

even realising it sometimes.

And so, you know, there's always said the easiest person to fool is yourself, right?

And so I really wanted to become a scientist at that level because I just, you know, I love

to really tease out and test things for myself really.

Brilliant.

So that gets you into endocrine disruptors, it gets you into the home sort of territory

of hormones.

What does that then take you?

Yeah, so with that, it took me to, within all the different types of diseases and learning

about the biology and the cell biology, I started to realise that there was a commonality

amongst all of the diseases with disruption to their mitochondria.

And so mitochondria always sort of understood as the powerhouses, the fuel system of cells,

but there's so much more than that.

I would say that they're conductors of what happens inside of the cells.

So depending on what kind of energy source, so what energy carrying source, that's carbohydrates,

proteins, fats and ketones, they will have different effects, signaling effects on the

mitochondria, but also different effects on the hormones that your body produces in response

to them.

And so within our field of, you know, weight, diabetes, cardiovascular disease, cancer

and these, often people are only thinking about things like metabolism, they think fuel,

glucose or fat and ketones and it's always the thought of metabolism in fueling, but they're

not realising a fundamental part of this is the hormones.

All of these fuel sources affect your hormones and it's your hormones that are dictating the

behaviour of your cells and the behaviour of the mitochondria.

And so this is why I think that it needs to be brought in that when you have a metabolic

issue.

Because when we have a metabolic issue, you've sent to an endocrinologist.

So it's the endocrine, which is the hormone system.

And so it's not one without the other, you know, and sometimes you'll see in vitrocellular

studies where they'll, you know, want to look at what's the effect of glucose on these

cells, but in our human body, when your blood glucose is elevated, your insulin is elevated

and that's your type one diabetic.

And so, you know, there's a lot of research that's not mirroring human physiology correctly

in terms of, you know, just this, with these kind of experiments, or even with animal experiments,

where they infuse them with a high amount of glucose and they don't have the consequent

insulin and all the other growth factors that come along, then we're misinterpreting

the biology and actual fact.

You know, so the endocrine system, it's something that has to be studied if you're studying

mitochondria and chronic diseases of aging.

So I mean, I've learned so much from you when I've been up there and chatting through

things.

And one of the things that really stuck in my mind is that I tend to sort of be dealing

with food at a fairly simple level.

So I think if you eat carbohydrate, your blood glucose level goes up, insulin gets called

upon to take, you know, get the blood glucose level back to normal.

But you taught me, remind me, that that's its emergency role, it's not its core role.

Tell us more about insulin and what it's doing in the body, in response to food or anything

else.

Yeah, so insulin, although, you know, I look at insulin in a pathological sense when

there's too much, it is life essential, right?

So we need insulin and it tells yourselves what to do with the type of energy that

it's receiving, the type of energy carrier, right?

So like I said, glucose, proteins, fatty acids and ketones, and depending on how much of

each one there is there, then insulin is going to essentially tell the cell what to do

with it, not just in terms of turn it into ATP carrying energy molecule, but in terms

of, okay, if it's more glucose and very low on the fatty acids and ketones, then first

obviously use glucose as a fueling substrate, and then it's going to affect other molecules

inside of the cells that will determine you should proliferate and grow more, or you

should spend more time cleaning up the inside of the cell, recycling, proteins and cleaning

up damaged parts at auto-phagy, might have, so insulin will have this effect of signaling

on the cells when a lot of insulin is being triggered, and then it will have a different

effect if it's at a lower level. So it's not a linear relationship where sort of more

will do the, what it does at the lower level, it actually starts to, at a certain point

where it's higher and constantly there's more of it, it tends to have what we would call

a pathological, meaning a negative effect on our body, unfortunately. And so with regards

to insulin, you want to treat it like this Goldilocks hormone, not too much, not too little,

that's the right amount. But how do you know what's the right amount for you? That's the

sort of big question. And in our area of research, the biggest problem with that is that we've

got these huge reference ranges, and it's just far too broad, not only far too broad

as in too high, the allowance of where insulin can be, but in terms of it's not really telling

you what's really the correct amount for you. So just like we would determine fat mass,

we would think there's a percentage that if you go under for a reproductive woman, she'll

actually not be reproductively capable, because the body needs a certain percentage for her

body. Just like we know that when you go above a certain percentage, you start to see

more pathological conditions develop. And so that's that percentage is determined on

her body, or you know, relative to what her body size is, muscle mass, and these sort

of things. And insulin is the same. It's not about just, oh, it's this number. What is

it negatively regulating in your body that we can then determine that it's not a healthy

amount for you? And most research at insulin is just looking at, is it putting glucose

away? And that's it. I know it's a solely glucose centric. And for sure, we know if your

glucose levels are consistently higher, first, usually always, and that's your type 1 diabetic,

they mean your insulin background insulin is always persistently higher too. But the reality

is is that your insulin in a healthy setting can be very, very low, and your glucose levels

are really, really well regulated. You don't need more insulin to keep glucose at a really

good healthy number. And natural fact, research has shown that the more insulin that your

body is producing to keep these sort of really good looking glucose numbers, the more risk

and pathology that you can develop. And I mean, I don't know if you want me to reference

and mention studies, because they're an amazing study, so I actually really show this. So

as an example, there's the cord trial, which was over 10,000 participants, and the average,

they were all diabetic, all type 2 diabetics. And their HBA1C, which is the average glucose

at exposure over two to three months, was above eight. And what they did, they split the

groups as an RCT, and so they split the groups into one group that was, you know, having insulin

injections to bring their HBA1C between 7.1 to 7.9. And then the more intensive control

group was to bring their HBA1C, which means glucose at exposure down to below six. And

after three, three and a half years, they actually stopped the trial, because there was

like 26 points, something more deaths in the more insulin group. So they did manage to

bring the HBA1C, which means less glucose, but the insulin has this, you know, too much

insulin. So regulating your glucose with too much insulin is pathological, right? So

if you only measure in your glucose, thinking whether my insulin's fine, you can actually

have a big problem. And this, this is, I would say, somewhat why we will even see cancer

in normal weight people, heart disease in normal weight people, you know, dementia in normal

weight people. And because the insulin's actually, it's like you're setting off little fires

in your house, and you're just putting them out, but their fires are going on, but then

you're putting them out, you know? And so how do we know your insulin is good for you?

What you really want to do is what does insulin absolutely control? It controls your ability

to make ketones. Like that, you know, it absolutely controls ketogenesis, so long as

you're not drinking ketones or guzzling MCT oil. And so the best way to actually really

know is testing your evening ketones. So before dinner time, testing your evening ketones

for about seven days straight. And when you've done that and your ketones are above 0.5,

then you know that your insulin is either healthy, safe low level for yourself. I know.

So it's such a great example because it is, isn't it? It's a sort of bit upside down

that we just focus so much on glucose. We're not looking at the thing that is bringing

the glucose down. And we're just assuming that if something has brought it down, that's

good. I liked that example a lot, actually. I mean, that kind of brings us into a couple

of terms that are just, we probably wouldn't have heard these very much 20 years ago, but

they've become mainstream in our world, which is insulin resistance and hyper-insulinemia.

Can you sort of pick up on those and explain those to people who may not be so familiar

with insulin? So in sort of the common research area of insulin resistance, people will

often mistake this for meaning the insulin is not doing its job so you just need more.

And this is the danger. And I see this a lot with diabetic research, diabetes research,

because they'll treat type two diabetics, kind of like type one diabetics in research.

And the sort of clinical way of understanding insulin resistance is that your cells don't

take up blood glucose in response to the insulin signaling to the cells to tell them to take

up the blood glucose. So really that term insulin resistance should only be applicable to the

glucose element. So it's glucose uptake insulin resistance. That's what it really means.

And in that setting, it's not a low insulin setting, it's not a type one diabetic, it's

actually a higher than normal or higher than is good for your self level of insulin. So

it's invariably if you're insulin resistant, you are hypoketanemic, meaning you're not

producing enough ketones because the level of insulin is enough to stop you producing ketones.

So that insulin resistance, meaning in terms of not taking up glucose in your muscles as

an example, at the same time that that's happening, the cells are all actually still seeing that

insulin signal. They're not not seeing it. They're just getting a different message. And cells

that are naturally hyper proliferative. So that's going to be your lungs, breast tissue, prostate

tissue, intestinal tissue, brain tissue, kidneys and liver. These are cells that are naturally,

they have to divide on a regular basis. These cells, they are negatively affected by the excess

insulin when a person gets into an insulin resistant state. At that point, the insulin is

triggering the grow and divide. Nothing to do with glucose. It's triggering the grow and divide

receptors, which means proliferate more. And there's doing it more potently, more strongly than when

your cells are not resistant to glucose uptake at the same time. And the thing is, in terms of

evolution, we have not evolved a system that would trigger a cell to proliferate and grow

while at the same time enable the cell to go through controlled cell apoptosis. It's

biologically inefficient, right? If you're building and growing, you wouldn't be

breaking down and destroying the same thing you've just built and grown. So when a cell

has it turned on to grow and divide, at the same time, it turns off apoptosis, which is the

cell controlled cell death mechanism. So that's how we define cancer, too much growing and dividing

and not being able to die, right? And so excess insulin, which is always the case in

insulin resistance, and the term is hyper insulinemia, so too much hyper. And so insulin,

emia,emia is in your blood, too much insulin in your blood. And so they always come hand in hand.

And that hyperincentemia in that insulin resistance state is actually triggering normally proliferate

cells to proliferate even more. And it inhibits apoptosis, which that controlled cell death we need

in order to maintain healthy organs and healthy tissues. So the more that switched off, the more

damage dysfunction inside of the cell happens. And then that that results in not just the potential

for cancer, but in terms of the mitochondria becoming toxic unhealthy, dysregulated and doing a lot

of other damage in the body. That's not necessarily just cancer, autoimmune conditions, dementia,

and things like that. So yeah, hyperincentemia and insulin resistance, they come hand in hand

together. But insulin resistance is usually only started to be detected once you're either outside

of the reference range or you have hyperglycemia. So that's tested by the HBA1C or using HOMAR IR,

which I would argue is the best one out of the three, but it's still not perfect because HOMAR IR

requires these big jumps in order to really see this change. So you know, sort of it's about 65 to

75 percent sensitive, but then that's missing quite a big group of people. So what you really

want to do is test your fasting insulin, test your fasting HOMAR IR, do that seven days before

dinner, repeated capillary ketone tests, do the glucose as well at the same time, of course,

so that when you do or at the end of the seven days, if you went to go measure your insulin at that

point, it would be related to those seven days beforehand of ketone testing and you'll have a

greater insight that that insulin level is actually good for you or possibly not so good for you.

And then you would know, are you now into your personalized hyperinsulinemia threshold?

It's very, very important because it is so personal that that level. And ultimately, if your

ketones are lower and you have normal level glucose, what you're really experiencing is what we

call hypo ketonemia, which is not enough ketones. Insulin compensated euglycemia, meaning

very well regulated blood glucose because of too much insulin.

That was a brilliant intro to why cancer, or there is certainly a field, cancer is a metabolic

disease. That was just an absolute perfect intro to how you can get cancer in the body. I mean,

that was just brilliant. So we're talking about ketones. I guess now we need to do

body's ketosis. We hear the terms nutritional ketosis and then therapeutic ketosis.

Talk to us a little bit about those. So ketones are molecules that we produce when we're fasting,

when we're sleeping, when we're born, babies actually require ketones. It's in breast milk and

it's passed from the mother to the fetus during pregnancy. We produce it when we go into fat

burning. So, you know, it's unfortunate that people have confused what's called ketoacidosis

with being in ketosis. And ketoacidosis is a state where ketones are exceptionally high, above 10

millimeters per liter, with exceptionally high glucose levels as well. Again, above 7, 8, 9, 10

and what's called bicarb, which is buffering in your bloodstream so that you end up with a change

in the pH level, becomes very acidic, your blood pH. So this is something you see in type 1

diabetics. You just don't see it in people who produce insulin. So if you've got a little,

extra heavy weight around your belly and carrying more weight than you want,

you produce insulin because the only way you can make all that extra fat is being able to produce

insulin. So, ketoacidosis is something different. Ketones, when we go and you're fasting or you're

exercising and you know, people often say you should exercise for about 40 minutes so you burn

through your glycogen and then you get into fat burning, which means you're going to stop

metabolizing the fat in your body. Actually, what's happened is you've actually lowered your insulin

enough that now the insulin's not blocking you from burning fat and using it as a fuel.

And so when that starts to happen and your liver starts to actually burn fatty acids as it's fuel,

there's a kind of spillover and excess and that excess becomes turned into ketones. And this is

predominantly liver, but it's not exclusively to the liver. So the liver is our major sort of

major source of ketones that we make our cells, but our kidneys also make ketones, the intestinal

cells, the the interocytes of intestine, they're a major source and of course, the intestines are

really large organ. They make ketones are retinal epithelial cells of the eyes, they make ketones,

they could stabilize the very external layer, about 10% every day and then they produce ketones and

feed that backwards to nourish the eyes. And so, of course, having too much insulin to block that

would be negative for your health of your eyes. And our astrocytes in our brain, glial cells,

they also perform ketogenesis and provide that for the brain. And with regards to

dementia, Alzheimer's Parkinson's disease and vascular dementia, this is really important to

understand not only the importance and the benefit of ketones for this group. It's also that when

you have hyperglycemia and hyperinsinemia, so too much glucose and too much insulin, which remember

that doesn't mean necessarily you're going to diagnosis type 2 diabetes because one meal can cause

the hyperglycemia for three hours with the hyperinsinemia that comes with it. So that's a transient

moment of hyperglycemia and hyperinsinemia. That's actually been shown to break down the

the type junctions that bond cells together. So the blood-brain barrier, it's really tightly linked

together. And when you've hyperglycemia and hyperinsinemia, it opens it up and what that allows is

easy passage of insulin straight into the brain because normally insulin, it goes into the brain

through a very, very controlled receptor-mediated method so that you don't get sort of sudden flooding

of the brain, of insulin. But when you're tight junctions of your brain are actually negatively

affected, then actually a lot more insulin can go into the brain and harm the astrocytes that are

making ketones for the neurons of the brain. And so that's with regards to just glycemia and insulin

together. It doesn't, again, if it's your type 1 diabetic, one doesn't happen without the other

in a normal physiology. But then you have other things like eating wheat or anything that contains

gluten, that contains glyodine, will trigger your intestines and your blood-brain barrier to produce

a zonulin, which will open up the type junctions of the brain again. And so these kind of foods will

allow background insulin into the brain and actually affect the physiology and affect the mitochondria.

Because too much insulin, chronically too much insulin, actually causes mitochondrial dysfunction.

It causes them to break apart more, changes their shape and their shape will then change their

behavior. So yeah, there's all of these other ways that you can have excess insulin exposure,

which is not solely down to carbohydrate. It's really important for people to understand. And I would

say in my field of research, it's a bit of a frustration on my side because there's only this focus

on glucose, the starchy part or the sugary part of carbohydrate and not focusing on

things that can trigger insulin receptors without affecting your blood glucose and without

elevating your insulin. So you can actually stay perfectly in ketosis and still not have

health benefits that you would expect to see when you're in ketosis. So not an example of that

would be certain types of lectins. There are certain plant lectins that actually trigger insulin

receptors. You won't measure it in your bloodstream as insulin, but it will trigger those

receptors and trigger those growth in a way that insulin would as well, but not affect your

blood glucose. So that would be conkinablin A, hemogloutin N, certain proteins like Amadin from

Almonds, these kind of things will actually trigger insulin receptors. And again, to really hone

in the point, you've got insulin receptors for glucose and you've got insulin receptors for

growth, division and apoptosis inhibition. They are different and the less, the less sensitive

the cells are to that insulin triggering of glucose uptake, the more activated and magnified

the signaling on the growth and division. And growth and division is, you could say a bit

explosive in the cell. That's how it's triggered. It's an explosive reaction. So you get that going

on in your mitochondria. And so, you know, at a very sort of simplistic way of describing it,

it's a fire in your mitochondria, essentially. And if that's going all the time, it creates

damage inside of your cells. That plant thing is really interesting because it helps to understand

why some people get into ketosis more easily than others. I've got a couple of friends trying it

in the new year at the moment. One has noticed that a square or two of 85% dark chocolate will

knock her out of ketosis quite quickly. More than the carb count of that chocolate would make you

think. And then there are others who sort of say, I'm okay with, I don't know, a particular vegetable,

but I go for kale or broccoli or something. And then suddenly I'm not in ketosis anymore. So,

what you're saying there, that certain attributes of plants, I guess, that are going to have an

impact on insulin, separate to the carb content of that thing that you've eaten.

Yeah, yeah. And there's definitely different kind of sensitivities. But we do see sort of

patterns, let's say. And we saw that in my PhD in the trial. And, you know, as an example,

very near carnival, but not totally carnival participants deciding to cut out just

cauliflower and broccoli had a huge jump in their ketones. There was no change in their blood glucose,

but there was a huge jump in their ketones. And you're like, well, hang on a minute, these are

typically ketogenically rated, you know, okay, to have and key share diets. And so, of course,

depending on what is it is you're trying to achieve, you know, might determine whether it matters

to you or not. You know, if having 0.5 to 1.5 ketones is working for you and a benefit,

then you might not need to be so strict. But there are some people who, you know, they have quite

a severe disease where they need to be, as we mentioned, nutritional versus therapeutic. So,

nutritional or rather, you ketonemia is classed as above 0.5. That's it. If you're, you know,

if your ketones are above 0.5 and you have normal glucose levels, you are in you ketonemia,

which means they're healthy, healthy, normal background physiology level of ketones.

So, that was, that was referred to as nutritional ketosis, but the correct terminology

is actually you ketonemia. Then therapeutic is essentially understood to be about half your

glucose level. It can be a bit less, so let's say, if your glucose is five millimolars,

then once you're at two millimolars on your ketones, you're considered to now be in a therapeutic

level. And that therapeutic level really means that you're going to see quite visible changes

in your health. So, for example, in a time course, so it's not going to take six months to see

that outcome or a year, you're going to see some significant changes. So, an example would be

people who get into really deep ketosis who are on anti-hypertensive medications, you know,

blood pressure medications. They actually usually need to come off their blood pressure

medications somewhere between seven to 11 days. And that's because their level of ketones are

such a therapeutic level that their body actually really does respond and go through a huge change,

huge changes as a result. And so, in regards to cancer, again, as an example, cancer patients,

they do need to be in what's called therapeutic levels, much higher levels, because they are

literally trying to outrace something that is, you know, very dangerous for them. So, they need

to kick in all of those mechanisms that come from therapeutic ketosis at a much deeper level.

And it's really important to point out, it's not about just having those high ketone numbers.

As I mentioned, you can drink ketones and have those high ketone numbers. But with regards to cancer,

yes, the ketones are protecting the cells are not using ketones as fuel, that would be, you know,

non-cancerous cells. But we need what we want to focus on is to stop the signal that's telling the

cancer cells to grow and divide. And that signal is insulin. And insulin has this sort of higher

arc, it's like the king and queen of hormones of growth factors. So, then insulin makes you produce

more IGF1, which is insulin like growth factor1. It makes you produce more lectin. It makes you

produce all these other growth factors, V, EGF, EGF, and all these ones. And so, a very small increase

in insulin, that's just enough to lower your ketones a bit, will increase all these other

growth factors, which are all signaling to the cell, grow, divide, make new blood vessels to take

more nutrients to them, grow and divide, and block apoptosis. As well as the fact that too much insulin

actually, it increases what's called PDL1, which is a receptor that allows cancer cells to be

invisible to immune cells, essentially. And so, it has this profound effect. And so, when you

know that you're getting your endogenous ketone production, so that means not drinking MCT oil

and not drinking ketone drinks, then you know you've done it because you've got the insulin really

low. And the insulin is going to lower all those other growth factors. This isn't to say that

supplementing with ketones doesn't have benefit. It does. But if you supplement at the expense of

not getting into the endogenous ketogenesis yourself, you don't get that benefit, especially with

regards to combating cancer, and also things like dementia Alzheimer's. Yeah.

We're going to come back to that in a second, I think, because it touched on some markers of

aging and longevity, which is a real research area of yours. We also touched on your PhD, and I

think now is a good time to cover that. And I was just blown away by your PhD, because what people

do in diet trials is they take average people eating the average diet, and then try to give them

a different diet, or they're supposed to keep some people on that diet, because it's the control.

And then they put some other people on a different diet, whether it's a dashed diet for hypertension,

or a Mediterranean diet, or whatever. But they're starting with what we know as metabolically

unhealthy people who are following before they flip the pyramid in America, following really

unhealthy dietary guidelines that are trying to get them to have 55% of their diet in the form of

carbohydrate. And they also don't study women, because women are complex and they have periods and

hormone changes. So you just like, right, I'm throwing all of that out of the window. I'm only going

to study women. I'm going to study 10 women who've been in ketosis for an average of four years,

who are metabolically healthy. I'm going to take all of their markers, and then you did it as a

crossover trial. So you don't need the control group, because for 21 days, you measure them in

their normal state. You then asked these poor women to follow the UK, I call it the eat badly,

plate, you know that they call it the eat well plate. You called it in your PhD, the standard

UK diet, which every day is a suck. So they were on this diet that sucks literally, and they did

that for 21 days, and then you put them back into their natural state. So I've set the scene,

tell us what happened, apart from that these women will probably hate you for the rest of their

lives, because you make them do that. It was, you know, it wasn't, it was an experience indeed,

and yeah, I mean, that is something you just said, women are not studied, you know, women are,

and so so much in physiology, medicine, pathophysiology, it's actually studied from men,

and then just slapped onto women, and it's like, well hang on a minute, we're quite different,

actually. And when women are studied, they're typically studied either postmenopausal, because it's

considered our hormone cycles are like complicated and messy and make it harder. And the women who are

reproductive, you know, having a menstrual cycle are usually put on some sort of hormone or birth

control when they're going to trials and all these things, because essentially to mirror again,

like being male and not having a monthly cycle. And certainly those women should be studied,

because we should understand how do those things interrupt with natural physiology. But at the end

of the day, you know, we should be studied in our natural physiology without all of these inter,

you know, interruptions and then things like that. And so I wanted to do that. I wanted to

understand how the women respond. And I would say, actually, you know, the expectation is that

with you've got a huge age, our youngest participant was 18, and our oldest participant was 37 or 38,

38 at the time. So that's quite a huge age, age spread, and two, three of the participants,

so two of the participants had children and then two went on to have more children. And amongst

the 10 participants, five or six of them were mixed race. So in totality of the ethnicities,

we actually had 10 ethnicities, you know, yeah, so you should actually expect less good data

with all those differences, right? So time of the month, we didn't time it so that you start the

trial. Everyone was at the same time of their, you know, menstrual cycle. We didn't do that because

the way our trial was structured, there was no way we could actually maintain the duration of each

phase that would actually fit with anybody's menstrual cycles correctly. So we were like, well,

that's out the window. And so all of those things together, you would expect a lot more noise

in your data. You would expect a lot wider differences in terms of responses and changes in

hormones and metabolites inside of the blood. And what we got was not the case, even with all the

genetic ethnic differences and age, age spread and menstrual cycle start to start to, you know,

start in the phases of the trial. Our data was incredibly homogenous with a very narrow,

what's called a standard deviation. So differences, they were much more similar to each other,

you know, and they were normally distributed. So this actually really gives us much more confidence

in those findings as well. In the sense that it's clearly the menstrual cycle, though it does have

an effect on us, it's not as impactful on these markers. And the ethnic differences also didn't

actually impact these markers. And the age disparities didn't, you know, massively affect these

markers. And so that gives us more confidence with a smaller group of people to start with in an

end of 10. And as you mentioned, because it was across over trial, it meant that everyone acted

as their own control. And so, you know, with regards to trials like this, if you're acting as

your own control, and it is across over study, it effectively changes your, your end number,

you could say, right? And so it was what's called statistically powered enough participants

inside of that trial. And when you get to much, much larger trials, there's always this risk that

the more participants you have in it, there's going to be more error because the more different

types of scientists are recording your data will bring in disparity and actually be less control.

So if you're able to hyper control what the trial actually is, which we did and our participants,

they were testing their blood coupons and glucose four times a day for 66 days, which means they did

256 tests over that 66 days. And we had 99.3 percent compliance. And so the level of controlling

that we did meant that, well, when we actually did what's called power calculations, it came back

and actually said to us in three different formats of power calculations that we actually only needed

for insulin nine participants and for IGF one, these were the two hormones we were very particularly

interested in. IGF one, it was three participants. And so we ran 10. And then with our final

actual data from the whole trial came through and we sort of, you know, if a curiosity state wanted

to see that power calculation again with the data that we had, it actually came back and said,

we only need five participants. So we did run the right number. And there are because, of course,

that's for those markers, not for the other markers that we investigated. And the reason why I wanted

to look at that is because, you know, in terms of like, we use BMI a lot to determine if you're healthy

or not. It's very common in the NHS and everything. BMI is considered, you know, the standard because

it's cheap and easy. And it's flawed. It's not, it's not, it's not ideal, actually, because, you

know, we know that about 40 percent of people who are normal weight actually get cancer,

cardiovascular disease, dementia, and all of these problems. And so BMI doesn't capture it. And

in the Enhame study, which is the National Health and Nutrition Survey in America,

they did a, theirs was on, I think it was, I think it was 12,000 people of data they looked at.

And too much insulin was more predictive of mortality, death than BMI. It was much more powerful

predictor. And so, you know, that's one of the reasons why, you know, in my PhD, we wanted to see

if we suppress ketosis, ketogenesis. So that basically means hypoketanemia.

Will that not only change your insulin in a way that we consider is not healthy?

Will that do it to all these other factors that we know are downstream of insulin? IGF1 being

the big one, right? And in IGF1, there was actually a study on the 30,000 people looking at IGF1

and mortality. And it is a U shape curve, because actually if you have, if you don't have enough,

just like insulin, if you don't have enough, you can die. So you need to have, you know,

but too much actually, if you consider this sort of middle healthy range,

if you're on the top end, it's negative for your health. And so IGF1 was shown second to insulin

being incredibly predictive for cancers in particular and earlier death. And so

with regards to the reference range for IGF1, you really want to be sort of between 120 to 160

in, I think it's nanograms per mil life to check that. But if you have low insulin and you have

slightly higher IGF1, it's not the same. It's rare that you would have low insulin and high IGF1

in actual fact, but you can produce IGF1 from exercise, which is great, because that's going to

stimulate the growth of muscles. So you can have transient increases. What you don't want to see

is this higher insulin, higher IGF1, and you detect that by a lack of ketones. And that's what we

want to see in this trial. So if you followed the UKEQL guidelines, it was, you know, in 2017,

the UKEQL guidelines had consumed 273 grams, I think of carbohydrate, spread over three meals with

snacks in between. And that's basically three oral glucose tolerance tests a day.

And then we were like, okay, we're going to get our very healthy participants. These are women who

have had no health issues, no overweight issues. And they're not athletes, you know, where they

do do research, there's always these really athletic people. And they're a unique group of people

themselves, you know. And so we need to study regular people, you know, and regular women. And so

we had, we measured everything in them beforehand. So we could see they were exceptionally healthy.

And then, okay, well, follow the UKEQL guidelines, but the health-ish interpretation of it,

you know, not going to McDonald's and eating junk food and things like that. And we did have

our participants photograph everything that they consumed. And in real time, send it into us so

it's timestamped. And we did that in truth, because it did two things. One is the expectation of

being audited. You know, there are people who really dislike ketogenic research. They really

dislike it. And so I just thought, you know, I'm going to be really frustrated here. We're going

to photograph everyone's meters. When they test, they're going to photograph their meters.

So it's not going to be reliant on the CVS file. They photograph their meters, they send them in.

Everything they, they're going to photograph with their hand flat down sky view,

so that we could proportional sizing as well. But also, you know, when you're photographing in and

sending in your records, you're not relying on memory recall. And it's memory recall is so inaccurate.

So we don't want to rely on memory recall. Whenever there was food that did have packaging,

that would have nutrition information, they were photographed that as well and send it in.

And, you know, when you photograph what you're eating and you send it to a scientist who

keep in track of it, you're also paying attention to what you're doing, you know. And, and we

were able to also then actually give some advice during the ketosis suppression. So essentially,

the carb phase, the phase that's making you produce more insulin. And we were able to give

some advice because our participants had been in ketosis for so long. They've forgotten the habits

that typical people have. So I remember when we were coming to the very last, really the very last

two days of, you know, each participant coming in because we don't even have one participant a day

because they've been the lab for eight hours. I remember asking some of them beforehand.

Has anyone actually drank any like fresh orange juice or something like that for the morning?

And they all replied back and were like, no, because in their minds, that's like, why would I drink orange juice?

And I was just like, oh my god, you know, most like regular carbuting people, they think that having,

you know, orange juice, freshly squeezed orange juice for the breakfast is good for you, right?

And so our participants really actually did do the healthiest possible version of a higher

carb, you know, ketosis suppression diet. And the results were quite spectacular in times of the

changes in the blood markers that we know are associated both as as indicators for some

and causative for others in pathology when they are elevated for a very long time.

And in our participants, they were only elevated for 21 days, right? And so, you know, they obviously

didn't develop pathology from that. And the most important part of our trial, which was the

third phase, which was going back to their lifestyle of being in ketosis. So eliminating all those

carbohydrates was that those markers all reverted back to their original baseline. That's really

important to have seen because it means that it was the intervention that did it. It wasn't,

you know, it was becoming winter and we had less sunlight and we'd become more sedentary and we,

you know, all these things that are possibly happening, it really means that intervention had the

it was the causal effect. It was the causal effect to make those changes that we saw.

And when you say those markers changed, I mean, in 21 days and quite early on in that period,

they were gaining weight. Their BMI was going up, their IGF1 was going up, their insulin was going

up, their fat mass was going up. These were marked changes in a really short period of time.

And as you say, they were very reversible when they went back to eating in a metaphorically

healthy way. But it really does make you think people following the government advice and it's

embedded into the school curriculum so that they're teaching kids this nonsense.

It's way more than 21 days that they're doing this stuff for.

Oh, yeah, absolutely. And I think one of the things that we want, I really wanted to also show

was we get a lot of people saying being in ketosis for the long term is not good for you,

you know, it's bad for your thyroid, it's bad for your cortisol, it's really stressful,

you know, it's a starvation diet. And certainly if you go on a calorie deficit,

nutrient deficit, you know, and you go into starvation ketosis, that's not good, you know,

but we're not talking about starvation ketosis here. You know, a well formulated ketogenic diet

is nutrient dense, bioavailable, doesn't subtract from the body and provides you the calories that

you do need because at the end of the day, you need to maintain your body, it needs a certain

amount of calories and it needs, you know, essential nutrients. And one of the things at first was

of participants, you could see after coming into the trial, the group average was about four years,

they were, they were extraordinary healthy, their muscle mass, fat mass was amazing,

respiratory quotient, which is where we're measuring the amount of oxygen consumed in carbon

dioxide released out, was showing us they were pretty, did just fat burners, which was amazing.

And and the other thing that we were able to show was their cortisol, there was, you know,

someone up, someone down, but it was just completely perfectly within the band of nothingness,

you know, normal. And so it wasn't stressful in their body at all. And even when they came out of

ketosis, because again, this is a very, very healthy cohort. So 21 days of, you know, essentially,

you know, suppressing ketosis and having more insulin, you could imagine it being

September at the end of summer, where you see all the berries and all the fruits and you might

binge for it before coming into, into Christmas, into the winter, sorry. And so the woman, they

certainly gained weight during this time, but they did, they did their, their muscle, their, their

lean mass actually stayed stable. And then when they went back to ketosis, their lean mass, so the

lean mass never changed, it really was just the fat. And of course, there's a water, there's a

water retention change in that. And in actual fact, when you measure, when you measure

fat distribution and lean mass, the way we did it was with the biological impedance seeker machine.

And when you go out of ketosis, so when you eat carbs, raise your insulin,

you change your water content in your body. And with that change in the water content,

it's the numbers are less favorable for when you're in ketosis. And yeah, our data was still

more favorable for when you're in ketosis. You know, and so yeah, these, these things, and just

being able to show the other thing was the thyroid, because we're often, as women told, it's not

good for your thyroid. Now, to be fair, in women who have hypersenemia conditions, they end up with

a lot of thyroid dysfunction. And quite often, it's a hypothyroid, so they're not producing enough

thyroid hormone that their body requires. But there is a difference between higher levels of insulin,

no ketones and low thyroid, versus low insulin high ketones and low thyroid.

The TSH and T3 hormone has been the two that predominantly looked at. Because what happens is,

when you've been hypersenemic, meaning hypoketanemic, so, you know, higher insulin to suppress ketones,

for a long enough period of time, what that insulin is doing is harming your mitochondria.

Your thyroid hormones are for signaling cells to make new fresh mitochondria to try to save the day.

And if you're doing that constantly over years, you're actually, you really are overworking your

thyroid, producing more of the hormones to try to fix mitochondria constantly. And eventually,

a few other things happen. So one of them is, you know, the more thyroid hormone you are actually

producing, the more hydrogen peroxide you actually produce, which is damaging for the thyroid.

And so there's this, you're going to be using up more of the iodine, more of the selenium.

If you have depleted in that, you're not going to be able to produce the thyroid hormone either.

Remember that insulin? If it's harming mitochondria elsewhere in the body, it's harming the mitochondria

in the thyroid as well, which means they're less capable to produce thyroid hormones as well.

Additional to the fact that when you're hyperincentemic producing too much insulin,

that actually coincides with not enough stomach acidity. Mainly because first,

the insulin, again, affects the gastric cells that produce insulin and damage their ability

to produce insulin. But the actual foods that are typically eaten on ketosis suppressing,

so carbohydrate foods, but including high fiber plant foods, they actually decrease the body's

ability to produce stomach acidity as well. That's going to negatively affect absorption of minerals,

iodine, selenium, magnesium, all of them minerals. But with regards to your thyroid,

it's going to negatively affect. And if you don't have enough iodine and selenium,

you're not going to be able to produce the thyroid hormones either. So that's in the hyperincentemia

state. So that would be the insulin compensated uglicemia. So you've got no

low to no ketones. You can have perfectly normal glucose because there's too much insulin

keeping the glucose looking nice and suppressing ketones at the same time. And so what we showed

was in our trial, there's low thyroid hormones, but not because there's a diminishing ability to

produce it. It's because there was a low demand because you're not damaging the mitochondria.

And we could see that through what's called the RQ because when you're measuring in the RQ,

the RQ is measuring what fuel is your mitochondria using. Damage mitochondria can't use fatty acids

very well. Then in that case, they'd be burning and using glucose. And so you produce more carbon

dioxide so your RQ value would be a higher value. And we see at least they have a different

RQ to regular people overweight or diabetics. And so if you're a regular person, you're not

diabetic, you're not actually overweight. You expect to be around about 0.85. And if you're

unwell, it starts to go even higher, 0.9, 0.95. But athletes, they kind of expect theirs to be

below 0.8. And after they've done about 40 minutes of exercise, it goes down to 0.75.

And that's considered, well, mitochondria now burning fat, which is great.

In our trial, our participants were already at 0.7 in the ketosis and some of them were even lower

and they weren't athletes. And that's telling you, they weren't damaging their mitochondria in the

first place. So that requires, it decreases the requirement of the thyroid to have to constantly

produce thyroid hormone. So it's not lower thyroid hormone because you're not good at making it

and there's something wrong that's dysfunctional. It's lower levels because you're not harming

yourself as much. So you don't need to bandage and constantly repair the damage. So it's really

important when we look at any of the hormones that we're never looking at it in isolation. And it's

the biggest problem in our healthcare system is they're looked at in isolation. And so, you know,

a lot of the time people will go into ketosis woman. And then their thyroid hormones will actually,

their T3 will actually go lower. And the doctors will panic and say, see, it's really bad for you.

You need to either go on, you know, thyroid medication or this diet is really bad for you. And it's

not the case. It's just you're, you know, setting off little fire bombs inside of your cells all the time.

So you don't need thyroid hormone to come in and try to rescue the situation.

That's brilliant. I love that. Whenever I'm up with you, you are so inspiring and you're such a great

cook, as I said, it just makes me think I should just be on a keto diet all the time. Are you on a

keto diet all the time? And do you think people should be on a keto diet all the time?

I think the natural evolutionary state that we would have likely evolved in is majority of the

time in ketosis. You know, if you, if you don't look at the last 150 years with that refrigeration

or that industrialization of what foods we produce, we just didn't, I don't think people were

eating three meals a day. They were eating at most, let's say, two meals a day. And of course,

the types of foods that we're eating are quite different. Again, you know, if we look at that

sort of evolutionary context, many weren't likely probably in like, you know, therapeutic levels of

ketosis and they could be in this euketonemia, this background amount. And in actual fact,

when I've measured a lot of people who are healthy, they actually are in euketonemia without

realizing it. And these are people you could say are very carbohydrate tolerant, right? So,

so just like we can say, I don't get drunk on two glasses of wine. Doesn't this mean the two glasses

of wine are good for me? You know, and it's the same in terms of, well, I actually stay in ketosis

on 75 grams of carbohydrate. I can eat 75 grams in a meal. And I guarantee you, I still think

ketosis doesn't knock me out. That doesn't necessarily mean it's good for me. And additionally,

doing it once in a while is not the same as doing it every single day or doing it every single day

three times a day, you know. And so, you know, it's not for me to go around saying to people,

oh, you shouldn't be and you should be in ketosis and things like that. People have different

things they want to seek out of life. It's fair enough. But I will certainly say people who are

diseased and unwell feeling pain in their body, even depression, a lot of these areas where they

would likely benefit from it's, it's lowering the inflammation that comes from the insulin.

Right. And so, it's the focus is lowering the insulin. The byproduct is the ketones.

The ketones themselves have benefits. They're antioxidative. They change the genetic,

regulate like genetic expression, epigenetic regulation. You know, so they have all these

other things that are fantastic, which you can get some of that from some types of supplementation,

but from some of them. But ultimately, it's the lowering of the insulin that you really want.

And different degrees of lowering insulin begets different benefits. And those benefits again

are seen differently depending on what age you're at as well, what your needs are at that time.

But in general, do I think that if it was a broad reaping statement, will being in ketosis be

more beneficial for people? Yes. But again, I'll also have it. If you were to drink soybean oil

and eat soybean protein, you will be in ketosis. And I put money on it. You will not be healthy.

Yeah. Good point. Good point. So, I like the thyroid diversion a lot because that's one of the

things that doctors get upset about. Another one, obviously, is, oh, you're eating too much fat

because you get into ketosis by cutting your carbohydrate and eating real food, not by, you know,

people who think, I've got to add loads of fat. And then, you know, no, no, no, it's getting rid

of the car first. And then, of course, the other one that we probably just sort of should touch

on before we finish is, in some people, and they tend to be the leaner people and the fitter people,

they go on a ketogenic diet and they feel amazing and all their markers improve, all the stuff we've

been talking about insulin, HBA1C, BMI, weight, energy, not feeling hungry, food noise, all the

rest of it gets better. But in some people, their cholesterol goes up. And of course, relationship

between total cholesterol and LDL cholesterol is very strong. So, those two markers go up.

What might be the pathway by which that happens? And is it something that would concern you?

So, straight out there, doesn't concern me at all. No, it's true, Lord.

You know, your LDL, the LDLs, they are a transport system in your body. They are essential.

In order, no one disputes between an ADEK is essential or an animal-based omega-6. No one

disputes these are essential for yourselves. Well, guess how they get transported to your cells?

Via the LDL system, that's how they go to your cells. And so, this system is more pronounced,

definitely, in people who are lean and going to ketogenic diets. The system sort of upregulates

and then you get a lot more of these LDLs going around. What you do actually get as a consequence

is more HDLs. And the HDL signal, when you get this high HDL, which has a much closer relationship

with good health outcome, the higher it is, not LDLs, an actual fact. But what it's telling you

is when you end up with a subsequent higher HDL, it means that the goods that were inside of your LDL

got delivered to the cells. And then you get these HDLs at the end. So, that means that the

communication between the cells and your cells being able to receive all these nutrients that they

need to have healthy functioning mitochondria got delivered and you ended up with HDLs at the end

of it there. And so, yeah, it's really a big problem when people are talking about lowering or

wanting, you know, panicking when they see this raise in their LDL. When an actual fact, you know,

first of all, if you, you know, there has been a very good study, and I can't remember the name

of the study, but they've done, you know, hazard ratios for looking at the markers that are most

predictive of morbidity and mortality. So, death, the biggest predictor is insulin resistance,

right? Hyperinsulinemia with LDL being literally at the bottom and being not so strongly predicted.

So, this is the first thing that I would say, but also in terms of low longevity studies,

actually seeing that cholesterol is, you know, the higher cholesterol,

it gets a much longer life expectancy. And specifically with cancer, low LDL and low

cholesterol in general, but low LDL and low cholesterol is predictive for a worse outcome in cancer

patients. Now, the, the LDL is, as I said, it's a carrier. What is it carrying? It is carrying

to the cells cholesterol, which is necessary for the cell to remain insulin sensitive. To be

insulin sensitive means less insulin is needed to do the job. If your cell becomes insulin

sensitive and less insulin is needed to do the job, it means you end up with less excess insulin,

triggering growth and division and inhibition of apoptosis. So, you want to increase insulin

sensitivity in all your cells to reduce the total amount of insulin being used. And LDL's carrying

all these essential vitamins in addition to omega-3 and omega-6, which are necessary for your

membranes of your cells, they're necessary to get them to improve cell membrane health and

insulin sensitivity. This is just a little tiny fraction of what they're doing. You know, the whole

system, you've got chylomicron remnants, VLDL's, LDL's that whole system. And this again feeds into

a problem in ketogenic research, in ketogenic diets where people go on high fiber, spinach,

kale, flaxseed, flaxseed, the actual seeds, the fiber, the psyllium husk, as well as the oils,

that all of these things actually strip your bile out of your system, which means it strips

your cholesterol, which lowers your LDL. But what's happening is you're actually stripping out all

those fat soluble vitamins, essential fatty acids, and torine, which is not an amino acid,

it's sulfonic acid. And torine is essential for healthy mitochondrial function. And you know,

we're talking about fibromyalgia, many other conditions that torine is fundamentally essential

for your mitochondria to work correctly. And the only way you're absorbing that torine is with your

bile to be secreted and then reabsorbed into the body. And high fiber diets, high seed oil diets,

they bind to that bile and they take it out of you, which will be depleting you of essential

nutrients. That's why I was saying you really have to think about not only what nutrients are in the

food, but do they contain other things that are taking things out of your body? And so this is where,

you know, it's not just the willy-nilly, just being ketosis and everything's going to be good.

If you eat the wrong foods and you're actually lowering your cholesterol when you need it to be

higher, because you need all those essential nutrients to be delivered to the body. So,

as an example, when I just mentioned about the torine and bile, it's required for the immune system.

So, the bile actually causes basing of your adipose tissues. That's making of mitochondria.

Those mitochondria transfer to your macrophages, to your monocytes and macrophages, so that your

immune cells have the mitochondria to then go ahead and do their job in immune surveillance.

And the immune system is so involved in the development of diseases like cancer or autoimmune

conditions, which can create other problems in the body. And so, you need to know that those

ingredients are getting to your cells. And that's through the LDL, the LDL system.

So, depleting it is not a good idea. You know, everyone goes around saying,

you're olive oil is so good, because it lowers your cholesterol. I don't think that's a good thing.

I don't either. I don't either. Wow. I mean, this has just been an amazing hour. Thank you so much.

My last question is usually, is there anything I haven't given you an opportunity to say that you

would like to have said, or something's popped into your head on one of the many topics that we've

covered? No, I mean, you and I, we can talk for hours on so many subjects. I think we hit the good

ones. Obviously, we can talk. And if anyone wants to write into you and say, can we talk about

something else in particular, we can. I think we hit the good ones. I think we'll be having another

chat about how cancer is a metabolic disease and therapeutic ketosis and all that kind of thing.

I have to say, because I do know you well, you have done amazingly well at keeping it

at an understandable level. The number of times I'm studying your kitchen and I'm literally

gawking at you, because I'm just trying it. I was probably doing it on the screen today. I just

have to take the information in and process it. And it's like, yep, okay, I understand what she's

saying. And then you're there on the next thing. But you've explained that so well. Thank you so

much for your time. And I'm sure you're going to be a repeat request very soon. Thank you.

Thank you. Thank you for having me.