Saturated Fat with Dr. Ben Bikman

Summary

In this episode of the Metabolic Classroom, Professor Ben Bikman clarifies misconceptions about saturated fat's role in insulin resistance. He challenges the narrative that saturated fat from meat causes insulin resistance, explaining the physiological process of fat digestion and its impact on the body. Bikman cites studies that show high saturated fat intake in a low-carb environment doesn't increase blood saturated fat levels or insulin resistance, suggesting that high carbohydrate intake might be more detrimental. The lecture aims to provide a nuanced understanding of saturated fats, their metabolism, and their actual effects on health.

Takeaways

• 🧬 Professor Ben Bickman, a biomedical scientist and cell biology professor, discusses the misconceptions around saturated fat and its effects on insulin resistance.
• 📚 Bickman's own research, published in 2011, showed that saturated fats uniquely activate the TLR4 receptor, leading to inflammation and the production of ceramides, which are linked to insulin resistance.
• 🔬 The study conducted by infusing lipids directly into the bloodstream or treating cells with fats, which is not the same as consuming saturated fat through diet.
• 🍽 The process of fat digestion involves bile salts, lipase enzymes, and the formation of chylomicrons, which transport fats into the lymphatic system and eventually into the bloodstream.
• 📉 A 2014 study by Volek et al. found that increasing dietary saturated fat intake did not lead to an increase in plasma saturated fat levels, challenging the direct link between diet and blood saturated fat.
• 🥗 The DASH diet, known for lowering blood pressure, was found to be effective in a high-fat version, with participants experiencing similar benefits and improved lipid profiles compared to the low-fat version.
• 🧬 A 2020 meta-analysis by Choy et al. showed that ketogenic diets, which are high in saturated fats, improved glycemic control and insulin resistance more than low-fat diets in overweight individuals and those with type 2 diabetes.
• 📊 Despite a decrease in dietary saturated fat intake over the past decades, insulin resistance has been on the rise, suggesting other factors, such as carbohydrate intake, may play a significant role.
• 🍚 High carbohydrate intake, especially refined sugars and starches, can lead to increased liver production of saturated fats through a process called de novo lipogenesis.
• 🚫 Bickman acknowledges that some studies suggest saturated fats may contribute to insulin resistance in the context of a high-calorie, high-carb diet, indicating the importance of diet context.
• 🔄 The overall message is that the relationship between saturated fat, diet, and insulin resistance is more complex than often portrayed, and the total dietary context is crucial.

Q & A

Who is the host of the 'Metabolic Classroom' episode discussed in the transcript?

The host of the 'Metabolic Classroom' episode is Professor Ben Bikman, a biomedical scientist and professor of Cell Biology.

What is the main topic of discussion in this episode?

The main topic of discussion in this episode is the impact of saturated fat on insulin resistance and the common misconceptions surrounding it.

What did Professor Bikman's 2011 study published in the Journal of Clinical Investigation focus on?

Professor Bikman's 2011 study focused on the role of the toll-like receptor 4 (TLR4) and how its activation by saturated fats can lead to inflammation and the synthesis of ceramides, which are known to induce insulin resistance.

What is the role of ceramides in the context of insulin resistance as discussed in the script?

Ceramides play a significant role in inducing insulin resistance by blocking the cascade of events that occur downstream of insulin binding to its receptors.

How does the body process dietary fats according to the script?

The body processes dietary fats primarily in the small intestine, where bile salts emulsify the fats, lipases break down triglycerides into fatty acids and glycerol, and the fatty acids are re-esterified and packaged into chylomicrons, which enter the lymphatic system and eventually the bloodstream.

What was the finding of the study by Volk et al. published in PLOS ONE in 2014 regarding the effect of dietary saturated fat on plasma saturated fat levels?

The study by Volk et al. found that even with a stepwise increase in dietary saturated fat, there was no corresponding stepwise increase in plasma saturated fat levels, suggesting that the body adapts to handle increased dietary saturated fat without significantly increasing circulating saturated fats.

What is the DASH diet and what does it entail?

The DASH (Dietary Approaches to Stop Hypertension) diet is a diet designed to lower blood pressure. It is characterized by low fat, low salt, and reduced consumption of refined sugars and starches.

According to the meta-analysis by Choy et al. in 2020, what was the effect of a ketogenic diet on insulin resistance in type 2 diabetic patients?

The meta-analysis by Choy et al. found that a ketogenic diet, which is typically higher in saturated fats, resulted in significant improvements in both glycemic control and insulin resistance compared to a low-fat diet in type 2 diabetic patients.

How does high carbohydrate intake, particularly of refined sugars and starches, potentially contribute to increased plasma saturated fats?

High carbohydrate intake can lead to increased plasma saturated fats through a process called de novo lipogenesis, where the liver converts excess glucose into saturated fats, which are then released into the bloodstream.

What was the conclusion of the study by Lucin et al. in 2018 regarding the combination of high carbohydrate and high saturated fat intake on insulin resistance?

The study by Lucin et al. concluded that when combining a high carbohydrate diet with overconsumption of saturated fats, it led to worse insulin resistance compared to a high carbohydrate diet with overconsumption of unsaturated fats.

What is the potential impact of high fat and high carbohydrate diets on metabolic health as suggested by the script?

The script suggests that diets high in both fat and carbohydrates can be particularly detrimental to metabolic health, as the combination of high insulin levels stimulated by carbohydrates and the presence of a lot of fat can lead to increased fat storage and potentially worsen insulin resistance.

Outlines

00:00

🧬 The Impact of Saturated Fat on Insulin Resistance

Professor Ben Bickman, a biomedical scientist and cell biology professor, introduces the topic of saturated fat's impact on insulin resistance. He critiques common misconceptions and highlights his own authoritative research in the field. His 2011 study published in the Journal of Clinical Investigation revealed that saturated fats uniquely activate the TLR4 receptor, leading to increased inflammation and ceramide synthesis, which is a key mediator of insulin resistance. The study's findings have been misinterpreted by anti-saturated fat advocates, despite the fact that direct cell incubation or intravenous infusion of fats does not accurately represent dietary fat intake.

05:03

🔬 Challenging the Saturated Fat Paradigm

The video script delves into the methodology and subsequent reflection on Professor Bickman's experiments, which involved direct infusion of lipids into the bloodstream and incubating cells with fats. He acknowledges the limitations of these methods as they do not mimic physiological dietary fat intake. The script transitions into a primer on fat digestion, explaining the process from consumption to absorption, and setting the stage for a deeper discussion on how dietary saturated fat affects insulin resistance.

10:04

📊 The Disparity Between Dietary Saturated Fat and Blood Levels

The script discusses a 2014 study by Vulk et al., which investigated the relationship between dietary saturated fat intake and blood saturated fat levels. Contrary to expectations, the study found no correlation between increased dietary saturated fat and elevated blood saturated fat levels, suggesting that the body adapts to higher intake by metabolizing the fats differently, potentially through burning or desaturation.

15:04

🍽 The DASH Diet and Saturated Fat Reevaluation

The discussion shifts to the DASH diet, traditionally viewed as low in fat and salt to reduce hypertension. However, a 2016 study by Chiu challenges this view by comparing the effects of a high-fat version of the DASH diet with the standard version. Surprisingly, the high-fat version, which included more saturated fat, resulted in similar blood pressure reductions and better lipid profiles, contradicting the belief that low-fat diets are superior for heart health.

20:06

🧪 Meta-Analysis on Ketogenic Diets and Insulin Resistance

A meta-analysis by Choy et al. in 2020 is highlighted, which aggregated data from 14 randomized trials on the effects of ketogenic diets, typically high in saturated fat, on metabolic outcomes in overweight individuals with or without type 2 diabetes. The analysis showed that ketogenic diets led to significant improvements in glycemic control and insulin resistance compared to low-fat diets, directly refuting the notion that high saturated fat intake exacerbates insulin resistance.

25:09

📉 Trends in Saturated Fat Consumption and Insulin Resistance

The script contrasts the decline in saturated fat consumption over the past 50 years with the concurrent rise in insulin resistance, suggesting that other factors, such as carbohydrate intake, may be more influential. It introduces the concept of de novo lipogenesis, where the liver converts excess carbohydrates into saturated fats, potentially contributing to insulin resistance more than dietary saturated fats themselves.

🚫 The Risks of High Caloric Intake of Saturated Fats

In conclusion, the script acknowledges that while dietary saturated fats do not appear to be the primary culprit in increasing plasma saturated fats or causing insulin resistance, especially in a low-carb context, there are studies indicating potential issues with high caloric intake of saturated fats in the context of a high-carb diet. It emphasizes the importance of considering overall dietary patterns and metabolic health when evaluating the role of saturated fats in one's diet.

Keywords

💡Saturated Fat

Saturated fat refers to fats in which the fat molecules contain only single bonds between carbon atoms, leading to a high level of saturation. In the video, it is discussed as a potential factor in insulin resistance, but the narrative challenges the common belief that it is detrimental, especially in the context of a low-carb diet.

💡Insulin Resistance

Insulin resistance is a condition where the body's cells do not respond properly to the hormone insulin, leading to high blood sugar levels. The video explores the relationship between saturated fat and insulin resistance, questioning the notion that saturated fat consumption directly causes this condition.

💡Toll-Like Receptor 4 (TLR4)

TLR4 is a protein receptor found on the surface of cells that plays a role in the immune system. The script discusses how activation of TLR4 by saturated fats can lead to inflammation and the production of ceramides, which are implicated in insulin resistance.

💡Ceramides

Ceramides are a type of lipid within the sphingolipid family. The video explains that ceramides are synthesized in response to TLR4 activation and are a main mediator of insulin resistance by blocking insulin signaling pathways.

💡Metabolic Research

Metabolic research encompasses the study of metabolic processes in the body, including how substances like fats and sugars are processed and utilized. The video's host, Professor Ben Bikman, has a background in this field, which informs the discussion on the effects of saturated fat on metabolism.

💡Ketogenic Diet

A ketogenic diet is a high-fat, low-carbohydrate diet that aims to shift the body's metabolism from primarily burning carbohydrates to burning fats. The video cites studies showing that ketogenic diets can improve insulin resistance and other metabolic outcomes.

💡De novo Lipogenesis

De novo lipogenesis is the process by which the liver synthesizes new fat from excess carbohydrates, particularly from glucose. The script discusses how high carbohydrate intake can lead to increased saturated fat production and release into the bloodstream.

💡VLDL (Very-Low-Density Lipoprotein)

VLDL is a type of lipoprotein that carries endogenous triglycerides from the liver to other body tissues. The video mentions VLDL in the context of transporting newly synthesized saturated fats from the liver.

💡DASH Diet

The DASH (Dietary Approaches to Stop Hypertension) diet is a dietary pattern recommended to prevent and treat hypertension. The video discusses a study comparing the traditional DASH diet with a high-fat version, finding similar or better health benefits with the high-fat approach.

💡Meta-Analysis

A meta-analysis is a statistical method that combines the results of multiple scientific studies to draw more general conclusions. The video cites a meta-analysis that found ketogenic diets improved insulin resistance and glycemic control compared to low-fat diets.

Highlights

Professor Ben Bickman introduces the topic of saturated fat and its effects on insulin resistance, addressing misconceptions and bad information prevalent in the field.

Bickman's authority on the subject is established through his extensive research and publications in high-impact biomedical journals.

A 2011 study by Bickman on the role of TLR4 receptor activation and its link to inflammation and ceramide synthesis, potentially leading to insulin resistance.

Saturated fats uniquely stimulate TLR4, which may result in ceramide accumulation and contribute to insulin resistance.

Bickman reflects on his own journey and the evolution of his understanding of saturated fats' role in metabolism.

The methodological critique of direct lipid infusion or cell incubation versus the physiological process of dietary fat digestion and absorption.

A detailed explanation of fat digestion in the small intestine, including emulsification and the role of bile salts and lipases.

The process of chylomicron formation and its role in transporting dietary fats into the lymphatic system and eventually the bloodstream.

Volk et al.'s 2014 study showing no correlation between dietary saturated fat intake and plasma saturated fat levels.

The DASH diet's multifaceted approach to reducing hypertension, with a focus on low refined carbs and sugars, not just low fat and salt.

A study by Chiu in 2016 comparing the effects of a high-fat DASH diet versus a standard DASH diet, finding similar blood pressure reduction and improved lipid profiles with the high-fat version.

A 2020 meta-analysis by Choy et al. demonstrating the benefits of ketogenic diets on glycemic control and insulin resistance in overweight and type 2 diabetic patients.

Trends in dietary saturated fat consumption over the past 50 years in the US, showing a decrease that contrasts with the rise in insulin resistance.

The role of carbohydrates, particularly refined sugars and starches, in stimulating de novo lipogenesis and potentially increasing plasma saturated fats.

Studies by Acheson et al. and Sevastianova et al. highlighting the link between high carbohydrate intake and increased liver saturated fat production.

Bickman's concluding thoughts on the nuanced relationship between dietary saturated fat, carbohydrate intake, and insulin resistance, and the importance of context in understanding metabolic effects.

Transcripts

hello and welcome to this week's episode

of the metabolic classroom I am

Professor Ben bickman a biomedical

scientist and professor of Cell

Biology hopefully that means I know what

I'm talking about thanks for joining me

today this is a topic that I've been

looking forward to discussing in part

because there is so much silly thinking

and bad information when it comes to

saturated fat and particular its effects

on insulin resistance this is something

you've likely heard many influencers

speak about especially those who

Advocate plant-based diets that uh

encourage you to avoid meat often they

will cite studies they will say well

saturated fat the saturated fat from

meat is causing insulin resistance so

that's why you need to avoid it I have

been looking forward to this topic in

part because it's actually one of the

areas that I am U most Authority on or

most authoritative on having worked in

this field quite substantially through

my not only my PhD dissertation but also

my postdoctoral fellowship that where I

focused on Metabolic Research for a few

years working um with Duke Medical

School all right so with that as the

introduction let's just Dive Right In in

fact let's start with some of my own

work interestingly enough it's some of

this work that is cited by the anti-

saturated fat Advocates and so in 2011 I

authored a manuscript that was published

in a very good Journal called the

journal of clinical investigation it's

one of the higher impact factor

biomedical journals in the field so PR

very well respected and very difficult

to get a paper accepted to publish in

that journal this study focused on the

on the role of a particular receptor

that is found on a on the cell so on the

surface of cells among the many many

types of receptors or doorways for

various molecules to come and knock on

there is something called the tlr4 or

the toll like receptor

4 what we found in this paper published

in 2011 is that when tlr4 was activated

it would induce a series of events and

steps that would increase inflammation

and that this process would result in

the synthesis and

acrel of a particular type of lipid

called ceramides ceramides are the main

molecule within a family of lipid or fat

called sphingo lipids named after the

enigmatic Sphinx because for so many

decades no one knew what these lipids

did uh now part of what I helped with

was identifying the fact that these

lipids do have a metabolic role to play

specifically

inducing insulin resistance so ceramides

are a main mediator of insulin

resistance and they do so by blocking

the the the Cascade or the series of

events um that is Downstream of insulin

binding its receptors so when insulin

comes and binds its receptor it would

elicit a series of second messenger

events we call it in cell biology so one

thing leading to another leading to

another leading to another so I use word

the I used the word Cascade moment ago

and that's a pretty good word you can

imagine this Cascade this waterfall of

events occurring ceramides block that up

it basically is damning the Cascade up

ultimately causing the cell to become

insulin resistant now having said all of

this what is the role of saturated fat

here well we identified in this study

through a series of

experiments that saturated fats uniquely

among the family of all fats saturated

fats uniquely stimulate ated

tlr4 thereby resulting in the

accumulation of ceramides and the

overall antagonism or the insulin

resistance um that that we're interested

in for the sake of this discussion and

was the focus of that manuscript all

right so let me say that again so

saturated fats were found to be a liend

or a binder or an activator of tlr4 and

when tlr4 was activated it would then

create ceramides or induce the synthesis

of ceramides and the accumulation of

ceramides and then ceramides would block

the insulin Cascade causing insulin

resistance so that was all accurate it's

all true and it's often cited my own

research by the anti- saturated fat

Army now let's take a step out of this

work and I had to do this myself as I'm

telling you this there's also this sort

of undercurrent of my own Journey

because I got done that work with this

uh strong conviction that saturated fats

really are a problem this was in we did

this work over actually a couple years

it was 2008 2009 when we were doing this

work you know it takes so long to get

stuff published and I really was doing

this work thinking boy saturated fats

are such a problem now how did we

actually conduct these experiments this

is part of the evolution that I had to

go through myself um which I was happy

to do because it forced me to change to

look at the experimental model and by

looking at the experimental model more

correctly and more lucidly you're able

to challenge the Paradigm so the

Paradigm here being saturated fat causes

insulin resistance via inflammation and

tlr4 and ceramides but how did we

actually show that well we did it by

directly infusing lipids right into the

bloodstream and by directly incubating

or treating or bathing cells with these

fats so it was a direct model we were

either directly bathing the cells with

the fats or directly infusing it

intravenously can you see the

problem is this a physiological model

these experiments that I'm very proud of

I'm very happy with the work we did

although I very much regret how

misinterpreted they've been and in

hindsight wish perhaps that we would

have clarified some of this in the

discussion of the manuscript R but is

infusing a fat intravenously or bathing

cells in a Cell culture the same thing

with saturated fats is that the same

thing as eating saturated fat of course

it's not of course not let's in fact

just by way of a brief physiological

primer let's go through the process of

getting fat from the diet into your

blood and then and then use that as a

segue to then dive into the studies that

actually explore

the role of dietary saturated fat on

insulin

resistance all right so much of the

action when it comes to Fat

digestion practically all of it is the

small intestine yes we've been chewing

the food yes we've been churning the

food around in the stomach but there's

nothing really happening until we get to

the small intestine at that point the

fat is interacting with bile salt from

the small from the from the liver that

have that has then been stored in the

gall bladder so the fatness coming down

the gallbladder contracts thereby

reducing the risk of gallstones moving

the bile into the small intestine and

then the bile will separate the fat all

out you know fat wants to Clump together

and so this the bile will pull it apart

into small little blobs that's a process

called emulsification you've heard of

emulsifiers or emulsification before

that's what's happening there with the

bile salts now the molecules are small

enough to be acted on by an enzyme and a

series of enzymes called lipase so the

Lipa starts snipping off the individual

fatty acids of triglycerides so here's a

triglyceride my Knuckles are the

glycerol backbone and then these three

fingers are the individual fatty acids

so the lipase comes in and we'll snip

one of them off all right there's one

fatty acid now that's just floating then

it'll come in and snip the other one off

and then we're left with a what's called

a monoglycerol or monoglyceride where

you have one fatty acid bound to the

glycerol backbone and then these are

small enough um to get moved in to the

intestinal wall so now they can pull in

and get absorbed by the epithelial cells

or the cells that are lining the

intestine once they get pulled in they

actually get reesterified that's the

technical term to say that they all just

kind of get lumped back together so

let's go back to me awkwardly acting

this out here here's the fatty acid

bound to the glycerol backbone but

you'll recall there's an empty spot for

two more so reesterification is taking

this fatty acid and boom popping it back

on taking this other fatty acid and boom

popping it back on so now we have a

triglyceride that's been reformed and

now within the wall of the intestine

with all of these reformed triglycerides

it will package them all up with the

lipids with these the the fats we've

eaten the triglycerides other lipids

like cholesterol and phospholipids and

some proteins and lump them together in

a bigger molecule called a kyom micron

now the kyom Micron is big big enough

that it's not easily moving into the

blood through into a capillary into the

bloodstream and so it doesn't go into

the bloodstream it goes into the lymph

system and so the lymph system is

carrying these kyom microns and then it

deposits them into the blood through

this area up in the thoracic cavity

that's where lymph meets back up with

blood so lymph comes from blood um

that's a topic for another time but

flowing slowly through the body

ultimately getting its way back to the

blood and so the kyom microns now these

big fatty protein complexes come back

into the blood then now the journey is

not over yet and remember we're talking

about the digestion of fats because the

idea is that if you eat saturated fats

you'll get insulin resistance so the

kyom Micron now is in the blood and now

it can be acted on so now we'll have

lipoprotein lipase a different version

of the lipase that was in the the guts

that was cutting off the fatty acids we

have now a different version through the

blood vessels through the capillaries

and they're cutting off fatty acids and

now absorbing them into the cell and so

the free fatty acids will be pulled in

but at that point it's possible that

they can bind any kind of receptors like

tlr4 all right and then we have the kyom

Micron Remnant having dropped off a lot

of fat throughout the body it can go to

the liver and get reprodu processed okay

now that is the brief as I said primer

on the digestion of fat so it's a little

bit of gastrointestinal physiology for

you so does eating fat elicit the same

response as directly infusing saturated

fat via intravenous or directly treating

cells bathing them with saturated fat so

let's in order to look at that I just

want to highlight a few

studies okay the first study is one by

vul v o k vulk at all and it was

published in 2014 in a journal plus one

and when I say plus I'm not saying plus

like a plus sign or addition but p s P1

2014 vul at all this is probably the

single best study that looks at the idea

of saturated fat in the diet and then

explores that effect in the plasma so

let me just before getting into that

study let me just emphasize what I'm why

I'm discussing this this

way the the idea so I've shown you

evidence that if a cell directly gets

saturated fat it is capable of causing

insulin resistance uniquely more so than

other fats are via

tlr4 as I explained at the beginning of

the

conversation now then does that mean

that eating saturated fat will increase

the amount of saturated fats in my blood

that is the question that we want to

know does eating more saturated fat

increase the saturated fats that are

actually being circulated around because

if so that could explain a mechanism so

this study by vadol was fascinating

because it actually took people through

a stepwise increase in saturated fats

and so it had this this very fascinating

experimental model where the amount of

carbohydrates and the amount of

saturated fats was being changed and so

it would go in the stepwise direction up

or down down so and and fantastic

changes I mean it would be multiples

more saturated fat in at the end or the

beginning of the stepwise change and you

would think if dietary saturated fat

directly connects to or directly leads

to increased plasma saturated fat well

then as they stepwise increase the

saturated fat you should see a stepwise

increase if they stepwise increase the

dietary saturated fat to be more precise

you should see a stepwise increase in

plasma or blood circulating saturated

fats and you didn't it was totally a

flat line even though they were eating

two or three times more saturated fat

which is substantial it did not change

their plasma saturated fat levels at all

they stayed they they actually went down

by about half with the onset of this

ketogenic diet and then it stayed down

that low even as saturated fat

changed so the stepwise changes the

study suggests that the body really has

an adaptation that even as you're eating

more the body is clearly handling it um

where you're not seeing these saturated

fats hit the bloodstream like you'd

expect it could be just that they're

getting burned it could be that they are

getting desaturated that happens very

readily where you take saturated fats

and you actually desaturate and

elongate so it's possible for the

saturated fats to turn into actually to

turn into oleic acid which is the main

fat in olive oil and then get stored in

in fat cells or something which is fine

all longchain fats are capable of being

stored so that's not inherently a

problem um remember because the main

thing we're looking at here is the role

or the degree to which dietary saturated

fat can increase plasma saturated fat

because if we can show that then there's

a mechanism to explain that saturated

fats could cause insulin resistance but

I just highlighted the study and I

encourage you to look it up vulk at all

in

P1 Plus plus one in 2014 where it looks

at the stepwise change in dietary

saturated fat and it had no effect at

changing plasma or blood saturated fat

levels now with that idea in mind I just

want to highlight uh it's a little bit

of a tangent but it's just such a kind

of funny study that I can't help but

show it by now you've likely heard of

something called the DASH diet Dash d

stands for dietary approach to stop

hypertension I think is what the a is

dietary approach or approaches to stop

hypertension and they

identified you know a diet that was

capable of slightly reducing blood

pressure and and that was relevant

because if you reduce blood pressure you

can reduce the risk of heart attack and

heart disease in

general the diet the DASH diet is famous

then all you'll ever hear about is that

it is low fat and low salt that's what

people want to brag about and use it as

evidence the problem is it is multia

faceted there are multiple aspects and

dietary changes that go into the DASH

diet including reduced consumption of

refined sugars and starches so it's

basically something like fact that

sounds like a somewhat miserable diet

which is probably why so few people

adhere to it it's very low in salt it's

very low in refined starches and sugars

and it's very low fat well I can get

behind one of those things I very much

am an advocate of reducing dietary

starches and sugars or refined starches

and sugars but that was all a part of it

there's many factors but the only thing

you ever hear about is the low salt and

the low fat well what if it's the low

carb that's actually benefiting the

people here as modest as the benefit is

now to with this study in mind the DASH

diet so chew at all Chiu in 2016

published a paper that actually looked

at it compared the typical DASH diet

which is low fat low refined carb low

salt with a really high fat version so

very high saturated fat that people were

encouraged to eat full fat Dairy

liberally so they were eating

substantially multiple times more

saturated fat than the other group and

not only did they enjoy the same

reduction in blood pressure that the

standard DASH diet did and remember

that's the main reason people do it at

all so not only did they enjoy the exact

same reduction in blood pressure but

they actually had better lipid

improvements their triglycerides went

down more and their vldl went down more

while the LDL stayed the same across the

two groups that is really impactful by

lowering triglycerides and lowering vldl

those variables are much more predictive

of heart attack risk than LDL is in fact

a paper was just published in the past

few weeks at the time of me recording

this in May

2024 that looked at varying blood lipid

categories in people with higher or

lower risk of having a heart attack and

the people with the lower the LDL but

the higher LDL had the lowest risk of

having a heart attack I'll say that

again people with the higher LDL but the

lower vldl had the lowest risk of a

heart attack that's exactly the lipid

profile we're seeing changed in the high

fat version of the famous and much

beloved I would say irrationally so DASH

diet all right now let's just go with

this a little further by highlighting um

so in general by highlighting a

metaanalysis that was published in 2020

by Choy at all Choy at all CI Choy at

all 2020 published in the journal

nutrients they did a a metaanalysis of

20 randomized studies looking at people

who were overweight with or without type

2 diabetes and the use of ketogenic

diets on a variety of metabolic outcomes

so again this is a meta analys which a

meta analysis which is attempting to

come up with a a singular conclusion

based on the combined outcomes of every

published in this case clinical study so

very very very relevant now just to

reiterate this is of course ketogenic

diet and ketogenic diets by their nature

are higher fat including often much

higher ins saturated fat and indeed

looking through sorry I said 20 randomiz

studies it was 14 randomized trials

looking at comparing it to low-fat diets

or high fat ketogenic diets and they

found that for these patients that are

diabetic so that means they're very

insulin resistant these are type two

diabetic the ketogenic diet resulted in

significant improvements in both

glycemic control and insulin resistance

compared to those on the lowfat diet so

they found that the ketogenic diet

despite eating multiple times higher

levels of saturated fat than the lowfat

diet had better improvements in insulin

resistance and moreover they had

substantial improvements and their blood

lipids but you can look at the other

details in that study but it directly

refutes the idea in a

metaanalysis that that a highs saturated

fat diet is going to cause insulin

resistance it directly they found the

opposite that in these studies where the

saturated fat consumption was high but

with carbohydrate consumption being low

there was a significant improvement over

better than the lowfat diet so that is a

direct reputation of the plant-based

Advocates who are calling for everyone

to avoid saturated fat this metaanalysis

directly refutes that so very high

impact I hope that leaves somewhat of an

impression on you now throughout this

conversation there's been one component

missing so remember I started the

conversation this little lecture um by

describing to you how saturated fats are

capable of causing insulin resistance

and now we've challenged the idea that

dietary saturated fat is contributing to

that and even if we zoom out to the

30,000 foot View and look at just Global

and or certainly within the US dietary

Trends over the past 50 years or so the

actual amount of saturated fat we've

been eating has been going down steadily

it kind of came up a little bit from the

1930s up through the 197 60s or 70s and

then it came down um and yet over this

same time period the amount of insulin

resistance globally certainly within the

US has just been steady going up up and

up and up I mean

substantially just at a surface glance

at this really high level at a

population level we can see something

doesn't work here now this is of course

correlational and I'm very Mindful and

appreciative of the weaknesses in this

but even if we use the terribly flawed

view of a correlational study we can see

that there's just nothing to this it

doesn't work this dog don't hunt as they

may say in some parts of the US again

saturated fat consumption has been going

down for decades and yet or at the very

least in the recent decade it's leveled

out but during this whole time insulin

resistance has been skyrocketing so

there's clearly another variable here

and among the many possible variables

let's just focus on

carbohydrates but even still in the

looking at them in the context of

saturated fats now you're thinking

perhaps what on Earth could dietary

carbohydrate have to do with plasma

saturated fat levels

we're not eating you could eat you could

be eating carbohydrates that don't have

a speck of saturated fat in them how

could that possibly increase saturated

fat well it can and of course insulin is

very relevant to this so um we know that

high carbohydrate intake particularly

refined sugars and starches because of

the increase in insulin is capable of

activating a process in the liver called

denovo lipogenesis

some of you with a little bit of kind of

Latin background you're hearing some of

the words here where you're hearing that

it is the synthesis of new fat so the

liver is capable of taking carbons

including those from glucose and turning

them into saturated fats and then

packaging up those saturated fats and

releasing them into the body being

transported on vldl so vldl is going to

be the vehicle that is transporting

these fats and the fat that the liver is

making is always is going to be a

saturated fat called palmitic acid or

palmitate so there are a couple studies

that I want to highlight the first one

is Acheson AC o n Atcheson at all 1988

this is old that's the year that the

Winter Olympics were in Calgary Canada I

remember going a banner year all right

um this study found that when a person

ate sufficient carbohydrates that the

liver glycogen got filled up but then

continued to eat carbohydrates which is

very easy to do most people are doing

this all the time most people never um

are restricting carbohydrates or fasting

enough to even have their liver drop

down even close to being zero so we're

always almost kind of filled up with our

liver so the study found atesin at all

1988 that if someone ate sufficient

carbs that the liver was filled and

continue to eat carbs which is virtually

every person on the planet that the

liver is capable of converting the

excess into fats increasing plasma

saturated fats all just because of the

the consumption of

carbohydrates another study is is

sevastova castanova I'm gonna say that

again sast

siast

sevastianova for a guy who speaks

Russian like me I should be able to get

through that sevastianova is the name s

v s TI a n o v a

sasona uh at all

2012 what this was a short-term study

finding almost the exact same thing that

the overfeeding of simple sugars

increased liver fat but also liver fatty

acid saturated fat

production so this directly challenges

the idea that s dietary saturated fats

are the problem in increasing body or

plasma saturated fats um this is

suggesting that you can find that effect

increased plasma saturated fat without

even eating saturated fats that just in

overindulging on carbs can do it and of

course the more refined the easier it is

for all of this to

happen all right now my concluding

thought having challenged the idea that

dietary saturated fat is the problem in

increasing plasma saturated fats which

can likely contribute to insulin

resistance I mean the plasma saturated

fats and then introducing this other

idea that the excessive consumption of

refined starches and sugars could

increase plasma saturated fats thereby

contributing to insulin

resistance but

I as a scientist have to admit that

there is some human studies that

challenge that suggest saturated fats

may be a problem in the context of a

hypercaloric high carb diet all right

those are two very very specific caveats

here that need to be mentioned so there

was a study published in the diabetes

journal and

the um lead author name last name is

Lucin l u k k o Neen in Diabetes Care

this was published in 2018 so not too

long ago and in this study again they

had a high carb diet but then had them

overeat so really getting hyper chloric

with eating saturated fats and

monounsaturated fats or just unsaturated

fats in general and they found that the

group that was eating hyper chloric high

carb sat High saturated fat had worse

insulin resistance then the group that

was eating high carb high fat with the

unsaturated group that that group didn't

have as bad as of insulin resistance is

the high saturated fat group so for the

sake of just blunt honesty if you are

eating a very high carb diet and you're

going to indulge in a lot of

fat then saturated fats might might be a

problem now you've heard me before speak

about the problem with high fat high

carb those should never be mixed that is

a particularly delicious and

particularly fattening mix where you

have the high carb stimulating insulin

which is going to signal to the fat

cells to store energy and then you have

a lot of fat for those fat cells to then

store it makes it all the easier for the

fat cells to get bigger so high fat high

carb is a particularly vicious metabolic

mix and should be generally avoided this

study suggests that if that high carb is

mixed with high saturated fat it's a

little worse even with insulin

resistance than high fat and high uh

than high carb with high unsaturated

fat but again as highlighted by that

metaanalysis if the high saturated fat

is coming in an environment where the

carbohydrate consumption is low then

there's no such concern and that

saturated fat is just going to be

burned all right that's the end

hopefully you feel like you are much

more educated with regards to the

intricacies the nuances of sat saturated

fat now you know the origins of some of

the arguments against saturated fat in

that there are studies that have shown

direct cell incubations or direct

intravenous infusions of saturated fat

is capable of causing insulin resistance

however that is not the same as eating

saturated fat particularly in the

context of a low carb

diet thanks for tuning in