Cardiologist (Dr. Nadir Ali) Explains LDL Bad Cholesterol Spike With Keto – Dr.Berg ｜ DrEricBergDC

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hey everyone welcome back and today we

have a real special guest dr. nadir Ali

is here and he is a keto friendly

cardiologist from Houston Texas so

welcome welcome to this channel can you

hear me I I can hear you well okay great

thank you

I am honored to be here on this channel

and I’m honored to be a part of your

program and as I told you I have had a

long-held admiration for you many of my

patients are avid fans of yours and your

Friday podcast so they look forward to

it they come and give me all kinds of

feedback I have learned how to

communicate with my patients based on

what you do to some degree Wow Wow thank

you that’s awesome well I’m really a

pleasure to meet you meet you in person

or actually sort of through the line

internet lines here you know just for

everyone’s knowledge you’re gonna be one

of the main speakers at our next Quito

summit coming up in August at the end of

August August 31st and September 1st

it’s uh I think it’s Labor Day weekend

and we’re gonna have a blast so I’m

really excited to have you come out and

speak you know you you bring to the

table something very unique I mean you

know one of the big things right now hot

topics is this cholesterol thing and the

LDL and people are concerned and you see

these things in the in the news where oh

don’t to key though it’s gonna raise

your cholesterol and you’re gonna die

have a heart attack

yeah I yeah and so I’m coming just from

your field I mean I guess that’s what

what you’re taught right in school like

I guess the whole cholesterol dogma has

been pushed so much it’s so ingrained in

us that it’s sometimes it’s hard to look

at the actual data what’s your what’s

your thought on that

that’s like delving right into it and

I’m glad you’re doing it that way

because we don’t waste time in

unnecessary stuff exactly but I’ve been

practicing for almost 30 years and as a

cardiologist and the dogma that has been

taught to us is that low cholesterol low

LDL is one of the best things for you to

do and unfortunately if you compile all

information about optimal human

nutrition about human brain size about

what we need to eat and how we need to

behave to reduce our LDL cholesterol C

Nevitt ibly it’s going to lead to very

poor health it’s gonna lead to obesity

insulin resistance diabetes hypertension

all the chronic diseases that are going

to reduce your quality of life that’s

gonna make you die earlier and so I was

kind of surprised that there’s such a

huge paradox between LDL cholesterol and

every other biomarker of health you can

take anyone you know they go in opposite

direction if you want to improve your

insulin resistance your LDL is going to

go up if you want to reduce your weight

your LDL is going to go up interesting

interesting so I started thinking about

this as a paradox but then when you put

everything together you understand that

that’s how our body is probably designed

to behave and so I go out there now for

the last five years it took me time to

understand why LDL goes up on a low-carb

diet

and it took me time to understand that

that is not necessarily bad and in some

ways having higher LDL cholesterol with

very good other biomarkers might be

something to celebrate not my own and I

could elaborate on some of that but I

wanted more interaction I wondered you

to kind of chime in and say hey I want

to lead this podcast in this direction

yeah exactly because I wanted to there’s

some there’s some things that I’m

interested in personally that I would

like to know your viewpoint on you know

cholesterol LDL this is called bad

cholesterol but really it’s a it’s a

cargo ship

it’s a transport ship and it delivers

cholesterol we need cholesterol I’m

hoping that most people know that our

body makes cholesterol but what I’m

interested to just start off with

talking about is your take on LDL

actually carries I think all of the fat

soluble vitamins but I’m an a de K k1

and k2 have you seen any data on that

especially even vitamin e to as an

antioxidant I think it does the data on

this is kind of not at least I’m not

aware of some very good data on that

okay that vitamin D does have its own

carrier protein and that may be the LDL

is a secondary mechanism for carrying

vitamin D around but I guess one of the

other major functions of LDL would be to

carry Co Q 10 because I’m not sure all

the muscle cells are capable of making

the Co Q 10 that they need for

mitochondrial function and but you’re

right LDL is a carrier molecule not just

for triglycerides and cholesterol per se

but for many antioxidants fat soluble

vitamins

Co Q 10 yeah and I do know that you have

all these phospholipids as well that our

I think it’s a that make up the cell

wall and so we have a transport system

of cholesterol cholesterol doesn’t just

float around by itself it needs to be

transported and I think that if you

could just touch a little bit on the the

necessary function of LDL that’s one

area I wanted to want to touch on and

then also I want you to maybe mention a

little bit about statins and what the

problem with statins that you run into

I’m sure that you know it’s a hot topic

with in your field I mean I’m a lot of

cardiologists prescribe them right so

let’s first talk about cholesterol in

general and then move on to allyl

cholesterol in particular cholesterol in

general is an extremely important

molecule for life there is no life on

earth without cholesterol every living

cell has cholesterol if you go back to

some of the earliest parts of evolution

when we started out as single-celled

beings in this world those single cells

also had cholesterol really if you look

at cholesterol it is an integral part of

every cell membrane the cell membrane

gets its structural integrity the

fluidity so that it acts as a barrier

because cholesterol is connecting the

phospholipids in such a way that it is

providing those functions

the second major way to think about

cholesterol is to look at brain function

because in our brain there are these

cholesterol rafts and these rafts are

locations where neurotransmitters set so

the structural integrity of the

neurotransmitter receptors

is because of these cholesterol rafts

and if you deprive the brain of

cholesterol the integrity of these

neurotransmitter receptors is affected

so there is a lot of data that comes out

and says that there are certain statins

that cross the blood-brain barrier can

have significant cognitive dysfunction -

and in fact cholesterol is so important

for the brain that it does not delegate

the responsibility to any other organ to

make cholesterol it makes its own Wow

and I often joke that I would not be

able to deal with the stress of being a

cardiologist or giving this podcast if

it were not for cholesterol because the

LDL molecule is supplying cholesterol as

raw material to my adrenal gland so that

it can make the stress hormone which is

called cortisone and and that’s an

absolutely amazing fact that many of the

hormones the backbone of that is a

cholesterol molecule and the carrier

molecule that is supplying that

cholesterol to make that is the LDL and

I often joke to audiences saying that

hey men look handsome because of LDL

cholesterol I like that and the reason

is is because the LDL is the one that is

supplying testes with cholesterol the

raw material to make testosterone and

similarly women look beautiful because

their ovaries also need cholesterol to

convert cholesterol to estrogens so

these are functions that are sometimes

completely skimmed over when we tried to

knock the LDL down like crazy and say

hey we the lowest is better and it made

no sense to me as a cardiologist because

I’ve been practicing for 30 years and I

have seen people come in having

extensive three vessels heart disease

with blockages everywhere with

cholesterol levels as low as 50 Wow Wow

and I have seen 90 year old women or

older with LDL cholesterol in the mid to

hundreds who I take them to the cardiac

cath lab and I find that they have the

most beautiful blood vessels that you

and I although maybe several decades

younger would be happy to trade those

blood vessels for them

Wow Wow that’s that’s fascinating so

I’ve been a bit of a skeptic all my life

about this cholesterol being a causal

factor in coronary artery disease

because it made no sense and if you

really take the trouble to talk to

patients you would find that they

complain of all kinds of side effects on

cholesterol reducing medicines it’s just

that the medical profession has moved in

such a direction that we rely so much on

information coming in from societies

that we have given up our clinical

acumen we have given up our critical

thinking ability we want to just follow

guidelines we don’t want to do our own

work we don’t listen to patients we

don’t want to be skeptics as a physician

I think it’s highly necessary for us to

be quite skeptical about every

information and use our clinical

intuition when we are taking care of

patients exactly I also was fascinated

that the LDL cholesterol is so involved

in host defense and this is not

something many people talk about because

host defense that means how we protect

against bacteria and viruses is in some

ways mediated by the LDL cholesterol

put out some elegant information from

different studies that I have looked at

in which like for example there is this

fascinating paper which looked at a

mouse lung and they infected the mouse

lung with bacteria and these bacteria

they elaborate a little protein that

goes in as a pilot to investigate and

see if the milieu is suitable to

establish an infection so the bacteria

themselves is smart they won’t go in and

start an infection without checking the

area out first and that marker protein

comes back and gives an information to

the bacteria it’s called quorum sensing

protein and it comes back and says hey

let’s establish infection and I was

surprised to find that in this paper

this elegant work that shows that it is

the LDL cholesterol that is going in

there and neutralizing this protein so

that bacterial infection cannot gain a

foothold Wow fascinating fascinating I

definitely want to get a copy of that so

um it yes it actually has ability to

attack pathogens it also has the ability

to bring antioxidants into a certain

area and dump vitamin E into an

epithelial wall to help protect against

lesions I mean now most the time from my

viewpoint it seems like people go on a

keto program and it lowers the LDL but

then you have people that have a higher

LDL lets us talk about what would be

some of the reasons why someone would

actually cut the carbs down and their

LDL would go up any reason for that yeah

that’s one of my strengths I think that

I’d like to take a little credit that

I’m the first one to point out in a

national audience now as to the

molecular mechanisms why LDL is going up

and and I’m so glad that

you brought that up because this is

something that has bothered me a lot you

know as a cardiologist for the last five

years I have been practicing a low carb

diet myself and recommending it to a lot

of patients and I have been seeing that

as many you know in large majority of

these patients as they lose weight as

their diabetes improves as they come off

diabetic medications as their

triglyceride levels go down as their HDL

level goes up the one troubling finding

that was happening is that the LDL goes

up and it goes up unlike what people

think it goes up almost in everyone it

may go up to a variable degree but it

goes up in everyone so I wanted to

explain why that is happening and in the

final analysis I think this is and

although this is my model and it’s not

being proven in studies yet but I think

that’s what we should do is that when

you are going on a low-carb diet by

design you’re burning fat we have very

limited carbohydrate reserves we run out

of them in a situation in which we stop

eating like intermittent fasting or

going on a fast for several days you’re

gonna run out of carbohydrate reserves

in about six to eight hours and then

your body predominantly becomes fat

burning so it’s burning triglycerides

and it’s there are certain tissues that

cannot directly burn triglycerides so

what it does is that the liver takes the

triglycerides and converts them to

ketones

so the liver is the only organ that has

the enzymatic machinery to make ketones

so it’s taking the triglycerides it

converts the triglycerides to acetyl co

a which then enters the mitochondria and

then the acetyl co it through a series

of enzymatic reaction gets converted to

HMG

Kawai now hmg-coa fascinatingly is a

branch point it’s the same raw material

that cholesterol uses to make

cholesterol in the body that means

hmg-coa can go on and make cholesterol

and hmg-coa can also get converted to

ketones that’s right

interesting so if by design you are

doing better oxidation of fat it just

means that you’re burning fat if you’re

burning fat you are making a lot of

ketones and if you’re making a lot of

ketones by design you’re going to make a

lot of cholesterol in the liver and I’m

not just basing this on hypotheses there

are a lot of animal studies that are

human studies that give you indirect

evidence that this is what is happening

and if you think it’s right I want to

take you through a few of these yeah

yeah I think you know it’s it’s it makes

total sense because ya could go split

off this way and make ketones or

cholesterol so I do remember that

chemistry so like wow I never actually

considered that viewpoint but that that

makes a lot of sense and I think the

this in this day and age the reason it’s

important to collaborate is because a

biochemist is not gonna completely look

at that point and say hey I want to

think about it that way right neither is

a nutritionist and not as a cardiologist

along because they don’t understand the

details of the biochemical steps in the

liver but when you put all of these

people together in a podcast like yours

or at a local conference it starts

gelling this information and that’s how

we would make advanced by collaborating

right so I to go back into this

information so there is there are these

drugs which are being used for diabetes

which are called sglt2 inhibitors in

Kanna is one of them Giardia –nz is one

of them and basically what these drugs

do is that our body filters sugar in the

kidneys but it reabsorbs most of the

sugar but these drugs poison the kidney

tubules in such a way that you don’t

reabsorb the sugar that you’re filtering

so basically you’re dumping sugar so

when you’re dumping sugar and if you’re

not eating carbs or if you are let’s say

fasting the body switches to fat

metabolism because you don’t have sugar

available you’re going to do now fat

burning so when they started using this

in humans they started noticing that

ketone levels go up they also started

noticing that LDL cholesterol levels go

up and fascinatingly in some of these

studies now that since there is no

conflict here in the sense that the

pharmaceutical companies and I’m sorry

for being a skeptic but the

pharmaceutical companies want to show

that hey dumping sugar and reducing your

blood sugar is beneficial for you and by

the way it’ll be helpful for you to

prevent heart disease and that’s what

they found but they could not explain

hey you’re improving heart disease but

your LDL levels are going up and so

there’s an accompanying paper that’s

done in a in a hamster which goes into

the biochemical mechanisms with this so

what’s happening is that as you are

dumping sugar you are not making more

ketones and as you’re making more

ketones the liver is synthesizing more

cholesterol and since the liver has a

higher amount of cholesterol

it doesn’t need cholesterol for itself

otherwise what the liver does is that

hey cholesterol is so important for me

let me soak up some cholesterol from

circulation and it has these LDL

receptors

these receptors are there that soak up

the cholesterol from the circulation and

remove it for liver to be able to use it

but since LDL since liver is

synthesizing so much cholesterol it

doesn’t need that cholesterol from

circulation so it down regulates the LDL

receptors and also since it’s making so

much cholesterol and since cholesterol

is not a metabolic fuel in other words

we can’t burn cholesterol like we can

burn sugar and triglycerides the only

way for us to eliminate it is in bile

well the paper shows that your

cholesterol elimination and bile goes up

so you can see that the feces are now

filled with cholesterol Wow Wow and

another fascinating mechanism that they

talked about is that the LDL cholesterol

is in some way an antioxidant it it is

fighting antioxidant injury and it gets

oxidized in the process when it gets

oxidized in the process it gets picked

up by the macrophages through a certain

receptor so the macrophages go around

and say hey this LDL has done its job

let me just pick it out from circulation

and this paper shows that these

macrophages that are laden with oxidized

LDL cholesterol their elimination

through the gut through feces is

promoted in the setting of fat oxidation

so here is a complete picture you’re

burning fat you’re making more ketones

you’re making more cholesterol in the

liver and hence you gonna make more LDL

because the liver has to mobilize that

cholesterol it’s going to down regulate

the LDL receptors because it doesn’t

need cholesterol anymore it’s gonna up

regulate cholesterol elimination so your

bile acid production goes up the

elimination of body goes

and it also improves the elimination of

oxidized cholesterol fascinating so so

um a couple things if you’re getting an

increase by all production you could

also have could be create a laxative

effect you could have a little diarrhea

maybe some of the side effects but the

question I have is that time so people

are probably understanding this now but

they’re thinking is this extra

cholesterol going to stick and my

arteries and clogged up an artery that’s

I think that’s the big question that

they are concerned about so I think that

one thing I would like to humbly submit

is that we don’t understand the

molecular mechanisms why we get plaque

in our blood vessels and I almost

hesitate to call it an adverse periodic

plaque because that gives it a

connotation that somehow cholesterol is

the culprit so I want to stay and say

hey it is plaque formation and to say

that the LDL is the primary culprit that

gets on to the vascular wall onto the

sub endothelium and I know I want to be

cognizant on by not using too many

medical terms that is the layer just

beneath the lining of a blood vessel and

then initiate a response in which you

are making plaque is by no means

scientifically agreed that that are the

mechanisms

it is quite equally possible that the

LDL cholesterol is there to help repair

an injury that happened as a result of

oxidative stress which means that

whenever you burn something you create

an injury an oxygen when it is used in a

certain way creates an injury at the

level of the vessel and that could be

from high blood pressure

that would be from result of an

infection that could be because you have

insulin resistant and as a result of

that you have systemic inflammation that

is leading to vascular injury and is

this vascular injury being promoted by

the LDL or is the LDL just there to help

prevent oxidative damage and in the

process you see it around and that does

not mean that it is the culprit and one

of the many people from whom I have

borrowed this line is that if you order

a scene of a fire you’re gonna see

firefighters but you’re never gonna

blame the firefighters for causing the

fire right right and so is the case with

the LDL I’m not sure it is there too

cause I don’t know if it’s the culprit I

don’t know if it is there to help right

the paradox is that you see vascular

damage in people with very low LDLs and

you see no vascular damage in people

with LDLs in the mid to hundreds and it

simply does not jive that it is a graded

culprit if it is a graded culprit you

should see consistency of effect right

and if it’s a graded culprit you should

see that hey if I reduce my cholesterol

LDL cholesterol down to 30 milligrams

per deciliter since this is my primary

hypothesis that this is what is causing

vascular injury I should see no vascular

injury and I can take you through many

papers in which they have dropped the

LDL down to 30 milligrams and have

changed the event rate either by less

than half a percent or have done it in

the opposite direction so to me that

makes no sense and this is the kind of

critical thinking that I want

physicians who are taking care of

patients to do is that you cannot rely

on relative risk reduction that many of

the papers talk about but you want to

look at absolute risk reduction you want

to look at the integrity of data you

need to be a skeptic and see who is

doing the studies and what is their bias

behind that right right yeah they just I

think they in 2005 they came out with a

rule I’m not sure how well drug

companies follow it that they have to be

more transparent upload all the research

on a given drug I don’t know if they’re

following that but before 2005 they you

could selectively publish what you

wanted to publish unfortunately so if

you’re if you as a doctor researching

and you’re only getting half the picture

you’re just you’re gonna see something

that’s not not the true data one thing I

was gonna ask you

being a cardiologist what when you’re

looking into an artery looking at plaque

do you find a certain pattern of where

that plaque is located is it always in

the carotid arteries is it in another

artery does it happen in certain high

pressure areas or does it just random

well to a large degree it does happen

with there are where there is shear

stress so you know shear it could be a

medical term so basically at a branch

point the blood flow is not laminar the

you know laminar is smooth blood flow

turbulence is when the blood flow is not

smooth and our areas of branch point

there is possibility of turbulence and

at this point there is a lot of stress

on the vessel wall and that can happen

as a result of high blood pressure that

can happen as a result of the blood

vessels getting constricted which means

getting smaller so you predominantly see

flag buildup

those locations but it can also be found

at other places that are more or less

random that you would say hey this is a

process that you can predict to some

degree that it will happen at branch

points and are places of high shear

stress but it can also happen in other

locations so like for example you

mentioned the carotid arteries the

carotid arteries bifurcate when I say

bifurcate they divide into two blood

vessels right here in the neck and at

this point one blood vessels going and

supplying the brain the other blood

vessel is supplying the face and at that

branch point there is more likelihood of

you getting buildup of plaque and

buildup of blockages and I’m trying to

stay away from saying buildup of an

asterisk erotic plaque right because

that implies a certain causation and

then you what about the coronary

arteries that is that more common than

the carotid so both occur concurrently

like if you have coronary artery disease

the likelihood that you can have carotid

artery disease is about 50% and if you

have carotid artery disease the

likelihood of you having coronary artery

disease goes up dramatically and what

goes up even higher a more a further

end-stage that means a more advanced

stage of vascular disease would be

blockages in the blood vessels of the

leg so if you have lock edges in the

blood vessels on the leg the possibility

that you have heart disease which means

blockages carotid disease the blood

supply to the brain and kidney disease

is very high so unfortunately people

with blockages in their blood vessels

that demonstrates that there is a more

advanced vascular disease present in

them and hence you would find it in

other locations as well interesting

the patients that come see you are they

coming with blood pressure or are they

coming because they already been

diagnosed and they need surgery what

type of clients come to see you so in

the first 24 years of my practice I

predominantly tried to work in the

cardiac cath lab so I would see patients

referred to me with blockages in the

blood vessels of the heart and I would

take them to the cath lab and put stents

in them and fix them and these people do

have high blood pressure

many of them are diabetic many of them

have I would say I hate to use the term

high cholesterol I would say poor

quality cholesterol I’ve started using

that term and poor quality cholesterol

and my view is somebody who’s got high

triglycerides and low HDL and if you

divide or if you evaluate their LDL

cholesterol properly it is the small

dense molecule and launch not the large

and fluffy molecule so they had a number

of these factors and I would open them

up in the in the cardiac cath lab but in

the last five years have gone through a

transformation and I said hey if this

nutrition works and me I should try it

in my patients and so now I spend more

and more time at least 50% of my time or