What is Fat Toxicity? Lipotoxicity Dr Nadir Ali Explains

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so I asked I asked Mr caliber the CEO of the hospital that it's three years since

the pandemic and we should have this in person and the reason I wanted to have this in person

is more for me than for you guys because I know that you all will show up on a Wednesday the last Wednesday of the

month and it forces me to improve and and understand this area

better and see how I can make a dent in terms of improve

improving our health for lifestyle so today's presentation really started

with uh a blank page I I didn't uh

copy any slides I didn't bring any previous presentation and and and make those slides so until they

get on there I want to kind of uh give you the setting for why today I

think is an important uh topic and that is because most people who come

to our office they think that we uniformly give one piece of advice

and that is cut out your carbs and eat a low carb high fat diet

and that may be appropriate in many instances but there are certain instances where a low carb high fat diet

is not appropriate so by no means am I saying that you have a high carb low fat diet

so the high carb low fat diet is a standard American diet that is the least appropriate diet of all

so like let's say you walk out of this room and you think that fat is bad

and you don't want to eat any fat at least don't go to a standard American diet sticking to a low carb high fat

diet will still be the best second option so this is a staggering statistic this

is very new in Texas you can see that roughly

40 percent of us are obese that means we have a BMI greater than 30.

and in the nation one-third of the nation is obese and if you look

at overweight and obesity it is roughly about 68 so normal weight

individuals are roughly only about 30 to 33 percent in the United States

and it's getting worse so I wanted to describe to you what is

fat toxicity like what is lipotoxic toxicity fat toxicity is called

lipotoxicity and you can see on the top right right hand side I think I can be there is I

can use this thing here and um you can see uh my marker out there those

are normal fat cells these fat cells are not overstuffed they are

not large these are overstuffed fat cells and these fat cells also have some

inflammation some of them are dead so there are inflammatory mediators in them

as well as cells that cause the cells to become swollen and red and inflamed

so the question is how does our body normally handle fat so here we are we are eating fat into

the gut

and you'd be surprised in healthy people that happens in a period of five minutes

after fat enters into the circulation so once it's dumping the fat into the

fat cell or it is giving fat to the exercising muscle the muscles we have in

our body for consumption or to store for future consumption it becomes much smaller and it's called

a chylomicron Remnant so this fat-filled globular globule become smaller

it's called a Remnant and that's cleared up by the liver

now you may ask me how do I know that I have normal fat

handling and you would know you have normal fight handling by looking at a few key pieces

of your blood work so you can look at your triglycerides if your triglycerides are less than 100

if you're good cholesterol or HDL is greater than 55 not less than 55 I just

noticed that I made a mistake out there and invariably when you have the situation the so-called bad cholesterol

which I call the other good cholesterol is over 150. and your total cholesterol usually is over 200.

so this is making it redundant it's showing a blood vessel where the fat globule is moving

so this is the blood vessel the fat globule is moving in here and here is a muscle cell or a fat cell

and in the presence of an enzyme called lipoprotein lipase you don't need to remember that it dumps the fat cargo

becomes a smaller molecule that gets cleared by the liver

so the question is how does fat toxicity happen

so let's say you are metabolically unhealthy you have become overweight

your type 2 diabetic you are insulin resistant now I throw

out a term called insulin resistance and I'll Define that later but for now just keep that in your mind

so if you are insulin resistant and you have obesity or type 2 diabetes

the fat cells are already filled and overstuffed and inflamed and they say we can't accept fat anymore

so the fat backs up in the circulation the muscles can take only so much fat

and by the way you will see that our muscles can also get fatty and I'll show

you slides on that so they refuse to accept fat so fat backs up in the circulation

the liver similarly will say hey I can't take any of these

fat globules or the remnant globules so they also hang in circulation

so the way you know that is that you will have high levels of triglycerides

low levels of good cholesterol and a series of other blood markers that I will explain to you

but what you will end up is what is called like topic fat deposition

so what ectopic fat is that fat that remains in the circulation is

trying to find a place to park itself and it Parts itself in your liver in

your heart in your pancreas and in your muscles

so this is the biochemical profile you will get in somebody so if you come to

us Channel I can look at your blood work and in a matter of a few seconds tell

you that you are at risk of lipotoxicity and the way she does that is that she

will look at your triglycerides see if they're high look at your good cholesterol see if it

is low she has got markers to see if insulin is working well and if insulin is not

working well you will have high insulin levels along with high blood sugar levels

there are markers of your liver being inflamed in the blood work one of the months that we use is ggt people are

very surprised they say hey this blood work says my ggt is normal but you're telling me that it is high because we

are used to seeing this marker for the last 10 years and we know that when the ggt is in the

teens like 16 17 18 or low 20s then your liver is good but if it's in

the high 20s or 30s or 40s we know that your liver is struggling

with handling fat there is another hormone called adiponectin that we get sometimes

the adiponectin is a fat hormone that I will elaborate a little bit later

there will be other markers there will be high blood pressure there'll be evidence of visceral obesity in other

words you will have high waist to hip ratio you will have high BMI

so I want to give you guys a very Elementary understanding

of how our body behaves when it gets fueled

so one of the things that people think is that insulin Works only on the liver but

it works on the liver it works on the muscles people think that insulin only

addresses blood sugar or glucose or carbohydrate but it's also involved in fat metabolism

so here is a person who has consumed some carbs these are sweet potatoes

it gets into the bloodstream as glucose and if you can see my marker out here

this glucose then gets into the muscle cell through a channel there is a a specific channel that sucks

the glucose from the bloodstream into the cells and that's called the glute4 Channel

you can just remember it as a glucose Channel so in the presence of insulin

and this channel the sugar is getting into the muscle and

if your muscle is healthy Physically Active

it has a lot of mitochondria mitochondria are engines inside the muscle that burn fuel

to generate horsepower to generate wattage and that horsepower is called ATP

so this fuel is then metabolized

by the engines of the cell which is mitochondria and it generates energy

and if you have had a little too much carbs or carbohydrates the rest of the

carbohydrates are then efficiently converted to glycogen so the muscle takes all the

carbs that you have eaten so one of the best advice I can give

especially as we get older is to improve your muscle mass if you

have better muscle mass it's just like a sump like a sieve that sucks in all the

carbohydrates that you have eaten either converts it to energy or makes it into glycogen

so large muscle mass is an important aspect of maintaining

normal blood sugars and preventing insulin resistance

now I said there's also roll of insulin in fat metabolism so what does insulin do to Fat so here is a person who's

consumed some fatty steak now instead of glucose there is fatty acids here

now these fatty acids enter the muscle through a mechanism I didn't draw that mechanism

and to get into the muscles it's you need insulin and an enzyme called lipoprotein lipase

and the fat that enters the muscle can either be burned for energy so you'd be surprised

that people who are Physically Active who are on a low carb diet are actually burning more fat and I'll

show you that in a subsequent slides but the fact that they cannot burn they

can store it close to the mitochondria close to the engines of the cells in what is called intra myocellular fat

imcl intramyocellular lipid so you'd be surprised

that the muscles can also store the fat you have eaten

so here is somebody and you know put an endurance that seed because I like cycling and sharing like cycling

but you could be a weight lifter and you could have good muscles and you would pretty much get to the same thing

so in somebody whose muscle is insulin sensitive that means insulin is working

well these muscles have a lot of capability

of storing fat they have very healthy mitochondria you will see these green little dots out

here these are mitochondria so they have capacity to store intracellular fat

which is healthy fat they have a very large engine so they

can burn the fat in addition because they're healthy they will also have a lot of glucose channels

so they not only will have ability to store fat but they will have ability to store glycogen

what they don't have is what is called toxic fat when the muscles get unhealthy

and we'll get to toxic fat in the next slide so you just keep in mind that there are some toxic fats

so if the muscle gets unhealthy one of the first thing that happens is that it loses its capacity to burn fuel

so the mitochondria becomes Shriver they don't they're not as good they're not burning as well they

are fewer in number so the fat in the cells get rancid you

know you can only store so much if it's not in Dynamic movement to burning

the fat gets rancid and as it gets rancid it gets converted to two compounds one of them is called ceramide

now if you go to my YouTube channel you'll see a a good presentation on ceramide but ceramide is

necessary in small quantities for ourselves but when the quantity is increase

the ceramide then goes and kills the mitochondria

and it prevents these glucose channels from being activated and so the muscle

can either store glycogen well nor can it use glucose well

and of course it has a lot of rancid fat that it is not able to use because there

is no capacity for it to burn in other words the engine is bad

so here is a I think one of the best slides I have created in order to show you what is the

mechanism for insulin resistance so let's pause here for a minute because

I want everybody to come along with me so you get you hear the term thrown out that that

there is insulin resistance so what is it so let's say that I have or one of you

has normal blood sugar of about a hundred or ninety and if you need about four of

insulin to keep it there 4 times 100 is 400 and this is a hypothetical number called 405 you

divide it by that if that number comes to less than one then you get a Homa IRS score that tells

you you are insulin sensitive that means insulin is working well but in layman's term

if you have normal sugars and low levels of insulin that means you need low levels of

insulin to hold your sugar but if you have normal sugars or slightly high sugars

and high levels of insulin that means that your body has to need a

lot more insulin to drive the sugar into the cells

so the reason we get insulin resistance and this has been worked out by some

very good intelligent people is through what we call as lipotoxicity

that means fat toxicity the cell is taking in fat it is not able to burn the fat

when it doesn't burn the fat the fat becomes Rancid and it creates ceramides and as it

creates ceramides it creates a series of reactions in which it goes to the

insulin receptor so here is an insulin receptor sitting on top of the cell there is insulin out there

and basically this fat through a series of reaction is inactivating the insulin receptor so

basically once insulin sits on the insulin receptor it creates a series of

reactions that makes the glucose Channel become

active and second glucose but this rancid fat is interrupting

all the channels through which the insulin receptor activates the

glucose pore or the glucose Channel and so the cell cannot take any glucose

so this is an important point and the important point is that insulin resistance

starves your body of fuel in other words the cell is starving it's not able to

get in the fuel and in some ways that will drive your appetite or want you to eat more because

what you're eating is not really getting into yourself

so the cell is energy starved and it's inflamed and then if you leave it like that for a long time it dies

so now the liver is the second target for lipotoxicity and so we need to understand how our

liver functions so let's say today I told myself that

it's a difficult day for me I need to fast to be as bright as Kathy

out there and so I'm not eating anything so in other words I'm fasting

so in the setting of fasting the liver is charged with providing fuel for our

body especially the brain so if you fast let's say you go on a fast every part of your body is willing

to fast the muscles will reduce energy the heart will slow down your blood pressure will drop

but the brain refuses to fast the brain says no matter whether you are sleeping or fasting or exercising I need this

much fuel per minute per hour so the liver is charged with that responsibility and it takes the fat from

the from the fat cells the fatty acids and through the mitochondria it converts

them to ketones so that ketones can supply the brain

it takes the glycerol which is part of your triglycerides as well as a little

bit of your muscle and converts it through a process called gluconeogenesis in other words it makes

blood sugar or glucose from fat as well as protein so that it

can supply the brain the brain can use ketones but there is an obligate requirement for glucose so it supplies

that so that's what the liver is charged to do but let's say

I want to spurge I had a good I had a good interaction with you all and I want

to go home and have sweet potato yeah so the sweet potato will give me glucose

and in the presence of insulin and because this liver is insulin sensitive

these channels are activated they take in sugar

and they convert whatever sugar they are taking into glucose that is not needed

for immediate burning by the muscles but there is one other important thing

that the liver does because as soon as you're eating food there is plenty of food available so the

normal liver at this time shuts down glucose production otherwise the liver is putting out glucose

and ketones for the brain but once you have eaten it needs to shut it down

now let's say that somebody is here who is eating a standard American diet a sad

meal and the sad meal has lots of refined carbs sugars as you can see

pastries bread so there is a glucose overload so in

other words that taking in a huge amount of sugar when you have that much sugar you will

need a lot more insulin for the sugar to get packed in so in other words you will raise your insulin levels

and if this person is still normal they'll convert some of the glucose to

glycogen they will still shut down the output from the liver

of the glucose it was producing when it was fasting so in other words the liver shuts down the glucose

but a large amount of this glucose is converted to Fat because when you eat a

large amount of carbs there are signals going to the liver to activate the fat manufacturing Machinery

so the fat Machinery is jacked up and the carbs that you have eaten

because we can store only a limited amount of carbs the carbs will get converted to fat

now what is standard and I must say that I didn't really truly understand what

liver insulin resistance is for a long time so in other words you say your liver

is not responding well to insulin what does it do so when the liver is not responding well

to insulin what it does is that it activates the curves that it gets

it will not use it to convert to glycogen so in other words it's not storing it as carbs

it diverts the carbs from glycogen to fats in other words an insulin resistant

liver is not responding to insulin in terms of storing glucose

but it is hyper responding to insulin to make fat

so in other words an insulin resistant liver will have high insulin and high fat manufacturing capacity

but it has another very important thing that we didn't understand and that is that despite that person eating a

sugar-rich meal the liver continues to put out sugar so

this is called hepatic glucose output and this hepatic glucose output is not diminished so you get a double whammy

you have eaten a large meal filled with carbs and your liver refuses to

recognize that and puts out more carbs so your sugar in the bloodstream will go up even higher

so this is in summary what insulin resistant liver does it has high sugar

output despite the fact that you have eaten it's activating fat manufacturing

machinery it is not only activating fat manufacturing Machinery but it's also

exporting fat which is called vldl which is which you will get in your blood as triglycerides

because insulin levels are high when your insulin levels are high the

fat cannot make any ketones so the brain could be potentially starved and if this process now people say okay

I I have fatty liver and I'm going to get fibrosis or

cirrhosis in the next few months it doesn't happen like that it takes

20 to 30 years of your liver protesting that hey look I am getting fatty I'm

getting insulin resistant before cirrhosis happens same is the case with pancreas so don't

think that you have a short period of time to intervene you have a long period of time to intervene then sometimes in

some individuals you can proceed to liver cancer so there's a lot of good work done on

the muscles for insulin resistance there is a lot of good work done on liver

but not as much for the pancreas so here is a fatty pancreas

and fatty pancreas is happening for the same reason you're consuming fat

the fat is not getting packed under the fat cells it's being left in the bloodstream you get ectopic fat

deposition in an area that the body does not want which is the pancreas

so here is a normal pancreas on CAT scan you can see a nice outline of it here is

a normal liver and here is another Imaging study that is showing that the pancreas is very

light in color because it's filled with fat and similarly the liver is very

light in color so Imaging techniques for finding out fatty pancreas are there

so I have all often heard people come to my office and declare that

well I'm slightly Pride pre-diabetic and this has been going on for 10 years or

20 years and it means nothing and they're wrong that's how the disease

process is the pancreas is struggling and telling you that hey make something

right and it lasts for 20 to 30 years before it falls off a cliff

they just don't know when the cliff is coming but there's that's not a normal situation for them

in the beginning when the pancreas is fatty it's actually making more insulin so it's it's it can create you to be

more hungry it can make you more obese and it can prevent fat burning

this is an important aspect that I may or may not be able to get into but

when the pancreas is first given an exposure to glucose from a meal you eat

a meal sugar gets into your bloodstream the normal pancreas has a rapid spike in

insulin so it the insulin goes shoots way up and there's a reason for that because when the insulin goes way up

it shuts down other hormones like glucagon but one of the first things to go in a

fatty pancreas is that rapid spike in insulin and of course the fatty pancreas makes

more glucagon which will create the liver to put out more sugar in the

face of you ingesting sugar so this is the work work of Lydia shishi

bank she is somebody who worked with Dr Roger Unger and what she showed is that on Imaging

studies she evaluated the fat content of the pancreas and if you looked at somebody with

normal sugar glucose metabolism the fat content was low

but here somebody who is supposedly with normal glucose but with a high body mass

index they are obese the fat in the pancreas was higher these are people

with impaired glucose tolerance there in other words pre-diabetic the so-called

people who have been like that for 20 years they have a little higher fat and as

they become type 2 diabetic their fat content is still high

so I had already gone through this so you can look at your blood panel go

home today look at it look at your fasting insulin level look at your fasting blood sugar multiply the two

divided by 405 you'll get a number if your number is less than one

you are insulin sensitive if it's between 1 and 3 your borderline but if

it's greater than three you are definitely insulin resistant here is I'll just skip through this

briefly but this is the fast insulin response a normal pancreas as it's

exposed to sugar the insulin spikes way up before it

comes down and this has certain key features in terms of dropping the other hormones

that will prevent the liver from behaving inappropriately

here is the person with a fatty pancreas the phase one insulin response is gone

even though they're making a lot more insulin and the hormone that's going to make

your liver function well in the setting of you eating refuses to go down so your

liver continues to put out sugar so these are people who are morbidly

obese you can see that they are making a lot more insulin than lean people so just wanted to show you that as you

become heavier the pancreas has to make more and more insulin

so we talked about the muscles they are fatty and Insulin resistant we talked

about the liver we talked about the pancreas now it's time to talk about the heart

so I don't know if any of you have this electrophysiologist the electrician of the heart his name is Sumaya Sharma or

Sam Sharma none of you are he's a good very good electrician but in

his previous life for three years he was working on hearts

that had gone through fat toxicity so in transplant center when the hearts

were taken out from transplant patients he would take them out and he would measure their fat content he's a doctor

here in this Hospital very good doctor so I thought I wanted to give him a shout out for that and what he did was

that he took 27 hearts and he measured the fat content according to what they had

so if these people had no real problems in other words

these Hearts were obtained not at the at the time of heart transplantation or but

for some other reason they didn't have much fat but if they had heart failure and the

hearts were obtained they had more fat if they had heart failure with obesity the fat was even higher

and if they had heart failure with diabetes these Hearts were fat infiltrated so in other words the hearts

had undergone lipotoxicity and here is a study that's done in

teenage girls and they took teenage girls that were lean and obese

and so they are measuring hepatic fat muscular fat and pancreatic fat

these are the lean individuals their weight is a lot lower see 53 kilograms

versus 105. their body mass index is much different

the obese girls have much higher insulin levels they have much higher levels of fat in

their bloodstream they have much lower levels of the good cholesterol the HDL cholesterol remember

that everybody focuses on the LDL the LDL is not really any different at all

look at their liver fat the liver fat is almost twice as much look at their muscle fat it's almost twice as much

their pancreatic fat is more than twice as much so they took a group of women who were a little

heavier and they did exercise training so 14 women very simple study

three times a week for 55 minutes they went through strength training and aerobic exercise so they taken

eight weeks three times a week one hour supervised physical training no diet

intervention nothing else was done they were just told eat what you want to eat

so this is their body mask index they're little heavy 33 25 and below is normal

body mask index you can see that it didn't change their weight didn't change in fact maybe went

up a little bit their fat Mass went down their fat free mass that means their

lean mass went up the resting metabolic rate which means

the number of calories that we're burning went up quite dramatically

fat oxidation went from 121 to 189 so in other words they were burning more fat

they were burning lot less carbs and there is something called our cues

in other words you can attach somebody to a machine they're breathing in oxygen breathing

out carbon dioxide if you're breathing in about like let's say 10 oxygen

molecules but breathing out only seven carbon carbon dioxide molecules that means

you're fat burning so the lower the number the lower the RQ the more fat burning

you are and they went from 0.75 to 0.70 so that means that they became very fat

burning this is another test to see

whether the engines in their muscle the mitochondria whether they increased in

number so this is a test to show whether the mitochondrial density was higher and

this is an activity of a mitochondrial enzyme and in all of them the enzyme

went up so this is a area that I wanted to touch

on really strongly because I want by a show of hands here how many of you are

taking cholesterol medicines so there's at least one two three okay so that few people taking

cholesterol medicines how many of you are taking four how many of you are taking something

called PCS canine inhibitor they call it repatha or paralleland it's an injection

that you take once every two months maybe some of you have taken it in the

past well you guys are lucky so

to the Statin users do you think statins worsen lipotoxicity

or make it better so yes I mean your doctor will not sit there and talk to you about this but

statins alter the way the insulin receptor sits on the membrane because the insulin receptor

sits on the membrane in a part where it is very cholesterol rich

so since it Alters it the insulin receptor does not function well

statins make the function of the mitochondria worse CoQ10 because CoQ10

comes from cholesterol and when you take statins your CoQ10 goes down your mitochondria don't

function well and if your mitochondria don't function well you have backup of fuel in your

muscles and so you'll be exposed to lipotoxicity and that's why

you have a higher risk of getting fatty liver and fatty pancreas okay you are not taking PCS canine Inhibitors but

have you heard about pcsk9 inhibitors so I won't go into that because I have a

a huge section actually I have a YouTube talk that is completely dedicated to that

but in brief there are a group of individuals who are born with PCS canine deficiency

so they're just genetically they're not making PCS canines like they are taking an injection

to inhibit their pcsk9 so it's like they are taking the drug that the doctors and the pharmaceutical

companies want you to take so if you are taking that drug would it

surprise you or if you have that deficiency would it

surprise you that these individuals are heavier number one

number two they have visceral obesity that means that they have more fat in their liver

in their heart okay that more of them are diabetic

so here is a slide showing that they have actually more visceral fat not only in the humans but also in animal models

and so these genetic variants are at higher risk of diabetes Higher by fasting blood

sugars higher body weight higher waist to hip ratios and the reason they get fatty

liver is because PCS canine comes and regulates a receptor that is picking up

fat from the circulation so if you don't have pcsk9 a lot more of this receptor

is expressed and the liver just imbibes in the fact that it cannot deal with and becomes

fatty and there are so many studies on PCS canine Inhibitors and I have just kind

of given you a little sound byte here that there is an association between an

increased risk of diabetes and the potency the more potent the PCS canine inhibitor you give the higher the risk

of diabetes the longer you give pcsk9 inhibitor the greater the risk of diabetes

and the duration of this that is the observation was noticed in

as short a period of time as 1.5 years now put that in context what did I tell

you when you get a fatty pancreas how long does it take for you to become a

true diabetic 20 years so when you when you notice this in a one and a half years

it should tell you something so this is the useful part of our

interaction today and all of you will be wondering how do I know if I have lipotoxicity and and we went through

this before but I want to make it redundant if your triglycerides are high normally the blood work says greater

than 150 I think that is way too high it should be less than 100. if your HDL is

less than 50 if your home IR is greater than one greater than three for sure

if your liver enzymes are high if you have low adiponectin levels and I will

get into that if you have high blood pressure if you have visceral obesity

that means visceral obesity meaning high waist to

hip ratio so adiponectin is a hormone that is evaluated elaborated by the fat cells

when the fat cells are happy and healthy they elaborate this hormone called adiponectin and what the adiponectin does is that it

goes and tells the fat cells hey hold on to the fat the body is not ready for the fat

you are the best source to buffer the fat now I must say in my clinical

experience I have a number of patients especially women

who are a little bit on the heavy side but their insulin markers are low their

insulin resistance markers are low the triglycerides are low the HDL is high in

other words they have all signs of metabolic health in every way they are metabolically

healthy and the reason is that for whatever reason nature gifted women with healthier fat

cells they can get heavier without having fat deposition in the

liver in the heart or in the pancreas men are not so lucky by Nature

so we check adaponectin levels if they are 20 or greater that means you're very

good if they're between 10 and 20 you're sort of marginal less than 10 that means your fat cells are hurting

and rdpronactin has many other activities on the brain on the liver it makes the liver insulin

sensitive it helps pancreas not die and it also helps with your immunity

so what should I do if I have lipotoxicity so I guess we we talk about this a lot

should I be on a high carb diet if I have lipotoxicity

no right because high carb diet is probably the worst because you're going to jack up

your insulin levels you're going to store more fat and you're going to make lipotoxicity worse you're going to make

insulin resistance worse if you learn nothing the low carb high fat diet although not

the best option is the better option than standard American diet

can I consume a standard low carb high fat diet in other words do I give you license if you have lipotoxicity to say

yeah you go eat that diet and you'll be fine and the answer to that is no in many

cases you need to go through a period in which you are doing three things to improve

yourself and I'll get into that so one of them is the role of fasting so people who are lipotoxic they have to

learn how to fast Nina can help you with that she's a coach on that Gabe and Chana can help you with that as to how

you do fasting is there a low fat low carb diet is it

sustainable long term so I used to think that low fat low carb diet is an oxymoron because as you

reduce the carbs you'll increase the fat as you increase the fat is only when you can reduce the carbs

but really truly there is and in one-on-one sessions you can sit with

Chana or Gabe or Nina and figure out how to cook a meal that is both low in carbs

and low in fat what is the role of exercise in lipotoxicity with

lipotoxicity you know you already have a fatty pancreas you know you have

your fat cells are full you know that you have a fatty liver you know that your muscles are filled with fat

and you potentially may have fatty infiltration of the heart and all of this is because of damaged

mitochondria so basically you have an engine with a horsepower of a moped

and that's not going to improve unless you do fasting unless you

practice uh low carb low-fat diet unless you practice what is called calorie

restriction how do you eat less and I have a YouTube video on that but more importantly you convert your

moped into a V8 supercharged engine

and that would be the role of exercise so I tell people that

look you need to exercise for about seven hours a week

both aerobic as well as strength training exercises because strength

training exercises increases muscle mass aerobic exercise is good at increasing mitochondrial density that means you can

burn more fuel so who can have a standard American Standard low carb high fat diet

so to have a standard low carb high fat diet you should be exercising you should

have normal body weight you should have low triglycerides you should have high HDL and these people

should actually be monitored on a regular basis for all these markers

so I think in a sense with time as you get more information

you are better able to individualize the diet for people

so I guess that's all I had [Music] and uh thank you

appreciate it [Music]

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