94. Dr Ankur Verma: Emergency Physician on Key Metabolic Risk Factors for Heart Disease (Not Cholesterol)

Episode Transcript
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Speaker 1 (00:00):
Okay, welcome back to the Regenerative Health Podcast
.
Today I'm speaking with DrAnkur Verma.
Now he is an emergencyphysician in New Delhi, india,
who is doing some veryinteresting research and
observation about certain groupsof patients coming in to his
emergency department.
So, ankur, thank you forjoining me.

Speaker 2 (00:20):
Hey, thanks for having me, Max.
I'm looking forward to this.

Speaker 1 (00:23):
So your work kind of stood out to me when you
published or you've popularizedor discussed some very
interesting findings withrespect to heart attack patients
who are coming into youremergency department.
So in this discussion I want toget deep into the
characteristics of people whoare having heart attacks,

(00:44):
because in India, in Australia,around the world, this is a
major cause, if not the mostimportant cause, of death and
disability in the world.
But maybe before we kind of getinto the nuts and bolts of what
we think and what you'veobserved is happening and who's
at risk, maybe talk a little bitabout the presentation of

(01:05):
someone who's coming in with aheart attack, because that might
make it a bit more real forpeople.

Speaker 2 (01:12):
Yeah, you know, it's quite common for people to think
that a left-sided chest painleading to the left arm is the
most common symptom.
But you know, whatever we'veread in our textbooks as the
textbook presentation isactually one of the rarest
presentations of those diseases,aren't they?
But you know, a patient with aheart attack does not need to

(01:35):
have just chest pain.
You know, there could beprofuse sweating which is, you
know, uncharacteristic of thepatient.
You know, if they feel that youknow that I'm just sweating
profusely too much today, it'snot normal for me they could be
having shortness of breath, theycould be having pain which is
going into the neck and jaw.
I've actually had patientswho've come in with diarrhea and

(01:59):
they were actually having aheart attack.
So those are some of thepresentations, but obviously the
most common is actuallyretrosternal chest pain or
tightness, you know, where youfeel as if an elephant is
sitting on your chest, you know.
And then just squeezing yourchest out.
That's the most commonpresentation.
And then obviously, you haveradiation to the different arms,

(02:22):
and you know it's been seenthat.
You know, if it's's radiatingto both the arms, that's more
ominous than radiating to theright arm, more ominous than
radiating to the left arm.
So, uh, you know and by ominousI mean you know the patients
are going to crash really reallyquickly if you don't do
anything.
Uh, so these are.
These are some of the reallytypical ones.
But then one needs tounderstand that if you have

(02:44):
certain comorbidities, like likediabetes, which is the most
common comorbid condition,especially in india, probably
across the world, right, youdon't come with typical symptoms
.
You probably won't even comewith sweating or shortness of
breath.
A lot of these people come with, you know, just upper abdominal
pain, which they usually tendto pass as acidity or probably

(03:06):
heartburn or something, and theydon't have these typical
symptoms.
Even their ECGs will not becompletely characteristic of an
MI.
You need to do your TROPS, youneed to do some ECHOs and then
diagnose the patient with an MI.
But I've had these silent onescome in just feeling uneasy and
they come in and they have anSTL-evited MI on the ECG and

(03:27):
then we do the STEMI code.

Speaker 1 (03:29):
But yeah, these are some of the symptoms which are
more common for patients who arecoming in with a heart attack
and talk about Indiaspecifically with respect to
this problem of atheroscleroticcardiovascular disease, Because
in Australia and New Zealand,America, US, Canada, obviously

(03:51):
it's a problem.
We have certain characteristicsI mean age of onset, obviously,
comorbidities but it seems tome that what's happening in
India is particularly bad andparticularly severe.

Speaker 2 (04:08):
Yeah, I mean, age is no bar anymore for having a
heart attack.
I mean, we published a casewhere we had a 17-year-old come
into the heart attack and thiswas way before the pandemic, so
it's not like it's not beenhappening over the years.
A lot of people don't actuallysurvive up to the hospital,
right, and you know they don'teven get an autopsy, so you

(04:30):
don't even know if they werehaving a heart attack.
But today's uh date, we get alot of patients actually uh, who
survive till the hospital andwe're able to diagnose them and
uh, and we're seeing people fromthe ages of 20 all the way to
about 80, 90 years old.
I mean, yeah, 80, 90 years oldused to be the ones that we read
about.

(04:50):
You know that that's whenyou're going to have a heart
attack.
But I still feel a lot of thepeople in India were having
heart attacks even at youngerage groups.
Most of them, or most of them,were not even diagnosed with
heart attacks.
Most of them, or most of them,were not even diagnosed with
heart attacks.
But we're seeing this and anduh, most a lot of people think
that smoking is one of the riskfactors.

(05:11):
I mean, we know that is.
I mean, you don't have to think, we know that, but most of my
patients don't smoke like Ithink.
If, if I remember correctly thestudy that we're doing right
now, about 75 to 80 percentdon't even smoke, right?
So we're looking into whyexactly are they having a heart
attack, right?

Speaker 1 (05:28):
and and that's something interesting that we're
digging into, and we've I'vehad some conversations with some
cardiologists, just just, youknow, raising some prickly
questions no, I love it, andthat's what that's what this
podcast and and yours as well isabout is asking prickly
inconvenient questions that thatchallenge uh challenge the
status quo.

(05:48):
So talk about these traditionalrisk factors, because there's
lots of papers essentiallyshowing that we can no longer
necessarily rely on thesetraditional risk factors per se
to help predict heart attacks.
So give us the background onwhat those traditional risk
factors are, and then we cantalk about what we think is also

(06:09):
going on.

Speaker 2 (06:11):
Yeah, if you remember , in our MBBS or our graduate
textbooks, we read aboutmodifiable and non-modifiable
risk factors, right?
So your modifiable ones werebasically smoking and your
lifestyle the food that you'reeating Hypertension, diabetes,
could be modified throughmedications.

(06:32):
And your non-modifiable oneswere basically your age and sex.
Males had a higher propensityof having a heart attack and,
you know, higher the age, morechances of a heart attack.
But it's surprising how wedidn't focus too much on the

(06:53):
modifiable ones and the mostimportant one, the most famous
modifiable risk factor, wasalways cholesterol, right, and
LDL, before the concept ofmetabolic syndrome actually came
about.
I think these were some otherones and so, and smoking was
obviously something that thatwas really focused upon, uh, and

(07:14):
rightly so.
But uh, people didn't focus onthe pathophysiology behind
hypertension and diabetes, youknow?
Uh, or cholesterol, first ofall, cholesterol was not rightly
so, but wrongly described to bea cause of atherosclerotic
cardiovascular diseases or heartattacks.

(07:36):
Hypertension and diabetes, yes,but what was the mechanism
behind getting the hypertensionand diabetes, you know, behind
getting the hypertension anddiabetes?
You know, that was somethingthat was never looked into or
never taught.
We were all taught to givemedications to try and pacify
the hypertension and diabetes.

(07:56):
Right, but it never worked.
It never works, right.
So all the patients and theycome in with heart attacks and
you're like, oh fine, you're adiabetic, you're bound to have a
heart attack someday.
Then what's modifiable about it?
Then right, yeah, I mean, ifyou're going to do that, if
that's what our attitude isgoing to be, all right, this guy

(08:20):
had diabetes and you know thisis one of the complications.
Then what are we doing about it?
We're just putting them onmedications and just adding it
on and on and on increasing thedoses and putting on more
medication and waiting for thecomplications to happen, and
then you can't do much about it.
You're just going to give moremedications for each

(08:42):
complication.
It doesn't work.

Speaker 1 (08:45):
And that's you as an emergency physician is that
you're at the bottom of thewaterfall.
People have people could havebeen like floating down the
river for 20, 30 years,collecting metabolic dysfunction
and and and cardiovascular risk, and then they fall down the
waterfall and you're there tokind of patch them up and and,
uh, try and prevent them fromdying.
But there was so much thatcould have been done in the

(09:06):
intervening preceding years toaddress the problem, but it
wasn't done.
And it's a comment about thestate of our profession which is
, it's almost this nihilistic,waiting for, as you say,
something to happen.
Oh, he's a diabetic.
We're waiting for him to havehis stroke or have his heart

(09:28):
attack.
We're waiting for his kidneysto pack in and get plugged into
the dialysis machine.
But it's so good that you'reactually kind of doing some of
this research to try andunderstand why.

Speaker 2 (09:40):
Yeah, I mean, once I got into my metabolic journey
and down the rabbit hole and Isaw the Matrix and I was like
what a second man.
Are we actually saving lives?
We're not.
I mean, we're saving thatpatient in that moment of time.
I mean they might come in andcrash and go into a dysrhythmia

(10:06):
or a VT or a VF and all of that.
And you know we do our CPRs andadvanced techniques or whatever
and save the guy.
And then they put a stent afterthat.
But then what happens?
Once he's discharged, right,he's put on medications, rightly
so.
Again, the guidelines say so.
So you know you have to putthem on medications, uh,
especially in the acute stages.
Yes, I understand, uh, and thenthey're given, uh, the wrong

(10:29):
dietary advice, and it's it'sthe advice that the patient was
usually having anyways,especially in india.
And and they're discharged anduh, and they continue with the
metabolic syndrome, uh, it justgets worse.
And we know, once you have aheart attack, you can always
have it, but should you, or doyou actually have to have

(10:49):
another heart attack?
Can it be prevented?
And not by medications, becausethat's not doing it right.
I mean, I, all of us have seenso many patients coming in with
the second heart attack.
Uh, they're eating apparentlyright and clean and green and
they're non-smokers, but theystill have a second heart attack

(11:10):
and that's blamed on the firstheart attack, right and they're
on statin therapy exactly yeah.
so yeah, we'll get into that ifyou want yeah absolutely so.

Speaker 1 (11:25):
Talk about these people Like.
What are the characteristics ofthese people there?
Obviously, and to give a bit ofa background, india has a very
vast and extensive culture ofvegetarianism.
So people aren't eating animalproducts.
People are probably not eatinga lot of fish either.

(11:46):
They're not eating seafoods,they're just eating wheat,
wheat-based products.
They're eating, um, you know,wheat-based bread.
They're eating rice rice whatelse?
What's this typical diet thatpeople are eating?

Speaker 2 (11:59):
yeah, uh, people do eat some seafood, but then again
, you know, uh, what I like tocall people in india plant
omnivores the one who you knowprobably say that, oh, we're non
vegetarians.
You know, if I ask them, howfrequently do you eat your meat
or your eggs, or your seafood?
It's like, probably once ortwice a week, right, and that's
accompanied with rice or rotis,which is wheat based, or naans,

(12:22):
which is, you know, like refinedflour.
So those are the plant-basedomnivores, because the rest of
the meals, so I give them anaverage, like you know, if
you're eating three meals a day,that's 21 meals a week.
How many times would you eatmeat?
It'll be twice.
Two out of 21, right, uh,that's just like five percent,
something I don't know, uh, or10%, yeah, so, and that's that's

(12:46):
about 30% of the population.
The rest, 65 to 70% of thepopulation, are pure vegetarians
.
And you know, if you, if youlook at breakfast all throughout
India, it's majorlycarbohydrate based and
carbohydrate loaded.
You know, if you go to south ofIndia, it's gonna be.
You know, I don't know, if yougo to south of india, uh, it's
going to be.
Uh, you know, I don't know ifyou've heard of these dishes,

(13:08):
but you know idli and dosa andvadas and you know these are all
cereal and grain based and andhave a lot of potatoes in them,
so it's all carbohydrates, a lotof oxalates.
Now you get you go to the westof india and you have these
rice-based uh uh breakfast whichis likeha, and I've had my
share, for sure, because I didmy medical from the west of

(13:28):
India and that was a staple.
You know we would play, youknow something like poker in the
night with just coins and justto time pass and whoever won for
like 100, 150 rupees.
You know we would bike it downto one of those railway stations
where you get really nice pohaat four in the morning and just

(13:49):
hog.
So, yeah, so that's, that'slike the staple breakfast of
west of india.
You come to the north of india,you might you must have heard
of chole bhature and parathasand all of that.
That's all again carb based andthe same with east of india.
So, and and if you go to themetropolitan cities, uh, it's
like english breakfast.
So you have baked beans andbreads and croissants and stuff

(14:10):
and, uh, people like to do thatfruits and juices and all right,
so people do that.
Uh, that's the most common.
This is the breakfast, right,so you can imagine what the
lunch and dinner is going to be,right.
So started, not a good start.
Exactly exactly.
So that's how the breakfaststarts in most of Hindead and

(14:33):
we're doing a lot of research.
So we're an academic departmentand the last couple of batches,
I've named them the metabolicemergency group or the emergency
metabolic group.
So their research and thesis isall based on emergency medicine
and the metabolic health of ourpatients.
Because I realized, uh, 90, 95percent of my patients who are

(14:56):
coming in have metabolicdysfunctions or complications of
that.
Right.
So they're coming in with heartattacks or strokes or diabetic,
keto acidosis, hypoglycemia,kidney, chronic kidney disease
and their complications, cancersand their complications, severe
infections or severe sepsis,right.
So those are the ones who areimmunocompromised and they think
that they're absolutely fine,but they've never got tested,

(15:18):
right?
All of these are coming in.
You know hypothyroidcomplications, asthma,
autoimmune disorders, aaa, pcosdissections, all of these right.
And then 5% of the traumas thatare coming in.
You can't do much about that,so you deal with them, but these

(15:39):
are the ones that are coming in.
You know kidney stones,gallbladder stones.
You know high oxalate diets,don't know.
I mean, as a doctor, you know,uh, and I accept, I accept my
fault of telling people drinkmore water because you've got
kidney stones or have some morebeer or, you know, avoid
tomatoes or you're dehydrated,that's why you're getting these

(16:01):
stones.
And and because we, we weren'ttold about oxalates or calcium
oxalate or where you get thatfrom, right.
So so diet's a problem.
You know all my gallbladderstone patients, they're all
vegetarians, right, and you knowwe forget our biochemistry as
to as to what the function ofbile is and what's going to
happen when, when it's notreleased, when you don't have
the right food, right.

(16:21):
So so all of these are comingin.
So we're doing a lot ofresearch and we're seeing a lot
of things, we're observing a lotof things, which is obviously
you can't do rcts.
Nobody can do rcts.
It's, it's not that easy, uh,especially related to emergency
medicine and their diets, right,because it's like a
cross-sectional study in thatparticular moment of time.

(16:43):
And so, yeah, these are allepidemiological association
studies, observational butmassive observations.
I mean, if you link that withthe biochemistry and the
physiologies, we'll understandwhat's happening, right.

Speaker 1 (16:59):
So these are non-smoking patients with
metabolic dysfunction.
So they've got signs of insulinresistance, pre-diabetes
diabetes and these are thepeople coming in with their
heart attack and again it'sflying in the face of these
traditional risk factors.
The question I also want to askis what are the occupation of
these people who are coming inwith heart attack?

Speaker 2 (17:24):
Yeah, so for smoking, most of them are non-smokers,
like 75% to 80%, just to beclear.
They have different occupations.
We've got government officials,we've got a lot of the labor
class coming in.
We've got a lot of businesspeople coming in, the service
class people, all walks of life,you know.
I mean from the rich to thepoor.

(17:45):
It's not sparing anyone, rightin different religions.

Speaker 1 (17:50):
Indoor or outdoor workers, are they mostly indoor
office?

Speaker 2 (17:53):
workers, both, both, but mostly indoor ones, mostly
indoor ones, probably theoutdoor.
So we're a private hospital,right, so not everybody can
afford us, but a lot of themactually do come in and you know
they get the free treatment forthe heart attacks.

Speaker 1 (18:13):
Yeah, okay.
So yeah, tell us what you'refinding, because obviously, b12
deficiency, hyperhobocystinemiaExplain these concepts, so
people can understand what theymean.

Speaker 2 (18:25):
Yeah, absolutely.
I mean, we all know howimportant B12 is for us.
That's the most importantwater-soluble vitamin, right?
And you get that only fromanimal products, and there are
actually a lot of cereals andgrains and vegetables that block
the uptake of vitamin B12 fromthe meat that you eat.
So if you're combining your,your, your chicken gravy or your
tandoori chicken with with uh,your carbohydrates and your

(18:48):
anti-nutrients, your b12 is notgoing to go up, it's going to
get blocked.
And it's so apparent because alot of my trolls tell me, you
know, I'm a non-vegetarian, myb12 is low, you know.
So you're talking crap.
I'm like you're eating it thewrong way, right?
I mean, when I started with mycarnivore journey, my b12 was
like 300 something.
Now it's 1060, something likethat.

(19:08):
Uh, because I stopped havingthings said that were blocking
my b12.
So india, like I said, ismostly a plant-based country.
No matter what people want tosay, it's mostly a plant-based
country and it's rampant.
B12 deficiency is in everybody,everybody, I think so, in our.
My patients, in a heart attackpatients.

(19:29):
We're looking at a few of thethings.
We're looking at their lipidprofiles.
We're looking at the diabetesdata with hba1c.
We're looking at the b12 levels.
We're looking at theirhomocysteine levels.
Uh, obviously, the otherdemographic and epidemiological
characteristics like age and sexand smoking and alcohol and
what they eat right and and notnot what they eat.

(19:51):
It's not a it's not a foodfrequency thing that we're doing
, but the dietary preference.
But if they're an om, if theysay that they're omnivore or a
pescatarian, we just ask themhow frequently they eat that
right and the rest of the timesit's obviously uh, plant-based
and uh.
And we're taking out thetriglyceride to hdl ratios and
it's massive.
I mean every one of them.
I think we've collected about120 patients till now.

(20:13):
Every one of them has a hightg2 hdl ratio which is more than
two.
Uh, I think three or four ormaybe you know benefit of doubt,
I don't remember the numbersoff the top of my head, but
probably you know.
You know, if I take them theupper limit, probably eight to
10 patients have normal B12levels because of
supplementation that they'redoing.
They're vegetarians but they'retaking supplements which is

(20:36):
cyanocobalamin, so they're like1500s and 2000s.
Some of them have normalhomocysteine levels.
Most of them have still havehigh homocysteine levels.
Most of them still have highhomocysteine levels.
The rest, everybody has B12deficiencies, and by B12
deficiency I mean less than 400,you know which is not even
optimum, because the referencerange goes from like 190 to 900.

(20:58):
And you know you getneurological symptoms when you
go below 400, right, so you needyour optimum levels to be above
400 or 500.

Speaker 1 (21:05):
So yeah, b12 deficiency, pick a moles per
liter.
I believe is the unit.

Speaker 2 (21:12):
Yeah, yeah, yeah, yeah, absolutely.
And you know I've seen B12levels as low as 30.
Wow.
And homocysteine levels as highas 223.
Wow, and homocysteine levels ashigh as 223.
Wow, in these heart attackpatients.
So, for your listeners,homocysteine is a protein which
actually balances out yourclotting.

(21:33):
It's supposed to help you healwhen you get hurt and all and it
clots your blood.
And methionine is an essentialamino acid which is converted
into homocysteine.
That's just one of its functionand it does its job.
And B12 remethylateshomocysteine.
That's just one of its functionand it does its job.
And B12 remethylateshomocysteine back into cysteine,
so it keeps it under check, youknow.
So our bodies like that, whereyou know it has checks and

(21:54):
balances.
But then if you don't eat B12in the right way, your
homocysteine goes out of control.
And all of these patients havehigh homocysteine.
So homocysteine is actually anindependent risk factor for
cardio, the cardioembolicdisorders, and by that I mean
you can clot in your lungs, youcan clot in your brain, you can

(22:15):
clot in your heart, you can clotin your legs, anywhere in your
body, right, uh?
So that happens, and highhomocysteine actually destroys
your glycocalyx also.
So I have this reallyinteresting conversation with uh
now the doctors nader, ali andmalcolm kendrick right.
And homocysteine actuallydestroys your glycocalyx also.
So when your glycocalyx isgetting destroyed, your nitrous
oxide is falling down right.

(22:35):
So your blood pressure is goingto spike up.
It's not going to be in controland then it causes injuries and
those injuries can lead toblood clot.
So you have an injury, bloodclot, and then you have the
homocyte which is causing ablood clot, and then you have
the body's defense mechanismcoming on as band-aids, you know
, and, and that, I feel, is whatis going to cause an

(22:59):
atherosclerotic block later on,when it keeps happening again
and again, and again and again,and and more so.
These I've had actuallypatients come in with the second
heart attacks and we had donethe b12.
At the first time it was low.
We did it again, it was stilllow.
Means what?

Speaker 1 (23:15):
that they weren't given the right direction for
dietary interventions yeah, andI guess, from my point of view
and looking at this problem ofatherosclerotic cardiovascular
disease, I absolutely agree witha lot of what Dr Malcolm
Kendrick says about endothelialdamage and damage to the blood

(23:37):
vessel wall and this glycocalyxas being this kind of primary
insult that therefore thendrives this pro-clotting,
pro-thrombotic environment whichleads to, over time, a
micro-injury which gets pluggedby a platelet plug and then
occasionally a macro-injurywhere you get a massive

(24:02):
endothelial damage and then ahuge blood clot that actually
occludes the lumen of thecoronary artery, leading to
massive AMI.
The point about nitric oxide isa fascinating one and the one
that I'm particularly passionateabout, because it's known quite

(24:22):
well by now that ultraviolet, alight, uh induces or um,
essentially liberates nitricoxide from, from the stores in
and around the endothelial layer, meaning that people who are
not getting out in naturalsunlight that's why I asked you
about the uh occupation of theseheart attack patients people
who aren't getting out inultraviolet light are therefore

(24:45):
not getting a vasodilating forcewhich is then going to push
their blood pressure up.
And actually also there's alink to an inverse relationship
between vitamin D andhomocysteine, meaning that maybe
it's the UV light that canpotentially offset some degree
of this hyperhobosystenemia thatwas um originated from a b12

(25:07):
deficient diet.

Speaker 2 (25:09):
Yeah, yeah, absolutely, and you know a lot
of my clients and my patientswho who are consulting me for,
you know, reversing disorders.
You know they're actuallyconsidering me for diabetes or,
you know, fat loss or weightloss and maybe hypertension,
loss of the periods and stuff,different, different things.
And when I get these, get themall tested they're all vitro

(25:33):
deficient with highhomocysteines.
We need to understand.
I mean, homocysteine has alsobeen linked with a lot of
dysrhythmias likesupraventricular tachycardias,
atrial fibrillation all beendocumented, all been published.
I've actually sent out a paperfor review which is linking.
I mean I've been seeing my purevegetarian patients coming in

(25:57):
with no known comorbidconditions, young ones between
20 to 30 having absolutelytanked b12 and really high
homocysteine levels, right, andI'm actually trying to
collaborate with somecardiologists who might, you
know, uh, do like a ct coronaryangio on them and then we can
see and and the lipid profileand see what's happening.
You know, and and that's youknow I forgot to mention in the

(26:20):
study of my heart attackpatients, most of them have a
cholesterol level less than 200.
Most of them have LDL levelsless than 100.
Maybe the average is about 105because of the omnivores who eat
some meat, so they spike it upa little bit and that's what we
want.
We want a little higher onesthere.
So that's also really, reallyinteresting.
We've also got a lot of them whoare already on statins, right,

(26:42):
the first heart attack, or theyhave diabetes and they've been
put on statins as per guidelinesand their levels are absolutely
okay.
You know, and these are theones the you know.
Another interesting part isthat the guidelines don't ask
you to do your lipid profileswhen you have a heart attack.
They don't.
They don't.
The guidelines don't say that.
You know you're supposed tostart them on statins, right,

(27:05):
it's a blanket rule that yougive them the loading dose,
which is obviously for the youknow, because you know
pleiotropic effect.
It has an anti-inflammatoryeffect at that moment, right,
and later on you're supposed tocontinue them on the statins.
And I asked my cardiologist whenwe were doing all of these
tests you know, like, like, thecholesterol levels are normal,

(27:26):
the lipids are normal.
Why do you want to keep them onstatins for forever?
Because that doesn't seem to bethe cause of the heart attack,
especially not the ones with thenormal ones, right.
But they can't help it becausethe guidelines say so when you
have vultures sitting outsideanywhere who can always
instigate the patient or, youknow, like you want, started on

(27:48):
statins, you know, is the doctortrying to kill you, it happens.
I've spoken to neurologists andthey're like.
At least a couple of them saidwe don't want to start our
stroke patients on high-dosestatins which can be harmful,
especially with the patients whohave diabetes.

Speaker 1 (28:11):
It's a very interesting situation where it's
almost like the patient isn'tstatining hard enough.
Why aren't you?

Speaker 2 (28:21):
statining hard enough , you've come in with your
second heart attack.

Speaker 1 (28:24):
You know, and they are, they're taking this
medication.
But it really speaks to thefact that the paradigm is
misunderstanding the true rootcause of these patients' illness
, Otherwise they wouldn't comein with another AMI.
And I'm reminded of a study, Ithink it was 2015.
I'll add it to the show notes,but I talked about it in a talk

(28:46):
I did at Regenerate in 23, sorry, 24, no 23.
And it was an analysis of about120,000 emergency and hospital
presentations with coronaryartery disease either ami or um
or coronary artery disease andthey measured the serum lipids
and the serum lipid levels.

(29:07):
Uh, over half of them were inthe normal range like in
inverted commas meaning againlike we're we're.
Are we missing something orwe're simply not looking at the
problem in the correct way?

Speaker 2 (29:20):
yeah, I think, I think that was the epic study or
something right 120, 130 000 uhpatients it was an
observational.

Speaker 1 (29:26):
Yeah, it was an observational cohort.

Speaker 2 (29:28):
Yeah, yeah, most of them were between 70 to 100 ldl
levels, and, and, and theconclusion was you need to bring
the LDL to less than 70.

Speaker 1 (29:37):
Yes exactly.

Speaker 2 (29:40):
I was like why is I mean you can't be chasing zero,
right?

Speaker 1 (29:47):
Well, that's what they want.
They want the apopoeia leveland the total cholesterol LDL to
be driven to zero in order toprevent this condition, so they
want the liver to stop working.

Speaker 2 (29:56):
basically.

Speaker 1 (29:57):
Yeah, and really I think both you and I what we're
saying is that this APOB-focused, ldl-focused paradigm of heart
attack prevention is failingpatients and it's kind of
missing the point here, and Ireally love it how you were
investigating a nutritionalaspect of it, and I previously
have talked about the way thatthe light and the light

(30:21):
environment is affecting it andis affecting the degree to which
the blood or the blood productsare liable to coagulate and
therefore clot over.
So have you ever measuredvitamin D?
Are you able to measure serumvitamin d?
Are you able to measure serumvitamin d when you do these
patients um initial?

Speaker 2 (30:42):
blood tests.
So not on these mi ones,because it's not in the research
protocol.
So, uh, we're not doing uhvitamin d in this, but, yeah, I
mean a lot of other physiciansdo get them done.
We're doing another reallyinteresting one, which is uh on
young adults with uh, no historyof diabetes, right?
So, uh, anybody coming from theage of 20 to 45 with the sugar

(31:03):
level a random sugar of 140 orabove, we're testing them for
their a1c's but what's that?

Speaker 1 (31:09):
in nano nanomoles?
A millimoles per liter, becausemy audience all right let me
just more of the metric.
And to clarify Ankur isreferring to the US unit of
lipids which is, I believe,deciliter, milligram per
deciliter.
Milligrams per deciliter.
In Australia and the UK we talkin millimoles per liter.

(31:33):
So, it's a different unit, allright.
Let me just uh 7.8 okay, yeah,so sorry, a random.
A random blood glucose above7.8?

(31:55):
Yeah, yeah.

Speaker 2 (32:01):
Yeah, yeah, and 45% of them turn out to be diabetic
and they didn't even know that.

Speaker 1 (32:11):
So it seems to me that there's this massive
iceberg of undiagnosed type 2diabetes and B12 deficiency,
hyperhobosy, cyst anemia,probably vitamin D deficiency as
well 100%, yeah, yeah, yeah,yeah 100%.
Talk about, because when Ivisited India, I noticed that
people were wearing long sleeves.
People wear long sleeves, longtrousers, people are avoiding

(32:32):
the sun.
Can you speak to people's sunexposure habits?

Speaker 2 (32:40):
It's really hot here.
You, you know when it gets hot,so people do want to cover up,
uh, you know, and we are nearthe equator, so uh, yeah, I mean
during during the summers, uh,or even during the winters, uh,
but uh, it depends on where youare actually.
I mean, if you're way up northin the hills and all you do want
to cover up, I mean if you goto the beach sides and all

(33:02):
people are actually wearingshort sleeves and stuff, but I
mean that's when they're on aholiday, right.
Or if you're living in Goa orKerala, people do get out a
little bit.
The metropolitan cities, I mean, you have your cars, you have
your houses, you have youroffices uh, you don't want to
actually come out.

(33:23):
And you know, unless and untilthe weather is nice, you know,
when it's a little breezy andstuff, people do actually try
and go out, but it's not, it'snot like a daily habit.
Uh, even for me it's reallydifficult because, you know, I
wake up at 7, leave at 7 30 forwork.
I don't wear sunglasses anymore, uh, to work.
And I've realized thedifference because you know, uh,
when I used to wear sunglassesto work, I would be yawning all

(33:44):
the way, uh, and then I realized, you know, the brain doesn't
know, or the brain is confused,that you know.
I just woke up and then it'sdark again.
Yeah, you know, uh, but since Istopped bedding into work, uh,
I feel energized.
You know, I wear the blue lightblockers in the evening so I
get my melatonin in time, so, soI, I do all of that and and

(34:06):
that's and it's really helpingme.
100 because I can, I can see mysleep, uh is, it's such a
beautiful sleep, right, becauseyou just passed out.
You have no idea what happened,even though you if, if you know
, if you're not that tiredduring the day, uh, if you don't
have major catabolism duringthe day, uh, the nights are like
, absolutely so serene, sopeaceful.

(34:27):
I mean, you know you getknocked out and you wake up on
time and and you're full ofenergy and you can do whatever
work you want to do uh in themorning.
So, yeah, I mean, uh, some ofthese habits actually do need to
get in uh to a lot of people inindia yeah, I, I strongly
suspect that.

Speaker 1 (34:46):
Um, and from from measuring my, in my clinical
practice, measuring people'svitamin d level, uh, again from
from michael professor michaelhollick's work on on-ranging
people in Africa, an ideal bloodrange is above 100 nanomoles
per liter.
125, which is, I believe that's40 nanograms per deciliter.

(35:11):
So most people aren't gettingnear that.
If they're just doingincidental exposure, meaning if
they're just taking off, rollingtheir sleeves up or wearing a
sword sheath shirt, no one'sgetting close to that ideal
vitamin d level.
So if people, unless you'reessentially taking your shirt
off and intentionally exposingyourself to the sun.

(35:32):
So I guess the reason why I'mbringing this up?
Because because from my pointof view I think this is an
intimate related aspect to thisatherosclerotic cardiovascular
disease, because if we'reunplugging from the sun and
patients aren't getting thesecritical light signals to
vasodilate, to regulate theircircadian function of their

(35:53):
cardiovascular system, thenthat's, that's just adding,
adding onto the problem.
And if, if we're addingcultural sun avoidance onto
cultural vegetarianism, it'slike it's like the ticking time
bomb yeah, yeah, absolutely man,yeah, you're absolutely correct
talk a little bit now about, um, like what can be done, because

(36:15):
you've obviously, you'reobviously uh identifying kind of
this problem.
Like what, what next?
What can you, what advice canyou give?
What, what are you doing?

Speaker 2 (36:25):
yeah.
So I mean, I have my own, uhside metabolic health practice,
right.
So, uh, getting a lot ofpatients through that and even
uh, on flow, uh, with myreal-time patients, we do give
them, uh, you know, a sort of arundown into nutrition or a
nutrition 101, and a lot of myteammates have actually started
to understand what what I'vebeen talking about, because

(36:47):
they're seeing it themselves andthey're all doing the research,
right, uh, it's, it's theirthesis.
So, uh, they're seeing thatwe're trying to get as many case
reports and case series becauseI think that's really important
.
A lot of people, you know, uh,you know just, uh, uh, don't
don't give importance to casereports and cases.
I think it's really importantbecause that's where the seed is

(37:08):
planted, that's where an ideais planted and that's where you
start.
That just opens the door intouh, what, what, what you're
looking at, you know, and andthen you see more of that
pattern happening, right, it'slike seeing the matrix, right.
So you know, a case report willlead to a case series.
A case series will lead to anobservational study.
That can lead to aninterventional study.

(37:30):
So people need to understandthat.
So we're doing so many differentstudies.
We're doing sarcopenia and diet.
We're doing urethra and renalcalculi and diet.
We're doing all the metabolicsyndromes coming.
That's, I think, my biggest one.
We're about to hit 11,000patients for that and then we're

(37:53):
going to sit down and analyzethat study.
So 11,000 patients have come inwith different diagnosis but
they all have comorbidconditions like diabetes,
hypertension, heart disease,strokes, alzheimer's cancers,
all of that.
You know their dietarypreferences.
That is like a 32-questiondietary questionnaire which has

(38:13):
everything sugars and alcoholand smoking and exercise and all
of that.

Speaker 1 (38:20):
Is that on presentation, like they come
into the department and theyfill out the form?

Speaker 2 (38:25):
Yeah, yeah, yeah, yeah, absolutely.
So we're doing that and so weget to talk to them.
You know, I mean heart attackpatients.
You know why do you thinkyou've had the heart attack?
Because nobody asks them thisquestion question and the
patients have stopped askingthis question.
Right, if they hit 40, 45, whydid I have a heart attack?
Uh, maybe a 20 or 30 year oldmight ask why did I have a heart

(38:48):
attack?
But they don't get the rightanswer.
Maybe it was cholesterol, youknow.
Maybe it was something that youate, but most of them eat what
doctors and and the dietaryguidelines want them to eat.
Right, and that's what theadvice is when they're giving I.
I remember I had this 25 yearold who came in with a stroke.
He had had two heart attackspreviously, age 25 incredible

(39:12):
age 25.
Yeah, he was on all themedications.
He was taking all hismedications on time, all of it,
right.
His lipid profile was clean,absolutely clean, right.
But his b12 was pathetic.

Speaker 1 (39:24):
His homocysteines were really high, pure
vegetarian and and maybe it's areally good point to mention
that we can't blame uh, familialhypercholesterolemia on these
really young ages of of uh ami,because that's uh, you know,
that's what, what can be areason, but this guy's lipid

(39:45):
profile is, as you said, it'scompletely in the normal range,
so we can't even thecardiologist can't even blame
that absolutely yeah and uh, andI mean the thing is that people
are not asking at least my team.

Speaker 2 (39:58):
I'm proud of my team because they've started asking
these questions.
I mean, they've started to havethese discussions with their
colleagues, their peers, youknow, junior residents or
academic residents and the otherconsultants.
And we need more doctorsactually questioning our own
practice, right, and we needmore doctors actually
questioning our own practice,right.
We need to understand andthere's something really nice

(40:20):
that I think Tom Cowan I hadheard him on a podcast who said
doctors have a thought disorder.
You know, once you've readsomething, we don't want to
relearn and unlearn, or unlearnand relearn things, right, and
we have this uh that thatwhatever we're saying is
absolutely right, it could beright.

(40:41):
I'm not saying that we'realways wrong, but uh, to
question ourselves and and thinkabout the pathophysiology, uh,
and and and relating that to uh,the way we live, I think is is
important for doctors to addressand uh, you know, uh, get
sorted.

Speaker 1 (40:58):
I've said this before , but I think the more
subspecialty training one does,the more convinced they are of
their correctness and theirposition and the more resistant
they are to changing.
And it's frustrating, but Ithink that seems to be the case.
Talk about your journey,because I guess you probably

(41:20):
wouldn't be doing this researchif you hadn't gone down this
path yourself.

Speaker 2 (41:25):
Yeah, absolutely.
I mean, everybody has a triggerpoint and because of that, I
actually feel that, you know,I'm trying to raise as much
awareness as possible so peopledon't wait for that trigger
point, because that triggerpoint just could be a cardiac
arrest and the family is likeyou know, this guy was healthy
and you didn't even know that hewas unhealthy, right?
Like I said, we're getting somany undiagnosed diabetic

(41:49):
patients who are young adults,right, and it's lucky for them
that they're coming into mydepartment and we're doing the
study and we're diagnosing themwith diabetes, so that something
is done about that.
Maybe they put on medications,you know, I mean, we do have a
discussion with them regardingthe diet, but then if they did
not come in and they were livingwith that undiagnosed diabetes,

(42:10):
they could have ended up with aheart attack and may not have
been able to be brought into myemergency on time, right?
So I don't want that.
I don't want people to havethose triggers.
My trigger was when I did mytest.
I just did my random routinetest in 2021.
I saw my triglycerides was 600.
And I knew something was wrongand I knew it was because of my

(42:32):
diet, but the thing was Ithought I was having the right
diet, which is a standard Indiandiet.
But I was always an omnivore,and a better omnivore than the
rest of India because I used tolove meat from the age of two.
I've heard stories of myselffrom my family, of you know how
they would cook a separate fullchicken for me and a separate

(42:52):
full chicken for the rest of thefamily.
You know that's how much Iloved it it.
But then obviouslycarbohydrates happen to all of
us and you know, and I callexogenous carbohydrates an
anti-nutrient along with therest of the list, right.
So all of that was there andobviously junk food and
everything happened duringcollege and post-college and you
know, I mean I still rememberwe used to have blue pepsis and
stuff and I'm like why anyways?

(43:14):
So we've done all of that,right.
And my triglycerol was 600.
So I cut down on my sugars.
It was an instant trigger forme.
I cut down my processed sugars,I cut down my intake of rice, I
brought it down, so it becamesort of like a low carb.
And then I read Robert Lustig'sMetabolical and that took me
down the rabbit hole, you know.
So I said triglyceride, why Ididn't even know about

(43:43):
triglyceride to htl ratio atthat time, because we were never
taught and none of the labsactually report that, right.
So then I realized mytriglyceride to htl ratio at
that time was 16.
Wow, right, yeah, eight timesmore than what it should be.
So probably taking time bomb, Idon't know, uh.
But uh, and so I went low carb.
I had been exercising for manyyears but obviously I used to
eat a lot, because my trainerstell me eat as much as you can,
eat as much as you want, becauseyou want to get the calories

(44:04):
back in, and you know.
And then exercise and you wantto burn it off and all of that,
you know, kiko brothers, uh.
And then I lost about 22, 23kgs, uh, but I still had
inflammation, because I've seenmy photographs from that time
because I'm still having alittle bit of carbs.
And then, uh, somebody sent mepaul saladino's, uh, carnivore

(44:26):
time reels.
I saw that I'm like this makessense to me and I had also cut
off red meat for the first fiveor six months because, you know,
I didn't know better.
Uh, but I was put on statins.
I was put on amlodipine for,for essential hypertension.
Yeah, essential yeah and uh, but.

(44:46):
But I stopped both of them atsix months and uh, once I went
down the whole rabbit hole, I, Iresearched, you know, uh,
everything out of it.
You know it's not like Ibelieve salarino at the first go
.
Or you know everything out ofit.
You know it's not like Ibelieve Saladino at the first go
.
Or you know, when I saw SeanBaker's podcast, I did my own
research.
I went and read all the books,all the papers that they were
citing.
I downloaded as many papers asI could got into it.

(45:08):
I actually asked my first yearPG residents to bring me their
biochemistry books, because, youknow, I don't know where mine
is.
And I started reading it again.
I, I'm like this makes so muchof sense, you know and it.
Well, why was first year ofmedical school not translated
into the final year of school?
You know, and uh and so, andthen I understood right and I

(45:29):
saw changes in my own health andmy family's health.
My uncle I reversed his 25years, 20 years of diabetes in
two months on carnival.
Uh, yeah, I mean, and I'm doing, I'm actually writing a case
report on that I reversed his 20years of diabetes in two months
on Carnivore.
Yeah, I mean, I'm actuallywriting a case report on that.
He's no more, unfortunately,because of the renal cell

(45:49):
carcinoma that he suffered from,because of uncontrolled
diabetes and the chronic kidneydisease that it leads to.
Right, so that's the mostimportant, or the major causes
of RCC, and this is somethingreally interesting that I really
have to tell you.
So I was having a conversationwith artificial intelligence,
you know, and I asked it what isthe most common cause of renal
cell carcinoma?
It said smoking, hypertensionand chronic kidney disease.

(46:09):
I said what if somebody doesn'tsmoke?
So it's hypertension andchronic kidney disease.
I'm like, what about diabetesin the like?
You know, textbooks don'tmention diabetes.
I said, yeah, but then what isthe most common cause of chronic
kidney disease?
And it said I see where you'regoing.
Of course it's.
It's diabetes, you know, andthat's, that's a critical
pathophysiology.
I said what about a diabeticdiet which is actually

(46:30):
prescribed?
And it actually said, yeah,diabetic diet has a lot of
carbohydrates which can actuallyworsen your diabetes.
And you know, it went the waythat.
I don't know, I wanted it to go, but you know, the conversation
was so interesting and finallyit gave me a whole flow chart of
diabetes, insulin resistanceand diabetic diet, 230 grams of

(46:52):
carbs, worsening insulinresistance, hypertension,
chronic kidney disease andfinally, renal cell carcinoma.
But that was nice.
So, yeah, I saw that he was onmultiple medications, changed so
many times over the past 20years.
I went through all his records.
He was always given thediabetic diet and once he was

(47:15):
told that you know, he needs togo into insulin and dialysis,
which he did not want, I put himon carnivore and two months his
doctor actually wrote downrecovered from diabetes and
hypertension, does not requireany more medications.
Wow, this took 20 years to do.

Speaker 1 (47:32):
Incredible.
It's stark, this contrast ofstandard Australian living or
standard Indian living, standardAmerican living, compared to
when you put patients back in anenvironment, and back into a
food environment that isancestrally appropriate.
What does a carnivore diet looklike in India?

(47:52):
Is it something that'saccessible to most people?
Is it?
Something that's accessible tomost people?
Is it something that people caneat or is it expensive?
Like talk about that.

Speaker 2 (48:05):
Yeah, I've had.
See, it's accessible.
We get mutton everywhere, whichis good, right.
We get beef in some of thestates in the south of India,
above Maharashtra and above.
You get a lot of buffalo meatwhich is equally nutrient-dense
as beef.
You get a lot of mutton, whichis really, really nutrient-dense

(48:26):
and has a lot of other aminoacids.
You get seafood.
You get chicken.
There are a lot ofpasture-raised chicken and goats
, especially the goats.
The mutton is pasture-raised.
You get a lot of eggs, right,so it's it's not difficult to
source.
The only thing is that indiaeats very less.
We eat like five kgs per personper year.

(48:47):
That's the average, which isinsane.
It used to be 3.5, so, yeah,it's increased a little bit in
the past couple of years andit's very easily accessible,
right, so you can do easily doeggs, pork, uh, chicken, mutton,
seafood five of them differentcombinations.
Uh, we do use some spices, uh,for indian cooking, that's okay,

(49:08):
I think, for the for the palate.
Yes, some of them have oxalate,so I I tell my clients to avoid
those, like you know, uh,turmeric or cinnamon or cloves
or black pepper and stuff.
But you know, just completelygo into.
You know the continental style,you know, just the steak and or
grilling gets a littledifficult for the Indian palate.
But you know, as long as youcan do mix and match, it's

(49:30):
absolutely fine.
I mean, you know, you, you, youhave so many options for eggs.
There's so many options forgoat, you know, you can grill it
, roast it, cook it in ghee orsomething.
So many options for eggs.
There's so many options forgoat, you know, you can grill it
, roast it, cook it in ghee orsomething.
So many options for pork youknow we've got pigry farms like
110 year old, 110 years old overhere and they have fantastic
pork.

(49:51):
So we do that and, and it's notexpensive, because I tried this
with one of my ward boys, youknow he came in with an HBA1CF11
to me and I put him onCarnivore and you know he was
doing fish, mutton and eggs andbrought it down to about 5, 5.5
in about one and a half monthsor something like that, and he's

(50:12):
sustaining it.
Yeah, doesn't earn as much as Ido.

Speaker 1 (50:20):
What's the access to?
To like dairy and and likedairy products.
What oils are people using likemostly, and what can they use?

Speaker 2 (50:25):
yes, a lot of people use ghee clarified butter
clarified butter, yeah, uh, butagain, uh, refined oils has
actually come in and, uh, a lotof people use refined oils.
But another one that's reallyrampantly used in India, which I
don't mind, is mustard oil,cold pressed mustard oil that
doesn't have omega-6, it hasomega-9 aerosol.

(50:46):
Very little research on that,right.
I think they've done someresearch on rats, where they
give them, like you know,massive doses and obviously
things happen to the rat.
So you know they've banned itin, which doesn't make sense,
because in india we've we'veused mustard oil for generations
and generations.
You know, I don't see itcausing much damage and I

(51:07):
basically use butter, lard,tallow, ghee, virgin coconut and
virgin mustard there you Canyou speak to the cultural
practices with respect to theconsumption of beef?
Yeah, I mean that's acontroversial topic in India,

(51:29):
but yeah, a lot of South India,a lot of South India actually
eats a lot of beef, and I'veread a few historical books
where it's mentioned that a lotof the religion uh, the
religious priests and andbrahmins used to eat a lot of
beef, and this has beendocumented by swami vivekananda

(51:49):
and br mbedkar in their books.
And you know, we have a verystrong caste system in india
from ages, right.
So you have the topmost andthen you have the brahmins, and
then you have the untouchables,right?
So apparently everybody used toeat beef and once the Brahmins
got to know that theuntouchables also eat beef, they
made it a sin to eat it.
So, yeah, I mean, people havetheir own beliefs and to each

(52:13):
his or her own.
I'm not advocating it foranybody.

Speaker 1 (52:20):
That's what I was getting at, because my
understanding is that obviouslyHinduism, the consumption of
beef is not common.
But if you dig back into theVedic texts and the old a couple
of thousand years back, it wasa thing that was done meat
consumption.
So somewhere along the lineit's been a social taboo to eat,
to consume beef.
But but historically, uh, itwasn't necessarily the case.

Speaker 2 (52:44):
Yeah, yeah, I've been reading that.
Uh, I think one of the I thinkit was a rig veda.
I'm not a scholar, but I meanI've read the translations and
stuff and uh it says that uh,the beef is so sacred that you
should feed it to the sacredguests.

Speaker 1 (53:00):
Well, I mean everyone's sacred, everyone
deserves to eat beef.
But understandable, it soundslike, even if I mean it's a big
jump to go to say consume it ifyou haven't for your whole life
and your parents didn't.
But it sounds like there's lotsof other options for people.
Yeah, yeah, yeah absolutely so.

Speaker 2 (53:17):
I mean, I think mutton is really.
It's great and you know you getminced ones.
There's a really nice recipethat we do, where it's just a
mutton curry and we put mincedmeat and boiled eggs inside and
just put in the slow cooker andit turns out absolutely
fantastic.
You should try that out withbeef, if you want.

Speaker 1 (53:34):
Yeah, you're making me hungry just talking about it,
but let's so.
It sounds like these changesthat you've made individually.
Now you're doing the researchin your emergency department.
You're educating some of yourcolleagues and your juniors how
do they feel when youessentially take the data and
you shove it in front of theirface about these characteristics

(53:58):
of people having heart attack.
And it's nothing like this diet, heart hypothesis or the lipid
hypothesis that you know you andI were taught in medical school
.

Speaker 2 (54:07):
I think that is a diet heart hypothesis that needs
to be rewritten.
Right, yeah, you eat the rightfoods and get your B12 up and
reduce your homocysteine levels,get your cholesterols up, get
your LDL levels up, you knowyou'll have good immunity.
Another thing that people don'trealize we missed on that
cholesterol is an importantprecursor for the insulin

(54:32):
receptors, right?
So the lipid rafts and all ofthat and I mean mean, if you're
bringing down your cholesterollevels and you already have
diabetes, it's only going toworsen your insulin resistance.
So I think there is adiet-heart hypothesis, but the
only thing is that they've gotit the other way around.

Speaker 1 (54:48):
That can be looked into right.
Yeah, and seafood too, and theomega-3 fatty acids from
marine-derived foods isenormously beneficial for
reduction in cardiovascular riskand it makes sense because of
its effect on clotting andcoagulation.

(55:09):
Absolutely so people arechanging things, I guess.
At least you're raising themessage.
I think you're showing peoplewhat's possible.
So how is your message goingdown with your private clients?
Are a lot of people adoptingsome of these techniques?

Speaker 2 (55:31):
Yeah.
So first my team Not all ofthem are adopting these
techniques.
My HOD did and he's reversedhis hypertension and prediabetes
, so he's doing really well.
Some of my juniors they'rewaiting for the right time.
Probably they're waiting fortheir trigger.
I've shown them their MRIs andthe visceral fat that they have

(55:55):
and the sarcopenia that theyhave around their abdomen, so
maybe that triggers some of them.
But most of them have startedeating more animal-based and
they're doing the same.
I mean, they're preaching thesame to their patients.
A lot of my other colleagues,you know the senior consultants,
were there neurologists,cardiologists, pulmonologists.

(56:17):
They've seen the differencebecause you know, I've been
working with them for the past10 years and they've seen me
change right and, uh, they knowwhat I'm doing is right.
They can't say what I'm doingis wrong because you know I I
look fitter than them.
Uh, you know yeah yeah, so, yeah, I mean, uh, and and if, if I

(56:38):
raise a question, it's going tobe a valid question, right, so,
uh, nobody can come after me forthat, uh, because, because
they're not raising thequestions themselves, right, so,
yeah, uh, that that's, that'ssomething that's really
interesting.
And my clients yeah, I mean alot of them are actually doing
this really really well.
Uh, some of them see the magicwith the weight loss that
happens in the first 10 days.
Right, that's way, what a waythat goes.

(57:00):
And you know, there's just more.
I think it's it's a good thingthat that that happens because
of the insulin sensitivitycreeping back in, because it
gives them more motivation.
Uh, if they see that right, and, and you know, I've reversed,
they've reversed their diabetesor high uric acid levels,
vitriol deficiencies,infertility, pcos you know I had

(57:24):
a patient who was advised IVFat the age of 29.
And you know, in two months ofcarnivore, she actually
conceived and is now a mother ofa seven-month-old baby.
So you know, things like thatNon-alcoholic, fatty liver,
hypothyroid, hashimoto's,rheumatoid psoriasis all of
these are doing fantastic rightnow.

(57:45):
I know I've had a fewvegetarians actually convert
into carnivore, yeah, so, again,I mean they needed triggers.
So both of them actually endedup with autoimmune rheumatoid
arthritis.
And ended up with autoimmunerheumatoid arthritis.
And you know, one of them wason methotrexate and was bearing
all the side effects and she hada baby and you know she wanted
to hold a baby for the rest ofher life, properly, you know, uh

(58:07):
, so she's turned carnivore.
And another friend of mine whowas a vegetarian, uh, she's been
diagnosed with rheumatoidarthritis.
So, yeah, she's done, she's,she's transitioning right.
So she's doing two meals animaland one meal, uh, still a
little bit of carbs and veggies.
So I'm going to wean her offthat slowly because, uh, she's
she's eaten vegetarian all herlife for the last 40 years.

(58:28):
So, yeah, it's gonna take sometime, but yeah, I mean, at least
at least they got motivatedenough.
Everybody wants that trigger.
So, yeah, my patients are doingquite well.
There are some who are stillwaiting for the right time to
actually start off, uh, andthey've understood everything.
Yeah, and we have this fastinggroup going on.
Uh, my carnivore consult,thursday fast, so we do like a
24 hour fast together.

(58:48):
Uh, it's a smaller community,so you know anybody who does
carnivore consistently with withus for like four or five or six
months and the same results.
I add them onto my uh fastinggroup.
Uh, so you know there's thatbonding and uh community
development over there, so so,yeah, it's a start.
Uh, let's see where it goes.

Speaker 1 (59:07):
My website's coming up soon, hopefully, so working
on that, so a few things goingon here the thing we didn't talk
about was this role ofepicardial fat in terms of the
pathophysiology ofatherosclerosis and
atherosclerotic cardiovasculardisease, and what I mean by that
is, if we take a scan of theheart usually the best modality

(59:32):
is MRI you can see that there'sthis ectopic fat, this fat that
shouldn't be there, you knowaround the artery and it's
sitting right next to thecoronary arteries and it's
releasing all this inflammatorycytokines which are going to be
provoking endothelialdysfunction and right there next

(59:53):
to them and also, you know,atrial fibrillation and other
kinds of cardiac dysfunction.
So are you, are you able tomeasure that?

Speaker 2 (01:00:01):
or I guess not necessarily on the patients that
come in um and with it no, notall of them I'll show you
something that's a ct oh yeah ofa trauma patient that came in.
So so you can see the amount ofvisceral fat here, right.
Yeah the abdomen's just packedwith it.
Yeah, yeah, so we do this andthen you know, when we do this

(01:00:23):
and apparently the patient doesnot have any comorbid conditions
yet.
But I think having this is amajor comorbid condition and
maybe over the next few yearshe'll end up with maybe diabetes
or heart disease or fatty liveror whatever you know, maybe an
MI, we don't know diabetes orheart disease or fatty liver or
whatever you know, maybe an mi,we don't know, uh.
So yeah, and, and when we seethis, we go and talk to our
patients.

(01:00:43):
You know, there's a lot of fatinside you, you see, and if you
see the whole city, he doesn'thave too much of subcutaneous
fat.
Uh, he's, he's like a basictoffee, uh, but but you can
still make out that he's goingto have some visceral fat inside
and then the scan proves thathe doesn't have epicardial fat
right now.
But yeah, I mean, if hecontinues the way, he's an auto
driver, he eats mostlyvegetarian, a lot of

(01:01:06):
carbohydrates, so we try andcounsel as many people as
possible, you know, and showingthem fat.
He's not educated, so it'sgoing to be very difficult for
him to actually understand, butthen a lot of people who are
educated also refuse tounderstand.

Speaker 1 (01:01:24):
Yeah exactly Ankur?
What research projects do youhave coming up?
Because, yeah, I want to knowwhat topics are you specifically
looking into or how are youlooking into?
Into this more?

Speaker 2 (01:01:39):
yeah, so we're doing a lot uh, like I mentioned
before, uh, you know, we'redoing uh geriatric falls with
fractures and sarcopenia anddiet right.
Uh, we're doing uh erythriticalkali with diet.
We're doing, uh we're going tostart uh cholelithiasis, which
is is gallbladder stones andtheir association with what
people are eating.
We're doing this big metabolicsyndrome and nutritional

(01:02:03):
association of about 11,000patients.
That's going on.
We're doing our heart attackpatients.
That's going on.
We're doing diabetes undiagnoseddiabetes in young adults and
got a few more.
We're doing non-alcoholic fattyliver and association with the
dietary preferences and whatelse.

(01:02:28):
Yeah, I think we're doing thatand we're going to start
probably when the new batchcomes in.
I'm going to do something withdysrhythmias, atrial
fibrillation and B12 and stuff.
Why?
Because, or maybe try and getscans done, if the ethics
committee actually allows us, sothat you know a lot of people
with atrial fibrillations haveepicardial adipose tissue, right

(01:02:51):
, and that's the fact which isthe trigger for the different
pathways.
And you know we go and do aradio ablation and burn that fat
off to stop it, right.
I mean, what if you just reducethe epicardial fat with the
right diet and the exercise andall the protocols and patients
don't have AF again?
Because you know they put onmedication, they put on calcium

(01:03:11):
channel blockers and stuff.
You know all of that.
So, but they still keep havingrecurrent episodes, right,
they're coming into theemergency and then you go to
anticoagulate them and they endup bleeding in the brain or
upper GI bleeds and so manycomplications Keep checking
their INRs to see if they're intheropuses or not, and you know
it's so painful even for thepatient, right?

Speaker 1 (01:03:34):
It's so painfully preventable.
As you say, they just repeatcustomers of their cardiologist.
They come in, they get anotherablation which attempts to
remove this pathological tractof cardiac wiring.

(01:03:55):
If they made these lifestylechanges then they could
potentially reduce that fat andbe less likely to go into this
malignant or pathological rhythm.
Absolutely.
I guess, my interest, like Isaid earlier, is that I would
really love to see a vitamin Dlevel on all these patients.
I'd like to, because that testis a really good proxy for

(01:04:17):
essentially total sun exposure.
It can be done on blood spots,so I don't know, maybe if that
might be a cheaper way of doingit, but to collect information
about sun exposure habits aswell.
Like I don't know if you knowabout the Pellylinquist Melanoma
in Southern Sweden cohort study.
That was like a 20-year studylooking at all-cause mortality

(01:04:37):
and they just asked I mean, itwas a more in-depth question,
but they just had four questionsabout sun-seeking behavior,
like sunbathing, and they wereable to show a dose response
between all-cause mortality andactual clotting, blood clotting
and I believe it kind of asksfor mortality too, with respect

(01:04:59):
to the most to the least sunexposure.
So I have a personal thoughtthat those of your patients who
are office workers, it workersand the more vitamin deficient,
more sun avoidant I think, themore likely they are to have
these problems.

Speaker 2 (01:05:19):
I'm sure they are.
I mean, we've got some profilesthat we run on some patients
who go into the IPDs right, andthat profile has vitamin Ds and
100% of them are deficientunless and until they're
supplementing.

Speaker 1 (01:05:36):
Yes, yeah, yeah, yeah .
Well, it's a massive tsunami ofdisease that you're fighting.
It sounds like initially withone hand, but now you've got
some team members on board.
So, yeah, I want tocongratulate you for all the
work you're doing and, yeah, Imean, I don't think it's more

(01:05:57):
important work that could bedone right now for the health of
the people in India.
So, yeah, well done.

Speaker 2 (01:06:04):
Yeah, thanks a lot, man Max.
It's important to raiseawareness regarding this and we
need to understand that.
You know, we became doctors toactually cure people, not to
make them sick.
It's not our intention to makethem sick, but then it's
important for us to realize thatwe're not doing what we

(01:06:24):
actually went out to do and thisis the way to do it.
You've got to get them rightthrough the right interventions,
and medicine is not one of them.

Speaker 1 (01:06:36):
Absolutely.
It's this sad state that, youknow, our colleagues, have we
become, uh, you know, justobservers of managed decline?
It's a managed decline of ofhealth and chronic disease, and
and that's definitely not whatyou or I signed up for.
So, yeah, um, fantastic work.
Where can people find you,follow you, you contact you?

Speaker 2 (01:06:58):
Yeah, I mean, I'm on Instagram and I go by the name
of thecarnivoreep.
Ep stands for emergencyphysician, so I'm there.
My podcast is on Spotify andApple.
It's called the Desi EM Projectand the same website is going
to be launched soon.
So yeah, fingers crossed, thathappens quick.
I am on X, not very active, butI'm on X.
That's A-N-K-S-V-2-5.

(01:07:21):
That's AnxV25 on X, I think.
Yeah, I mean, if people areprofessional and get onto
LinkedIn, so you'll find methere.

Speaker 1 (01:07:30):
Amazing and Facebook.
Everybody has Facebook yeah,great, great Well, thanks very
much An much, anchor.
Thank you for your time.
I really appreciate the chatright.

Speaker 2 (01:07:41):
Thanks a lot, man max .
It was a pleasure having uhcoming onto your show.

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