Diet Doctor Podcast #29 — Dr. Spencer Nadolsky, DO

September 26, 2019 0 By Ronny Jaskolski


Welcome back to the Diet Doctor podcast
with Dr. Bret Scher. Today, I’m joined
by doctor Spencer Nadolsky. Dr. Nadolsky is board-certified
in family medicine and obesity medicine, but as you’ll hear, also has a great deal
of experience and interest in lifestyle medicine. He was a division one wrestler; he has spent a lot of time learning
about exercise physiology and wanting to take that knowledge and help people improve their life
and their heatlh with lifestyle. And he got a little flack for this it sounds
like in his medical training, which is really interesting,
and we’ll get into that. But he also has specific interests
in weight loss and in lipidology. And he’s not the typical low-carb person. In fact, he is frequently thought of
as anti-low-carb, but as you’ll hear in our discussion today,
he really has an open mind and that’s one of the reasons
why I wanted him on this show. Because it’s good to get
different perspectives. He’s going to give you
a different perspective on lipids than you hear in the low-carb community. He’s going to give you a different
perspective about calories and insulin and the carbohydrate model than
you usually get in the low-carb circles. But he also has an open mind and he realizes there’s a place
for different treatments and different tools, and that’s one of the things I hope
you’ll appreciate about him. Not all of you may agree
with everything he says, but I hope you’ll appreciate his approach. And more importantly,
he’s interested in learning more and he wants to help foster more studies so we can learn more about LDL
and hyper responders and is it a problem or is it not. Because we can talk hypothetically
all we want. What we need is that data and Dr. Nadolsky is someone who’s trying
to be on that frontline to help us get there. So, I hope you enjoy this exploration
of some different ideas, and I hope you enjoy Dr. Nadolsky’s
open mind and his approach. So, sit back and enjoy this interview, and if you want to learn more,
you can go to DietDoctor.com, you can see the full transcripts, and of course access all the different
information we have on DietDoctor.com. Dr. Spencer Nadolsky,
welcome to the Diet Doctor podcast, thanks so much for joining me. Thanks for having me,
it’s good to be local. Is it not great that you’re a local and you’re able to stop by
for an interview today? A true pleasure. Now, you have a really interesting
background that I want to get into so people can learn about you and what
brought you to this point of your career. So, tell us a little bit
about after medical school, what happened to you, where did you go,
what did you do, tell us about your training. Yeah, I want to back up
before medical school because the exercise science
and nutrition science are actually what got me into athletics. My dad was a wrestling coach,
football coach, brother was a really good wrestler
as well in college. We used science to get good at athletics. And so, the thing was
I didn’t feel much fulfillment out of helping people
get better performance. I really wanted to use that science for
the betterment of the general population to reverse or prevent, cure if you want
to say, chronic disease. So, I went to medical school
with that thinking. I wasn’t sure if I was going
to do endocrinology or some sort of preventive medicine
or family or internal medicine, but eventually after medical school,
I decided on family medicine. So, I went into training at VCU
over in Virginia with a real focus on nutrition, exercise,
and lifestyle medicine, with a good combination of pharmacology
and everything like that to combine it, to really hone in on helping
prevent/cure chronic disease. Yeah, so actually, you’re right. We should start well before medical school
and even before college, because you were sort of a champion
wrestler and football player and not just your average athlete. I mean, you were sort of state champion
or something. Yeah, and the story behind that is
my brother was good all throughout high school. I came in and I didn’t actually start– he was like five foot nothing
when he was a freshman. He’s now like five five. I was like five ten, now I’m like six two, I had to really grow into my body
whereas he was a little bit stockier. He was like a four-time state finalist,
two-time state champ. I didn’t even start in my freshman year. So, I had to really look into nutrition
and exercise science to build muscle,
improve my performance to get good. So, then once I became a state champ,
really thought this is cool, but then again,
wanted to use that information, just to give a fraction of it
to the general population because that’s how you really prevent
and cure chronic disease. Yeah, so you came into medical school
thinking prevention, thinking I’m going to help people
with lifestyle, which is really kind of the opposite
of what most people come in with. And I think if a lot of people
come in with that, it’s probably beat out of them
during the course of their training, because you don’t get a lot of it
and you’re inundated with pharmacology, you’re inundated with these rare diseases and we don’t talk enough
about exercise and nutrition. So, did you find it hard, like it was lacking
as you were going through the schooling? Yeah, medical school, you know, everybody jokes about doctors don’t learn
much about nutrition in medical school. It’s actually true. I mean, you know, when you go through
medical school, you’ll see in the guidelines, yes it’s number one, lifestyle is number one,
but anyway, let’s learn about the drugs. So, and it wasn’t so much medical school,
but it was during residency, there was actually a time when
one of my advisors said they thought that I was a bit overzealous
about nutrition with my patients. Really? And my response was… this is an intern. And I said, you know what,
I’m not overzealous, you’re under zealous. Wow, you said that as an intern? Yeah, and you know what,
it’s kind of funny but I became the intern of the year and by the end of graduating
medical school, they said you know what, I’m really sorry, you were right,
I was wrong. And actually became a champion
for pushing lifestyle as medicine. And I think, you know, it is…
it’s really important. It’s starting to become more common
in medical school, you’re starting to see
all these programs out there. I know we can get into the new ones
of what types of nutrition they’re pushing. But at least it’s becoming
more mainstream now. Right, so, when we talk about lifestyle… I mean, there’s a whole bunch
of different pillars of lifestyle, with the main tune though being
with nutrition and exercise. So, let’s talk about exercise.
You’re the Doc Who Lifts, right? That’s your nickname, the Doc Who Lifts. So, so much of what we hear lately
is that you can’t outrun a bad diet. Exercise is not the path to weight loss. Nutrition first and it’s not
about exercising more. So, exercise has sort of been knocked down in terms of its place
and lifestyle in some circles. Now, personally, I have a problem with that because I think it’s important
and I’m sure you do as well. So, give us your thoughts about that.
Is it true you can’t outrun a bad diet? What is the place of exercise
in health and weight loss in your mind? There’s still a very strong place. And the exercise physiologists,
when you go to these obesity conferences, I go to the obesity week
where everybody has the obesity society and then the surgeons
and everybody in between. So, the exercise physiologist kind of pushed
back and it’s like wait a second, no. Exercise does have its place. The problem is if you don’t take
into account the nutrition, it’s really hard to outrun
or out-exercise a bad diet because of the compensatory mechanisms
of our appetite and everything like that. But if you have just a little bit
of nutrition going for you, the exercise can very much optimize your
body composition and weight loss efforts. Most importantly though, the energy gap
after you lose weight using nutrition… really bringing your physical activity back, we’re starting to see a lot of the data that
show that those who keep the weight off are the ones who are most physically active
because of that energy gap difference. Interesting, yeah. And when we talk
about exercise, there’s really… I guess three different kinds
that people talk about now. There’s the high intensity interval training,
the resistance training, and then there’s the slow steady distance
or sort of the zone two training. Now, do you have a favorite
for weight loss? Do you have a favorite
for metabolic health? Do you have a favorite for general health,
or what’s your general approach for those? Well, we have the weight-lifting zealots. I’m a little bit of a meat head myself,
so of course I love lifting weights. But I would be wrong to say
that’s the only way to do it. Ideally – and you’re a cardiologist,
so you’d appreciate this – I think you know, the synergy between angiotensin
receptor blocker or ACE inhibitor and then like a thiazide together, I think of like aerobic training and resistance
training is like a good combination medicine. So, ideally, a combination of all of it. You’re not going to be able
to recover every day if you’re doing high intensity interval
training and lifting. So, ideally, you’d have some steady state
in there to help with recovery. It could be very good for endothelial
function and everything like that and just being able to recover
while burning more calories as well, just from a weight loss standpoint. Yeah, so, it’s a good analogy,
the two drugs. So, the two drugs you were talking about they work better together
than they do individually. That’s a good analogy with the exercise,
that they do work better together. Now, some people though,
they haven’t exercised at all, right. They’ve been overweight their whole life,
they’ve been fairly sedentary. And just the thought
of high intensity interval training, it’s like oh my God,
how do I even get started, or resistance training,
what do I even do? So, how do you help people
get over that initial hurdle to sort of help them get started
to help them help themselves? I actually went to the gym
with my patients and that seemed to have helped them
overcome that thought of fear and it’s like nobody really cares. You’re at the gym,
you just got to get in and get out. So, people are scared of weights. They don’t know what they’re doing,
if they have good form, they think people
are going to make fun of them. And so, actually going with them
helped a lot and that’s I actually think
having a gym clinic would be ideal, so if you have your preventative
cardiology clinic. You could have
your cardiac rehab but actually having a gym with that clinic,
I think, would be perfect. But it is tough to get over. That’s fantastic that you’re able
to go to the gym with your patients. And I remember when I was doing
my preventative cardiology fellowship, I would have my office visits,
walking the track. Yeah, that’s great. I love that. It’s such a better way
to interact with the patients. And sort of help them in the gym,
even more important. But you know form, you know weightlifting. Most doctors don’t, let’s be honest. Most doctors have no clue
where to get started. So, I think the key is working
with a professional, finding somebody who can really help you
get started. It doesn’t have to be the diet. You can get a good strength coach
or whatever to work with but just understanding that resistance
training, any type of activity
is going to help the patient. Yeah, and one of the worst things
that can happen though is that someone starts and gets injured and says this is not for me,
I’m never going to try it again. Yeah, they feel like
it’s punishment, whatever. You want to get them in
and not feeling too bad at the beginning. Yeah, and what about people
who just like hate exercise? There are some people out there
who just hate it, they don’t like the way it feels,
they’ve never done it before. How do you help them sort of
psychologically to get over that hurdle to start exercising and sort of convince
them that this is a big part of their health? Somehow finding any physical activity
that they enjoy, whether it’s hiking. You know, ideally get everybody
to get to working out, doing some planks, bench press, but not
everybody is going to do that, you know. I’m not silly to think
that everybody can do that. So, any type of physical activity,
you know. If it’s dancing, whatever,
somehow– getting a bike, going for walks, anything will do. Yeah, it’s an interesting
sort of hierarchy. More physical activity, then sort of the zone
two aerobic, cardiovascular exercise, then the resistance training then
the high intensity interval training, like taking them step-wise through
in a safe manner and sort of educating them
about how each one impacts their health. Yeah, yeah, yeah. Now, you have mentioned a couple
of times with exercise the calorie balance… maintaining the calorie deficit. So again, there are two schools of thought. There’s the calorie in calorie out model,
there’s the carbohydrate insulin model. So, the calorie in, calorie out
is about energy balance. All you have to do is expend
more calories than you take in, whereas the carbohydrate insulin model
says not so fast, it has more to do with the type of calories. Paint it as a black and white picture.
What’s your take on that? So, actually throughout medical school,
worked with big time low-carb doctors now, you know, Dr. Phinney, Dr. Westman. Yeah, two of the best. And many more. So, as I came through that lens,
I then became a little skeptical because I started having patients
who would come in and saying, I basically ate a low fat high carb diet
and lost 100 pounds. And I was like, gosh, that doesn’t seem
to make sense according to, you know,
basically what I learned. And the whole insulin carbohydrate
hypothesis made sense, because in medical school
we learn that insulin is anabolic, because if it’s high you’re building fat. But then as I started getting more
into the path of physiology and you start becoming insulin resistant
and lipolytic because the insulin is not even working,
etc, etc. and then having some of these patients that
were losing weight on a high carbohydrate, low-fat,
vegan type of diet. And it was like, okay, maybe there’s more
to it getting more into the science. I became good friends with Kevin Hall,
you probably know who he is. And a lot of these other scientists. And so, the way I view it
is that the hormonal hypothesis is… those are very important because those can
tell you where you store your energy, and also not only that but maybe changes in appetite and inflammation
and things like that. So, it’s very important and it goes along with the calories in,
calories out energy balance hypothesis, so… I kind of view them as together
and you can’t separate them, because obviously you can’t give somebody
100% fruit juice… yeah, sure if they drink 800 calories
of apple juice a day, they’re going to lose weight,
but how are they going to maintain that? They’re going to feel
miserable type of thing, so that’s where my stance is right now. You brought up a lot of topics
we need to unpack there, so
one is the short term versus the long term? And anybody can lose weight on a calorie
deficit high carb diet for the short term, and the questions are what does it do to
your metabolism and what does it do
for long-term weight loss. And I don’t know that we have great data
to support that, you know. When you compare low-carb
versus low fat diets for weight loss, the low-carb diets uniformly work better
at six months and 12 months and a lot of the studies,
the curves kind converge and compliance goes down. And it makes it really hard to know
scientifically what the right answer is. Right, I think a lot of it also is
with our current environment, my personal bias is that it would be easier
to stick with a low carbohydrate diet, because if somebody
is saying eat whole grains, you know. I have a box of cookie crisps that I just
bought like for dessert purposes, like if I needed a little sugar fix
once in a while. A cookie crisp but it’s a children’s cereal. It has whole grains, 10 g of whole grains
per serving and it’s like… I wouldn’t give my daughter this cookie
crisp cereal for breakfast every single day. It would be easier just to say,
hey, go to a low-carb diet then get that completely out of your vision
anyway. So, that’s why I do think that a low-carb diet
in this current environment is easier to stick to, that’s what I think. -Yeah and controlling cravings.
-Right. I would agree with you completely. There are some people who can do well
on a low fat, higher carbohydrate diet, and they’re not the people
with addictive personalities and cravings and they’re not… somehow, they’re able
to control their hunger. That’s not everybody. There’s a large population out there
who need to control their cravings. So, do you find that on the low-carb diet
that cravings are better controlled? Yeah, so, this is
when I get into Twitter things… when I say
high carbohydrate to patients, they’re not getting like legumes and
like lentils in their like form, you know. In their whole form. They’re going out and getting French fries
and potatoes and cereals, pastas, breads. And it’s just hard to control this. I mean, I don’t need to control
my caloric intake but like, if I tried to cut back on some
of those things, it would be tough to do. So I do find that completely cutting those
things out and going to a low-carb. At the most, your carbohydrate may be
some more fibrous fruit at the highest, but vegetables, it just completely cuts out
their cravings and things like that. Yeah, yeah. And then, the next concept
is that of insulin resistance and talking about insulin resistance
and hyperinsulinemia, they frequently get combined together,
but sometimes they’re two different things. I think that’s really interesting because those people who do eat
a higher carbohydrate vegan diet can be having trouble still
with hyperinsulinemia. Whereas with the low-carb diet, you mentioned
there is some insulin resistance there. But I think we need to sort of differentiate
the insulin resistance with hyperinsulinemia, so the generalized insulin resistance
versus the more localized insulin resistance like the muscle level
with still lower insulin levels. So, do you differentiate in your patients
with those and kind of look for that? Yeah, so anybody that has any signs
of hyperinsulinemia and insulin resistance, regardless… I’m trying to help them lose
weight in any way possible, so like looking at the path of physiology of having the ectopic fat in your pancreas
and all over the place. Any type of weight loss. But, again, I tend to find that, you know, most of the time, they’re just getting
too many calories from things like croissants, donuts,
which are high in carbs and fat. So, going to a lower carb diet
tends to cut those things out anyway. They’re usually not replacing
those things with like lentils as I said. So, I tend to try to go
for weight loss in general. I do use weight loss drugs if needed if I find that they’ve tried multiple times
and that they haven’t passed. So, I have my obesity certification
everything like that, so I do use things like GLP1 agonists,
you know. If they’ve tried multiple times, for some
reason their appetite and cravings, even on like ketogenic type of diets,
but I do use those in general. I try to get them to cut calories, but they tend to be more of those
hyperpalatable high carbohydrate foods. Yeah, so, let’s talk about specifically
a ketogenic diet, right. There’s low-carb
and then there’s ketogenic. So, you know, in people who need
weight loss and who are struggling with it. And before you got o weight loss drugs,
will you sort of try a ketogenic diet, or does it sort of depend
on the circumstance? Yeah, I try, and pretty much
I get a good diet history on them. Most of the time, they’ve tried Atkins
in the past and maybe it wasn’t very well developed
or anything, like formulated. Most people have tried Weight Watchers
in the past, counting calories. Once they’ve come to me, a weight loss
doctor, they’ve tried multiple things. So, yeah, I do tell them like
a well-formulated ketogenic diet can be therapeutic in appetite regulations,
similarly to these drugs that we use. So, if they’re willing to do that,
we definitely do that. Sometimes people just
aren’t willing to do it, and I especially like the Virta studies; if you can monitor them with the ketones,
you can see that they’re adhering. But a lot of the time patients are like,
I’m not going to do that. Yeah, it’s overcoming that initial hurdle
so many people have; I need my carbs and you know, fat is bad and the things we’ve been taught that
aren’t necessarily true or aren’t true at all and we have to counteract that. And even brought up the point about whole
grains, this concept of healthy wholegrains, it’s one word,
it’s healthy wholegrains, it’s one word. The cookie crisp cereals,
that’s wholegrain. Right, that’s the society we’re in and that’s why it’s so important to be able
to break down these barriers that people have or these concepts that people have. But the message can get confusing because on the one
hand, keto may not work for everybody. And lower fat, high carb is not going
to work for everybody, but people want the sort
of this black and white, just tell me what the diet to follow
is that’s going to work for me, where it’s not always so clear cut. And there’s not even necessarily
a progression, I guess that’s what I’m trying to get at,
do you have a progression? Like try keto first, then try low-carb…
but isn’t a progression but– It’s hard.
I try to individualize for each person. I know some good fitness companies
that do only calorie counting. So, if it fits your macros, basically
they Tetris together their food and put it all into the My Fitness Pal
or Lose It app. And some of them can short-term,
you know, seems like one, two, three years, they can do really well,
but it’s kind of like an external device, they’re using an external device, maybe not hunger cues
to then follow their caloric deficit. And there ends up being a selection
and survivorship type of bias because these companies are known for doing well
with this particularly method, so when they see people doing well
they hear that, “What’s their method?”, and they go, “Oh, I could probably do that”, and then they get more success
with that method. And then the same thing you see
with the whole foods plant-based people, you know, they’re all yelling at each other,
this is how I lost 100 pounds, it’s like that’s how you lost 100 pounds. Then you get a carnivore person
who’s lost massive amounts of weight, and obviously I can do this and the vegans, you know, are saying
that’s not possible, that’s not good for you. And it’s like that person lost
100, 200 pounds from what it was, and that’s pretty good for them, and if they can stick to that,
more power to them. That’s kind of the way I am now. #It’s a good approach to realize the way
and there are lots of different ways out there. But also that weight loss is a new metric,
that’s so important. It’s weight loss, it’s how do you feel,
insulin levels. Quality of life is very important. Quality of life
and all of your metabolic metrics, and then of course
also your lipid metrics. Which I know is your personal favorite and you have an interest in lipidology
and so do I. So, lipids are a fascinating topic because for so long it’s been
whatever lowers your LDL is good. That’s kind of what we’ve been taught. Now, you started as a skeptic
to the LDL hypothesis and then you switched to become
more of a believer of the LDL hypothesis. Yeah, so tell us a little
about that progression for you. So, kind of going to medical school
with that low-carb lens, there tended to be a lot more
of the LDL skeptics in that arena and so, you know, reading he same type
of cholesterol type of books, and they brought up a lot of good points. And back then, I believe it was
the enhanced trial with Zetia and Simvastatin. One of the things that stuck out in my mind
was look, they lowered the LDL further but the CIMT wasn’t any different
and they didn’t have the hard outcomes yet. Right, so that was a study–
just to bring everybody up– it was a randomized trial where half
the group they all got CIMTs, carotid intima-media thickness test and the other half of the group got
Simvastatin plus Zetia medication that lowers cholesterol even further,
which they did. But in the end, there was
no plaque progression, or a change in their CIMT, so the conclusion was it’s not all about
the LDL, the lower LDL just had no effect. There are multiple other things
but for some reason that one stuck out and I was like, sure,
maybe yeah, they lower LDL but maybe there was
something about them, they call it the pleotropic effect
that improved the outcomes specifically,
obviously secondary outcomes for cardiovascular events and death. But it was then after
the Improve-IT trial came out that it showed no,
it actually did lower outcomes once they looked further past
the surrogate marker of the CIMT. It actually did improve outcomes and this drug works in a different way
than statins do, basically decreases the absorption
of cholesterol in the intestine. And that’s like okay, maybe there is
something to this LDL hypothesis, and so I started going to the NLA meeting,
Dr. Dayspring, if you know who he is. Yeah. He was in Richmond,
right where I was working, and I reached out to him and he became a mentor of mine,
sent me a lot of lipidology books, I said this is super fascinating, I’m really
into the physiology of atherosclerosis. Still with a skeptical mindset but you know like thinking this is something
that needs to be looked at further because I’ve got some of these patients and now, I’m a whole lot fascinated
by this whole lipidology thing, I’m a NLA member,
I’m about to take my lipidology boards. I do believe in the LDL hypothesis, but I do understand that atherosclerosis
is much more complex than just simply LDL particles
being retained in the wall. Right, and there’s a lot there to talk
about with the cholesterol, so gosh, where to begin. Going back to the Zetia trial though, the improved trial where adding Zetia
to a statin lowered it further and did show a reduction
in cardiovascular events. Not all cause mortality,
but cardiovascular events. But put into perspective though, it’s one of those trials where they’re going
to say it was a 20% reduction, when in reality it was a less
than 1% absolute risk reduction. So, less than 1% of the people
saw benefit in reduction of heart attacks, but it was a benefit. And that’s one of the dilemmas we fall into
is seeing a benefit but seeing such a small benefit is okay,
it’s statistically significant, is it clinically significant
for that one patient you’re seeing and does it then confirm an entire model
saying that LDL is the more important thing. And these concepts don’t have
simple answers to them obviously. So, it’s clear that LDL is involved but like
you said, there’s more to it than just LDL. So, part of the problem I have
is controlling for metabolic health. Like all those studies, every LDL study has been done in a low fat
or high carb or a standard American diet type of setting, and they don’t generally control
for metabolic health. So, now, what is your take on putting
LDL into perspective with HDL, triglycerides, the ratios, the metabolic health? Do you think it has
the same prognostic value with high HDL, low triglycerides
and good metabolic health? Yeah, I do think
it’s an independent risk factor. Risk factor I will say
because there’s multiple risk factors I do think that in order
to initiate atherosclerosis you do need
LDL particles otherwise how are they going to get in there and there are some other theories
on that as well. But I actually think that metabolic health
is very important as well. There are other independent risk factors. So, say for instance a smoker
with hypertension… they’ll have accelerated atherosclerosis
with the same amount of LDL particles as you know, compared to someone
who’s very metabolically healthy. So, that area underneath the curve
will be accelerated for atherosclerosis for those people
with multiple other risk factors. Now, you can look at somebody
with familial hypercholesterolemia and that’s– when you go into med school it’s like yeah, those people don’t have
any other issues, it’s just a genetic cause
of their LDL receptors not working or their APOB is not connecting to their LDL
receptor or whatever it is… they have a high area under the curve
of LDL particles. But then when you dive in deeper, there might be more problems with people
with FH and the scavenger receptors. Lots of other things that can’t necessarily
extrapolate that data to someone who has
a low-carb ketogenic induced– I actually have a…
I’ll add a document, I do want you to publish this blog
for Dave Feldman because he’s asked me to write,
if I’m going to argue against someone who doesn’t believe
that the ketogenic induced LDL, if you want a hyper lean mass couple
responder, if they’re not a– what would you do to argue against that? And I’ve listed out
all the different arguments actually being
in some of the Facebook groups, and a lot of the ketogenic proponents, they do have a lot of good arguments
against the LDL hypothesis based on their hypothesis, so yeah. But I’ll add you to that document
because I think you’ll appreciate it. Yeah, I will because I think it’s important
to recognize it, you know, a low-carb individual who has
a rise in their LDL is very different than someone
who has a genetic mutation that’s going to cause
a problem with the receptors. I think you can’t compare those two
and say they’re the same. And then someone who’s improving their
blood pressure and improving their weight and the visceral adiposity
and their metabolic syndrome, that’s going to carry a different weight than somebody
who does have those problems. So it puts us in this realm of– we don’t have
the data to say it’s safe, but we can also say
that none of those people are represented in the LDL
or statin trials, so where does that lead us? So, you can either say that we go back
to the data we already have and say it’s potentially harmful, or you say
we’ve made some many improvements and all these other things are improving
that we’re going to continue to monitor. So, if you were
to recommend to somebody that they continue to be monitored
with an elevated LDL on a low-carb diet with all the other health markers improving, what would you say, or how would you say
they should be monitored moving forward? So, actually, when this happens
to my patients– so in my articles I go
through the multiple mechanisms because I think there’s multiple
mechanisms that are increasing LDL, not just Dave’s hypothesis
of the energy model. I believe that’s partly correct, but I also believe there are some other
things down-regulating LDL receptor activity. I believe soluble fiber
and some of these other things, saturated fat versus monounsaturated. So, I actually do my best to add in things like
Metamucil and things like soluble fiber, change all their fat to monounsaturated,
then we see their baseline off of that. Then, I talk about the risk, and I go,
we don’t have the data, but you’ve improved
all these other risk factors, you’re feeling so much better. We talked about quality of life… If you’re feeling miserable
on multiple medicines and you have a lot of excess weight versus you’re on a ketogenic diet, you feel
amazing, you’ve lost this excess weight. Who am I to say then, you know,
this isn’t good for you? We don’t have the data, so I’m talking
to them like I’d be talking to you, like another physician or scientist
that’s looking into this. And I lay it out for them
and they have autonomy. Other doctors I have seen…
these low-carb groups, the doctors fire their patients
because I think they don’t want to get sued. I am not exactly sure,
but I tell the patients, I go, “Look, I think there may be
an increased risk, “but I don’t know, if you feel better “you have autonomy, you can choose this, “you can choose to go on a statin or not, “you can tell me, ‘Off!’
or you can just drink butter and not do any of the monounsaturated fat
that I recommend.” So I think patient autonomy is important
but I lay it out for them. Yeah, it’s frustrating
when I hear people saying, “My doctor yelled at me and he fired me
because he wouldn’t work with me.” And it’s not our role
to dictate to people what to do. I think they’re scared
about getting sued maybe or you know, those insurance companies, like we get these letters saying patients
should be on a statin-based diet or this this and this
or this drug and this and this. And insurance companies are telling us
how to practice medicine, also interesting. Yeah, it’s also interesting. We talk about this topic a lot
and for a good reason, because it is sort of a paradigm shift,
but it’s interesting to think that the percentage of people
who have this dramatic rise in their LDL. -Actually is pretty small.
-Yeah. When you look at he studies on people
who are overweight and diabetic, it’s almost non-existent in those studies, it really is sort of the people
who are already lean and don’t need to lose as much weight
and are already metabolically healthy. So it really is a specific subset
but it’s a fascinating subset because it brings up into question
the whole LDL hypothesis. You know, there are plenty of so-called
black swans of the LDL hypothesis, whether it’s the Kitavans or whether it’s the people with FH
who have greater lifespan as they age if they don’t get premature
cardiovascular disease. There is so many paradoxes
for the LDL hypothesis and it just tells you
that it’s not so cotton dried, and I guess that’s my problem
with the whole lipidology world. They do sort of paint it as a little bit
too black and white from my standpoint, and I can understand why,
but do you see that too? Do you think it’s a little
too black and white? Hopefully, I don’t get in trouble, but they’re heavily involved
with pharmaceutical companies, I see, and I think it does needs to be
a little bit more nuanced, because it’s like, look,
why don’t we just talk about it as we don’t have the data of these patients
that are on low-carb diets that have explosive levels of LDL? Why don’t we just say that
based on our information on patients that seem to be metabolically
unhealthy and maybe with FH? Let’s talk about it more in the grey zone
as opposed to black and white. So, I agree with you, I think we need to be
a little bit more open-minded. And it’s hard to separate the industry
influence and the pharmaceutical influence because that’s who funds a lot of the–
you know, you go to the lipidology meetings and who has the boots,
who pay the money to be exhibitors? It’s a lot of the drugs. So, one of the most recent drugs
that came out, the Vascepa, the Icosapent. So, that’s basically
the high dose Omega-3. -EPA only.
-EPA only, yeah. Huge reductions in events. So, for people with high triglycerides,
adding that… adding it to a statin, right? Adding that to a statin
for people with high triglycerides, they showed like a 5% less reduction
in cardiovascular events. It didn’t even follow the APoB,
they’re not even sure what they followed, They think that maybe there’s differences
in the endothelial function, they showed these molecular changes
and everything like that. But there was a very big industry
kind of push when I was at the meeting, so I’m kind of skeptical,
I think money influences a lot of things and I think the stuff needs
to be studied a lot more. Yeah, and how much to react
to one study as well. Reproducibility of a study is such
an important concept that just gets lost, one, because the studies
are expensive to do. So, if a company can spend the money, get
a positive result and cash in on it, why wouldn’t they
from a business standpoint? But from a science standpoint, we should be demanding
reproducibility of these studies and that’s something
that’s sort of got the– Yeah, and I know there’s a lot
of low-carb CEOs out there, you know, they’ve got a lot of money,
they could fund some of these studies. That would be nice. And speaking of which, you’ve mentioned
Dave Feldman’s name, it sounds like you’re in the process
of working with him on trying to develop a study
to help answer those questions, so tell us where you are with that. Yeah, it’s a very important question. Needs to be answered,
at least get some more clues into that, otherwise you’re going to see people
yelling at each other on Twitter, you’re going to see the lipidologists
and the LDL proponents, like Ivor and some of the other guys. I mean, it’s all good fun and it’s actually
good learning if you really get down into it. Dave and I kind of came together, he’s got the group
of the lean mass hype responders. And it’s just… I am baffled because I didn’t even think you could have
some of these exponential increases in LDL. I mean I saw it in practice, but not to levels where people would have
homozygous familial hypercholesterolemia. And that’s where you would have two
knockouts of various parts of the genes having to do with LDL receptors and APoB. So, LDL sea levels
are like 400, 500. 400, 500, 600. And so I’m seeing this in the group, and I’m
like no way, it’s got to be something else. But then you see their LDLs
before they went on a ketogenic diet and they are like 130s, 140s, 150s. And so, I’m actually writing… I’m going to publish a case series
on about five of these individuals. I actually brought it
because I’m going to UCSD next year and the reason I am going to UCSD
next year for preventative medicine is to get a Master’s in public health,
get some more bio stats, and also to get some more mentorship
to put this study into fruition, make it come to life. And basically, I’m going to publish this case
series because people don’t believe it. I’ve actually talked
to multiple doctors out there, I’ve sent the lipid profiles
of some of these patients and they think no way,
they have to have thyroid, they have to have type 3, whatever,
they have all sorts of things, and I’m like no,
it is ketogenic diet induced. We can’t find anything. I can’t see anything with the snips,
there is no LDL receptor issues, their urines are fine, you know, they don’t have nephrotic syndrome
or something like that, their thyroid is fine, they don’t have
a family history of hyperlipidemia, they do not have anybody with coronary
disease in their family, they’re lean, no other medical problems,
ketogenic diet, you know. 400, 500 LDL mg/dL. So what we want to do is we want to basically get like 50
of these lean mass hyper responders and then we would really want to get
a control group of low-carbers who don’t have this massive increase,
with similar metabolic profiles and then just watch progression. Now as we talked before, probably we will never going to have
the hard outcomes we’re looking for but at least progression in atherosclerosis. And I’d like to look at the lumen
with like a CT angiography. I don’t think a CAC score would do it,
I think too many people… If they are young,
you’re not going to see that calcification. So the CAC being the coronary artery
calcification score which is the noncontrast CT that shows the presence or absence
of calcium in the walls of the artery. But the CT angiogram injects the contrast
into the veins and you actually do see the arterial lumen,
you see the whole artery, and you will be able to detect any plaque. So it’s a little bit more sensitive
than just the calcium score. And as I’m learning more into it,
because I really want to understand, I do want to work with cardiologists who
understands the imaging a little bit more. As I am learning, you can actually look
at the plaque quality a little bit more with the CT angiography. So, I do think that we would need
to do that and say, “Well, look, you know… three, five years
we’re comparing the groups.” Is it similar progression? And it’s not just like a 20, 30 ml/dL increase
that you see with some of these individuals, we’re talking massive increases;
100, 200 ml/dL. We should see an effect… similar timeframe,
area under the curve, APoB, LDL particles that you would see with someone
with familial hypercholesterolemia. Yeah, they’ve had it since youth, but you should see
in a similar timeframe that progression. If we don’t see that massive progressions
or any progression or any difference you know, maybe there is something
else going on there, that’s protective. Just the study that came out
is talking about scavenger receptors and how we thought that the LDL particles
moved passively– you know, depending on their size
in the endothelium. Just this new study showing that maybe they had to go
through their scavenger receptors, you know. So, scavenger receptors are called
scavenger receptors because they tend to pick up
more of the modified and oxidized LDL, not so much the normal LDL, they’re not
like the normal LDL receptor basically? Well, so something that’s just published,
you know, you maybe want a link to it, it’s just interesting because as we thought the LDL articles move passively
in and out of the endothelium regardless of whether
they’re oxidized or not. And there are scavenger receptors
in the endothelium and it may– so hypothesizing further,
trying to argue for– so I am a LDL proponent, but arguing if I were a ketogenic proponent,
and LDL… more of an LDL skeptic… Maybe there’s something protective
about the ketogenic diet that down-regulates this process. And I just think it’s fascinating
because I just want to look… Dave and I talk about it.
It’s a win-win situation… I just want to see…
maybe this would be a breakthrough, and if it does show massive progression
as I would predict, then you know,
that’s the data we need to know. -We need to know that, absolutely. But if it’s protective that actually has
major public health implications, because then we can say look,
we have this amazing tool; places like Virta, whatever,
is going to skyrocket, people are going to love, you know,
a low-carb cardiologist, you would be like, look we had this tool
that is actually protective, don’t worry about your LDL particles. Or if you have these patients
who have massive increases, like hey, actually this is dangerous, we have some strong data here
to show that, either way I’m just interested in the data. I think it’s fascinating. And that’s one of the reasons,
one of the things that sort of attracted me to you
and wanted to have you come on the show is because you’re not
one of these people just dig your heels in and say this is the right way,
this is my way and I’m going to defend it. You want to know…
you want to help your patients and I think that’s the world more of us
need to live in. It’s don’t be so ideological,
but really search for the data, understand the data and understand what
we don’t know and what we need to know and help us get there. And we talked a little bit–
I guess this segues a bit into people… who they are in person
and who they are on Twitter and it’s humorous because people can be
such jerks on Twitter and it sort of makes you lose sight that what we’re really doing is trying
to help people improve their health. So why do you think that is? That people just become
so just snarky on Twitter? You live behind the computer, I mean
you talk about trolls and things like that and just say things you wouldn’t ever say
to somebody’s face. As a physician you have to have
that bedside manner you would never– I won’t say never I know some doctors
that tell their patients they’re fat and whatever things that are just like,
“Oh, my gosh… I don’t know how you became a doctor.” But in general
when you’re behind a computer you don’t have that personal connection, like can you imagine me saying certain
things right here to your face are here that are just like all my gosh…
that some of the people say on Twitter… Like swearing, almost threatening
in certain ways. I think if we step back so take for instance,
I don’t know, vegans or whole foods plant-based
individual proponents and then the people on the other end to be
like the carnivores like Dr. Baker and how a lot of people is yelling at each
other and kind of making fun of each other and I don’t mind teasing each other
in good fun but I think when you step back and go
to someone like Disneyland and Walmart and see there’s a lot of people… they’ll never follow a whole foods
plant-based or a carnivore. I’ve tried to prescribe a carnivore diet
as much as I like– Personally I don’t think
it’s probably optimal but I’ve actually prescribed it
to patients who I thought it would fit and they just wouldn’t stick to it,
which is interesting. So if you take a step back most people
are just eating just absolute horribly. If we can even get them closer
aligned to any type of these diets, ketogenic, low-carb high-fat,
whatever you want to call it or a vegan-esque type of diet, I think we have proven most people
just have no awareness. And so I think if we all kind of– We’re all trying to help people. I do think more people need to come across
the party lines or whatever, go to each other’s conferences,
understand where you’re coming from and I do think, you know,
there’s industry involvement that’s kind of pushed us maybe one way
or the other and there is influence there and I would be naïve to say,
no, it has nothing to do with it. I think we do need to be skeptical
about a lot of things and I think we all should just come together
and realize we just try to help people. Yeah, I think that’s a great point. I mean so often we lose track
of what we agree on because we are focusing so much
on what we disagree on. Well, that’s important
because the details matter. It’s so important to realize that our goal
is to help people live better, healthier, happier lives. And there’s more than one way to do that. So give us an idea…
what is a day in the life of Dr. Spencer? What do you eat? How do you exercise?
How do you live your day? What are some of the main things you do
during your day to improve your health? I am very relaxed now
because of my job. I will be going back to training next
in a few months actually but wake up, get my coffee, black coffee,
I don’t add anything to the coffee. I don’t have much of an appetite
in the morning so I drink basically
an egg white protein shake and I have a little bit of fruit with that,
brush my teeth… Exercise, lifting weights, whether I run, bike,
lift weights or now I am getting into jujitsu, because it’s not as hard in the body
as wrestling was… Lots of vegetables, lean protein, a little bit of healthy starch,
healthy fat thrown in there. That is kind the way I do it. Eight hours of sleep…
very standard kind of boring stuff, but like the stuff
that we know is good for you. Very, very simple. Very simple and obviously
it’s working for you. Your metabolic health
has probably doubled and it’s as good as it can be, right now. Yeah, so since medical school I’ve got
my NMR a few times a year basically, watched LDL particles change
and insulin is always very low. Actually is interesting, my A1c
on a lower carb diet… I’ve gone ketogenic… actually starts going up
a little bit interestingly… may have something to do
with the red blood cell life… Anyway, we don’t have to get into that,
but yeah, very metabolically healthy. There’s some variance depending
on what kind of diet I am doing at the time. And sounds like a lot of exciting things
on your horizon starting with the preventive–
preventive medicine fellowship? For me it’s technically a fellowship
because I am already board certified, but it’s a residency for people
who aren’t already board certified. Plus a Master’s in public health from that
and then working on a lot of projects so I look forward to seeing more from you
coming on the pipe. So thank you for taking the time to join us. Thank you for having me on.