#1Welcome back to the Diet Doctor podcast
with Dr. Bret Scher. Today I’m joined
by Dr. David Diamond. Now, Dr. Diamond
has a PhD in biology and he is a professor at the department of
psychology at the University of South Florida. Now, interestingly, his work
is in cognitive and neuroscience and he’s done this for decades. But because of a personal journey, he has now gone down this whole path
of cholesterol and statins and low-carb lifestyle, and really trying to say,
what does the science say, what does the science support
in this realm. Now, this is a polarizing topic,
especially with mainstream medicine, mainstream cardiology being very much in
the camp of LDL is causative of heart disease. And Dr. Diamond is on the other side
of that, saying wait a second, I don’t think the evidence
supports that statement. Now, I’ve got to be honest,
this is a very important topic for me, a personal topic for me. I had a huge list of notes and I kind of went
a little bit all over the place because I was just so interested
in talking to him and talking about the different topics
and getting his thoughts on different things. So, I apologize if this interview doesn’t flow
as seamlessly as I would have liked. But I think we cover
a lot of different topics. Now, quick disclaimer; if you have
high cholesterol, if you are on a statin, please do not make any medical decisions
or changes based on this discussion. This is merely to explore some evidence, to explore one side of this equation,
hopefully in a balanced way. But if you are going to make any changes or any decisions about your medications or
your health, please talk to your doctor first. Do not make any decisions
based on this discussion alone. Now, with that disclaimer,
we talk a lot about the science, we talk a lot about the practicality
of how this implies to individuals and a low-carb lifestyle, and we explore a number
of different topics about cholesterol, LDL, statins, and their benefit. So, a couple of quick definitions,
which I think we go over, but relative risk reduction
versus absolute risk reduction. So, if you have a one percent risk
of something and you can reduce it down
to a half of a percent, the difference, the absolute difference,
is a half percent, that’s the absolute risk reduction. Relative risk reduction however, I would say that’s 50 percent reduction because half percent
is half of one percent. So, we talk a lot about that, Dr. Diamond has been
very vocal about sort of truth in advertising between those two things. We talk about Mendelian studies and basically that’s just a natural history
experiment of genetic mutation and following what happens to people
over time with that genetic mutation, that’s called a Mendelian
randomization trial, I think I use that term a little bit in here. I think hopefully
that’s all the definitions you need, and I hope you enjoy this discussion
with professor David Diamond. You can see the full transcripts
on dietdoctor.com. Again, please realize
this is not medical advice, this is just simply exploring a fascinating
topic with a fascinating human being. So, enjoy this discussion
with Dr. David Diamond. Dr. David Diamond, thanks so much
for joining me on the Diet Doctor Podcast. #2Thanks for inviting me, Bret. #1It’s a pleasure to have you here because
you have been a spearhead in this movement of questioning the role of LDL,
questioning the role of statins and more importantly,
how does that apply to a low-carb lifestyle. But this… this is not even your job,
this is not your profession. I mean, you have a regular job as a
professor in the department of psychology, so tell us a little bit about how you got
from point A to point B here. #2Right, so, my training, my primary
expertise is in neuroscience, studying the brain and memory,
which I started over 40 years ago. But what happened about 20 years ago was that I found that I had
extremely high triglycerides, I was actually diagnosed
with familial hypertriglyceridemia, which happens to about 5%
of the people in the population. I eat some bread and my triglycerides
go sky high. My triglycerides were about 700, 800 and these people who have
high triglycerides also have low HDL. So, my ratio of triglycerides to HDL, which
should ideally be like 1:1, or 2:1, mine was about over 20:1. #1Wow, that’s amazing. #2And, so… and it was for about 10 years. My doctor’s keeping track every year,
I’m getting blood tests, I’m working out like crazy,
I’m on a low fat diet, and every year I just got fatter and fatter
and my triglycerides were up. Finally, my doctor just sat me down,
said you know, you’ve done your best, your diet and exercise have failed,
just like they say in the commercial. You’ve got to go on a statin
as well as other medication. And I just figured, well, you know,
I’ve got a background in biology. I know a lot about the brain
but not much about heart disease. Least I could do is read a few papers
before I go on the medication. I read a few papers and by this time,
I’ve now read a few thousand papers. And that has helped to guide me
and my decision not to use medication. Instead, I learned about the value
of low-carb diet. I was able to cut my triglycerides
by 75%, raise my HDL 25%, lose a good bit of weight, feel much
healthier now than I did 20 years ago. So, I’m a strong advocate for a low-carb diet but also realizing
that medication wasn’t appropriate. And in the process, I’ve been in a sense
indignant about the statin research. I actually express this when I give my talks about how I realized
that the cholesterol theory, which is cholesterol causes
heart disease through LDL, it’s really not well-supported and frankly, what I express
is the obscene profits that have been made through the food and drug industry that
have maintained a hypothesis that has failed. #1Very controversial and interesting theory
which you back up with a lot of research. So, I want to talk about that but I think your example is a perfect example
of what’s happening in this low carb-world and the medical world in general that whether it’s an engineer
or whether it’s a scientist, frequently an outsider from the medical
profession has a personal experience, but then they have the tools
and the knowledge to dig deeper and provide us
with a whole new perspective. And I think that’s so valuable because,
you know, in the medical world, if you’re in your own echo chamber,
only hearing the same people, the same experts,
the same drug companies. Although, we fall into that same risk
I guess, in a low carb world, right. We can be our own echo chamber too, so we have to reach out into other areas
and keep our ears open for other opinions. Now, one of the things
that you’re very critical of is evidence and how we portray evidence. And we talk about evidence-based medicine
all the time and we talk about what is the evidence
for keto, against keto. What is your perspective as you’ve looked into things about the state
of evidence in the medical world? #2Well, I think it’s very important
that I don’t come in with a bias. You know, I’ve actually been
very well-funded by drug companies in my neuroscience research, and I’m not personally or professionally
opposed to any drug company research. I had never seen the distortion of data… distortion of the presentation of data
before going into the cardiovascular field, before reading papers on effectiveness of treatments with cardiovascular,
particularly lowering of cholesterol drugs. And I have to tell you that I was astounded, I was offended when I saw how the data
were manipulated to greatly overstate the benefit
of cholesterol lowering drugs, which actually goes back decades, originally talking about cholestyramine
in a 1984 paper in which you had, starting off
with about half a million men, they got that work down to about 600
people at the highest levels of cholesterol, and using an older drug cholestyramine,
which lowered cholesterol. The amazing thing
was after seven and a half years, there was virtually no effect and there was
no real statistically significant effect. It was a 0.4% difference
between treated and untreated men. And I look at that, and what they should
have said, you know something, we were wrong… lowering cholesterol
didn’t have any benefit whatsoever. But they turned that 0.4% into a 24%
improvement in outcome. And so, this manipulation of the data and that’s using relative risk
rather than the actual outcomes. So, to me, this is just not right in how you report the data
to the public and to the medical field. #1Yeah, you’ve been very vocal
about the relative risk versus absolute risk. So, the absolute risk in that setting would
have been the 0.4%, but when you do it in a percentage,
it’s a relative risk, so if you have a 1% risk, you lower your risk
to 0.5% percent, that’s a 50% reduction. Now, what’s interesting to me,
as a cardiologist, I’ve inundated with that type of relative risk
reduction publicity, and to me it was just how it was done. Until I started, you know,
digging a little bit deeper and realizing it’s a completely different
conversation if you have the absolute risk reduction. But the fallback is there is a change,
there is a difference. So, even in the statins, and I guess maybe
we’re jumping a little ahead here, but even in the statin trials,
if there is a 1% difference, it can be a statistically significant
1% difference, which then they publicize as a 36%
difference. But it’s hard to argue
if there is a difference, so the question becomes
when is it a big enough difference to make a clinically useful intervention,
and that’s a hard question to answer, isn’t it? #2Right, the first thing is that we need truth
in advertising, we need accurate reporting. So, what’s very important is to report
both – the absolute risk and the relative risk. They should both be in the abstracts, they should both be presented
to doctors and to patients. People should know both. What is actually the difference
in the rate of events in people of placebo
versus the treated people? You shouldn’t only be told
the relative risk because that’s deceptive, and we know it’s both in doctors
and the public. When you hear about a 50% reduction
in risk and that’s all you hear, you think that half of all people
are now not going to have a heart attack. And that’s exactly what doctors
interpret that. So, again, first… I’m not against reporting
a 50% risk reduced with statins, but that’s got to come along
with the absolute risk as well. People need to have both data forms. And the second thing is, you are right. There are numerous studies
showing benefit with statins, and that benefit typically
is on the order of single digits. There’s never been a statin study I know of in which you actually have
a double-digit improvement. And I have to just briefly tell you, in my field of neuroscience
where we actually study depression, is such a great controversy because people with mild to moderate
depression, given a placebo, have actually a rather dramatic effect
as a benefit. And the controversy
actually is that the antidepressants only improve outcome by 10%
compared to placebo. Well, there’s never been
a real 10% improvement outcome of any kind with statins. So, I agree with you completely, there are studies that have shown
the benefit of statins when you’re looking at coronary events, as well as coronary mortality
and all-cause mortality and those numbers are relatively small,
but they are real. #1Yeah, I think that’s a great perspective
that you bring from the field of psychology
and depression and they’re looking for a 10% benefit and
we’re talking about 0.5% to 1% benefit. And it’s interesting that the phrasing,
the wording of these studies, that they’re blockbuster,
that they’re revolutionary. I think we’ve sort of lost perspective of what blockbuster
and revolutionary really are. Like treating tuberculosis, that was
revolutionary, that was blockbuster. Sanitation, anesthesia, you know,
those were blockbuster. A half of a percent difference,
is that a blockbuster? But then people say, cardiovascular disease
is the number one killer in the world. Millions of people are going to suffer
from cardiovascular disease, so if we can make 1% difference
and that’s a lot of people. And in a way, that’s a valid argument when
you’re talking about a population basis. #2I agree completely.
If statins had no adverse effects and you say 1% of the people
from having a heart attack, I’d be all for it. Maybe I’d take it myself if we were absolutely certain
there were no adverse effects. I mean, this kind of grabs you. You think that a hundred people
are going to take the drug and l one person out of a 100– 99 take the drug and then
there’s no benefit whatsoever, but again it gets down to adverse effects. Now, what has happened is people
are really not aware of the adverse effects. They’ve been greatly minimized
by the key opinion leaders. And I’ve also talked about this. Now, we actually were invited to write
a commentary recently by Plus One. And in that commentary,
which just came out a few months ago, we reviewed the literature
on adverse statin effects. And it’s not small, it’s extensive. We reviewed about 60 papers published in
peer-reviewed medical journals of about 20 different categories
of adverse effects. The most obvious is development
of type 2 diabetes. And this has really been minimized
by the key opinion leaders. But when you actually look carefully, and you have an RCT and an actual trial
in which you get blood samples and you look at the A1c levels and you look
at fasting glucose and other insulin measures, you actually find that over the course
of six years – this is in men – that there’s a 5% increase
in new onset type 2 diabetes. So, this particular one was done in Finland
funded by the government in which you have a spontaneous increase
in type 2 diabetes with placebo as 5%. But in those that were on statins,
it was actually 11%. So it’s doubling in the rate of type 2 diabetes,
which is a relative risk measure. But we’re not talking about 1%, we’re talking about a 6% increase
over the course of about six years, and so, that’s just one adverse effect. There are really
well described cognitive effects. We’ve published a paper
on cognitive effects in statins, and there’s actually a beautiful paper that has shown that people diagnosed
with dementia, older people diagnosed with dementia, which, when they were taken off the statin,
their dementia disappeared. Put them back on the statin,
the dementia returned. This is not something that doctors
are aware of, the extent of the adverse effects
of the statins. #1Yeah, it’s very interesting, because when
you talk about adverse effects of statins, the most common is the muscle aches,
that’s what everybody talks about. And the argument is you can’t compare
muscle aches to heart attacks, right? Those are not on the same level, especially when the vast majority
of the muscle aches disappear when you take…
when you remove the statin. But even with the muscle aches,
there’s significant controversy. I mean, you look at the trials and they report one in 20 000, you know,
risk of significant muscle aches, and of course, these are designed
by the pharmaceutical companies so there’s a run in period
which weeds out a lot of the other people who would be intolerant,
so, they’re not included in the trial. But then, my favorite
is how you called out Roy Collins and, you know, how he would state
there’s one in 10 000 risk of statins but yet his commercially available
product to test for statin myopathy risk, quotes a 29% risk. So, where do you see
in trying to evaluate the evidence? Where do you see
the muscle aches really lie? Where do you think that is?
What is the real number? #2This is very interesting because
you listen to the leaders of the field. Steve Nissen, for example,
calls it the nocebo effect, in which the patient is told
that the statin causes muscle aches and therefore, they say they have
statin-induced muscle aches. But he calls it actually a nocebo,
meaning it’s all in their head. And there are some very poorly designed
studies that support that. What I am presenting today is actually
Steve Nissen and Christie Ballantyne
and Steve Nichols strong statin advocates, talking about muscle pain caused by statins,
they’re not calling it a nocebo effect. And their estimate is 40%
of the people taking statins stop taking it in part because of muscle pain. So, I caught them on a video in which they’re being candid about
what actually happens in the clinic, why people stop taking statins. #1-Interesting.
#2-Yes. #1And it is difficult to decipher
the real-life effect, the physiological effect
versus the placebo or nocebo effect. That’s why you need a randomized control–
placebo controlled trial, but those trials frequently excluded people
who were at risk of having muscle aches. So, I don’t think we know the true answer. But the bottom line is if you think
it’s causing you muscle aches and you’re not going to exercise
because of it, we have to ask is it impacting
your health favorably. And makes you wonder, doesn’t it? #2Well, that’s another important point. What happens is we know that statins
interfere with metabolism, you have less coq10, which muscles need
to be able to have energy. And there’s some very nice work from…
out of UC San Diego– Glome?… it’ll come to me later. But very nice work showing that many
people have fatigue much more rapidly, especially under exertion conditions,
and so, we do have less energy. People have less energy
when they’ve taken statins, and we do have muscles breaking down, which contributes then
to kidney disease, kidney injury. There’s well-established
actually public papers. So, I think we are looking
at very real physiological effects that have adverse effects globally
on the body. #1Yeah, so, we started with the muscle
aches and then, diabetes is the next big one. And what’s interesting about the diabetes is people say, well, look, if you’re having
an increased risk of diabetes, but you’re still showing a reduction
in cardiovascular events, doesn’t matter. And that’s very interesting
when you’re in a five year trial. But when people are on these drugs
for 20 to 30 years, we’re left to determine
how are we going to interpret that data? On the one hand, people say, well, if the cardiovascular benefit
is one year or five years, it’s going to be 2 years
or 10 years and 4% at 20 years. Okay, maybe we can make that reach,
but how is the diabetes going to impact that? And we don’t know the answer
to that question, do we? #2No, we don’t because most of the trials
are stopped at about three or four years. It’s Beatrice Golomb by the way– #1I knew you were going to get it. #2She came back to me, and she had done
some beautiful work looking at statin effects. What you’ll find with the statin advocates– I look at this, really it’s outside
my primary area in which I was just a basic scientist. I am still a basic scientist
looking a brain function. But to see people who I now consider
advocates for statins, that’s not the way science is done. And what’s happened
with the statin advocates is they consistently take
that number needed to treat– which may be small after one year–
and they simply change it… one out of 100 people
will actually have a benefit from statins. And then they’ll say, well after 20 years,
you only have to treat five or 10 people. Because that benefit
will accrue over 20 years. And they refuse to say
the adverse effects can also accrue. So, if you’re looking at 6% additional
people who develop diabetes after about five or six years,
what’s going to happen after 20 years? And what’s going to happen if there’s actually an exponential increase
in adverse effects? But once tissue starts breaking down,
then you’ve got to be even more concerned with that happening at an even more rapid
pace, especially with elderly people. And by the way, also,
the way I also present this is if the tobacco companies had the control
that the drug companies have now, overlooking only with the onset of starting
to take the statin after only about four years, you look at the development of cancer, it’s
only four years that you’ve started smoking, we never would have known
about the link of lung cancer to smoking. So, understand, these trials were stopped
really before most cancers can develop. But when you look long-term and there’s actually a nice epidemiological
study looking over 10 years, you see twice the rate of breast cancer
in women who are on statins chronically compared
to equivalent groups of women either with high cholesterol,
low cholesterol. And so, there’s also evidence of cancer
in men as well, but you’ve got to look
at older population more vulnerable
over a longer period of time. #1And that’s interesting because that’s
where there’s some contradictory evidence, because there’s meta-analysis showing
no increased risk of cancer as well, and all has to do with which trials
you’ll include and how long is the follow up, and it becomes confusing
and it’s difficult to say with certainty. But then you hear these statements,
the preponderates of evidence, right. Taking the evidence as a whole shows
that statins reduce cardiovascular events. That’s also difficult because where does
the preponderates of evidence come from? It’s mostly the Pharma sponsored trials. So how do we interpret
Pharma sponsored trials, I mean the data is still the data, we can’t–
it’s not like they’re falsifying the data, but what is the impact the pharmaceutical
companies have on the data we’re seeing? #2I actually give pharmaceutical companies
a lot of credit. I don’t see any evidence of fraud. The deception is how actually
the clinic directors present the data to the public
and to the medical community, and again, that gets back
to the relative risk versus absolute risk. The fact that they report such miniscule
beneficial effects… to me, I give them credit. That clearly to me doesn’t appear to give
me any reason to accuse them of fraud because they’re showing so little benefit. And again, I don’t think we want
to automatically demonize studies that are funded by Pharma. These are very expensive studies and it’s very difficult to get government
funding for long-term studies on cardiovascular disease. The other challenge is it’s a very low rate
at which people develop heart attacks. About the only time you see a high rate
of death is with heart failure, of which statins are actually
no benefit at all, people with high cholesterol live much longer
than people with low cholesterol following heart failure. But when you’re looking at heart attacks, you’re actually seeing in the general
population such a low rate that frankly, to give the Pharma credit, it’s difficult to much of a reduction
in heart attacks. You even take people with high risk
of heart attacks and you’ll only get about typically 3, 4, 5%.
who will have heart attacks and you’ll have a low rate of mortality. So, this is part of a methodological challenge
for this area of research. So, now like in a cancer study you may have 50% of the people
die in a short period of time. But in these heart disease studies
I don’t think people appreciate that there really is relatively a low rate
in placebo treated people. And this is why I tell people… I show them
studies such as the Lipitor study, which was famous in the Lancet
early… around 2000. Or the British Heart protection study, you’re only looking at about 3% or 4%
of the people who died. They’re terribly uncooperative
as a way to put it. And about 97% of the people
don’t have heart disease, and the way I also present this to people,
I say, listen, you can go to your doctor and say, if I don’t take the statin,
if you give me a placebo… what’s the likelihood in the next five years
that I’ll have a heart attack? And the answer is 97% likely
that you will not have a heart attack. And so, to me,
that’s the reality of it as well. #1Yeah, so, that goes down to the–
from a doctor standpoint, the shotgun approach of let’s give this drug
to as many people as possible hoping one is going to benefit
versus the more… the more laser beam focus of let’s really
find out who’s at the highest risk and then maybe add a statin
as part of their regimen. So, how do you interpret the calcium
scoring data that’s come out recently? You know, another big study,
Walter Reed, that showed absolutely no statin benefit
if your calcium score was zero. It showed a very small benefit if your
calcium score was between one and 100. I think it was… the number needed to treat
was about 100 over 10 years. But then, as that scores go over 100, all of the a sudden the number needed
to treat to save one cardiovascular event– not death but cardiovascular event–
goes down to 12. So, how do you think about that more laser
focused approach than trying to better identify
who might benefit from a statin as one part of their overall
treatment program? #2Right, so I think there is evidence. Actually, going back to before that,
25 years ago, now including the calcium scores for people show that the people more vulnerable
to develop heart disease are actually… do benefit from the statins. And, so you’re absolutely right. That study showed that the people
who have a high calcium score showed a benefit
of reduced coronary events, no difference in mortality
as you say as well. And I think it’s actually important
to go back this relates– Well, first of all,
when we’re talking about calcium score, I want to point out, everyone agrees
high calcium score is unhealthy. I mean, it is a fact. The interesting thing is numerous studies
have now come out showing that people on statins
have increased their calcium score. This is also– there’s no difference
of opinion on this– the remarkable thing to me is now that
we say, well, that must be a good thing because increasing calcium
stabilizes the plaque. This, to me, came out of nowhere. It’s like increased calcium score is bad
unless it’s induced by the statin. Then it becomes a good thing.
So, that’s remarkable to me. So, what I will yield here is that there is
evidence of benefit of statins given to people with high risk. And the important thing actually is
there’s an analysis of people in the 4S study that was done 25 years ago
using someone on statin and actually, that was one
of the biggest effects ever in which actually had
a 4% reduction in mortality. And for secondary prevention,
people already had a heart attack. #2And frankly, I had to go back 25 years
to find any study as good as the 4S study. It shows how weak
the effects have been since then. But even accepting it was a study run by Pharma,
the data were analyzed by Pharma. It’s okay, a 4% reduction in mortality
for people at high risk. A reanalysis of that study came out
seven years later published in Circulation and it showed the entire benefit was in people that basically had
metabolic syndrome, people who had low HDL, high triglycerides
and high LDL, the entire benefit. Now, when you look in the 4S study,
which is so important, the people that had the same high LDL
but high HDL and low triglycerides, secondary prevention,
no benefit whatsoever. And this is so important,
getting back to low-carb, because that’s exactly what happens
when people go low-carb. Their HDL rises, their triglycerides
drop just like it did for me. So, what this is saying
is you have a choice, okay. You can take a statin and basically
have a crappy metabolic syndrome, or you can go low-carb,
make all those improvements and the statin won’t have
any benefit over that. #1I think that’s a great perspective, I’ll talk about that real quickly, going back
to the statins causing an increase in calcium. I think that’s a great point. The immediate reaction from the community
was oh, this is a good thing. And to be honest, we don’t know,
could be perfectly correct. Well, there’s a mechanistic way
to think that that is correct but to not have the evidence
and just dismiss it because of a mechanism. Would get thrown out
if it was contrary to the common belief. It shows how a common belief
can really direct a conversation. May not be- may be right, may be wrong
but it’s just a perfect example. So, that was good. Right, now getting back to the LDL
and the environment it’s in, and that’s something I think
we really lose perspective of because even going back
to the Framingham data, same thing. There was an association, all–
a complete, total association between rising LDL and rising cholesterol
and risk of cardiovascular disease. But when you see
the Framingham offspring data and they break it down
according to HDL levels, all of a sudden,
that association is lost at higher HDL. So, it shows there’s something to this
more than just LDL, and it probably has to do with metabolic
health like you said, a revaluation of the 4S trial, says that. Now, that being said though, you know,
LDL is causative of cardiovascular disease. We heard it in 1980s
with Brown and Goldstein, we heard it again last year
with the European society of cardiology. The definition of cardiovascular disease as an APO-B containing lipoprotein
in a macrophage in arterial wall, therefore, it is causative. Now, with so many people certain in the
medical community that it is causative, what are they missing? #2So, when you say it’s causative,
you’re just quoting– I don’t know your opinion on that- #1Sorry, I should say
I am quoting the literature, right. I am not stating my opinion; I am quoting
what I see in paper after paper after paper. #2Sure. And just to mention
Brown and Goldstein, they stated as a fact that
LDL causes heart disease in a complete absence
of any evidence. hey did an elegant work linking LDL
abnormalities to familial hypercholesterolemia, but they never showed that LDL
was actually causative of heart disease. This is again where we have
to really look at the evidence. It’s all I really care about. So, we have a drug that lowers LDL
as much as statins and also raises HDL, this is CETP inhibitors. So, the great thing about this drug is a completely different mechanism
from statins, and initially killed people,
and so those trials were stopped. So, people are dying with lower LDL
and higher HDL, but after that they were able to clean up
the drug, so it has almost no side effects. The CETP inhibitors, drug company
has invested over a billion dollars. This was to be a blockbuster, because
not only did it lower LDL, it raised HDL. This is one of the biggest failures ever
in Pharma history. So, these are the people who primary,
secondary treatment with the drug, dramatically lower LDL, and absolutely no difference to coronary
events or mortality, so no benefit, no harm. This, to me, is sort of the death note
for the LDL hypothesis. This is saying, no, you’re lowering LDL and you’re making no difference
in coronary events. So, that’s the first thing. The second is we have
to realize there’s… there’s a lot of money involved
in blaming LDL for heart disease. What we got is a new generation of drugs. Well, let me back off, a lot of people say it doesn’t matter
whether statins lower LDL or not, as long as statins provide a benefit,
we don’t care about the mechanism. And that’s one side of the argument
which actually we can talk about. If statins have a benefit and they don’t have
any adverse effects, fine, who cares how they work. But what has happened is we have
this new generation of drugs, that’s the PCSK9 inhibitors. This drug specifically targets LDL. So, if we actually look objectively
at the research and we drop LDL and we simply accept that LDL doesn’t really
cause heart disease and statins work and we stop right there,
that would be fine. But because the drug companies
have invested over a billion dollars in the PCSK9 inhibitors,
we’ve got to continue to target LDL. Now, part of this is I just want to talk
about familial hypercholesterolemia. These are people with extremely high
LDL levels, two, three times normal. And in my papers that I’ve written
which I’m covering in my talk today, I’m covering how people with FH,
people with LDL, 200 to 300 or more, live a healthy normal
life… that they have a normal lifespan. These are people who live
into their 70s and 80s with total cholesterol of 400
and their LDL 300. Well, that’s clearly counter
to the idea that LDL is killing people. It doesn’t make sense. #1Yet there’s a subset that clearly develop
cardiovascular disease at a young age and die at a young age, but when taken as a whole, the overall life
expectancy is not that much different. And when you compare those who get early
cardiovascular disease to those who don’t, it doesn’t seem that LDL is the predictor,
does it? #2Right, absolutely.
So, again, and let’s be clear on the numbers. When you look at – it’s a ratio –
of the age of death versus decade of life… so the first thing is, only about 1%
of people die in their first 20 years. In modern society, we have
very low mortality rate, first 20 years. And when you look at rate of death
for people with FH, that that is not statistically different
from people in 20 years, 20 to 30, 20 to 40. There is no overall difference in death rate. It is remarkable;
there is a greater increase, there are greater incidents of coronary
events, but the actual death rate, this goes back whether you’re looking
at the 1960s, to Harland’s work… though the decades there have been
a dozen of papers published. And Mundal et al,
this is beautiful work out of Norway in which you’re looking at about
5000 people documented FH in which you have no increased rate
of death all-cause mortality at any age. And in fact – this is untreated, so this is not looking at statins having
an effect for people 70 years of age with FH, they have a significantly lower rate of death
for the next decade compared to the general population. #1-Yeah, and that’s –
#2-So, LDL is clearly not relative. Now, we published a paper. My medical colleagues and I published
a paper on medical hypotheses in which we reviewed the FH literature, and this is so important
and it’s ignored by the statin advocates. You have so many papers
that have shown that what kills people with FH
is coagulation factors. These people naturally,
it comes along with high LDL, they also have a genetic anomaly in which they have significantly higher
coagulation factors, higher fibrinogen, higher factor 8. And their platelets are much more reactive
to epinephrine. So, you put some epinephrine in a dish
with platelets, platelets coagulate, okay, they aggregate. Someone with FH, put their platelets
in a dish, put in some epinephrine, they’re 100 times more sensitive
to epinephrine than a controlled population. Now, you don’t hear much about that because no one’s excited
about reducing platelet aggregation, I mean who wants to give aspirin
to someone who’s got FH, right? There’s no money in platelet aggregation,
far more money in targeting LDL. #1Yeah, so, what’s interesting about that is people have a problem mechanistically
understanding that because there can be, you know,
20 or more different genetic mutations than the LDL receptor to cause FH. So, how can they all individually
also effect coagulation? It seems like a disconnect. The LDL receptor genes
also affecting coagulation genes. So, people have a real hard time
mechanistically understanding that. Are you able to explain that? #2I think that it’s a different gene. There’s actually a very nice study showing
different gene forms for prothrombin, which is involved in coagulation. And it’s the subset of those
also have FH and equally high LDL between those who have cardiovascular
disease and those who don’t. But a subset of those also have
the gene anomaly, which dramatically increases prothrombin and those are the people
who have cardiovascular disease. So, it looks like it is potentially linked
to the LDL gene anomaly, but it is a separate gene. And so only a subset of people with FH now
have this reactive, and those are the ones. The other thing to keep in mind,
people with FH are just like everybody else. They are susceptible
to the same risk factors. So, people with FH that smoke have
a dramatically higher rate of heart disease, much more than the general population. And if you talk about
stress reducing heart disease, well, the FH person
is going to be more sensitive to stress. And diabetes, so higher blood sugar
is going to trigger platelet aggregation, so that FH person will be more sensitive. But to the individuals
that don’t have these risk factors and yet have sky high LDL,
no heart disease. #1Yeah, I think that’s one
of the most important points to the make. It’s that the augmented facts,
we know smoking is bad, we know diabetes, hypertension,
metabolic syndrome are dangerous
for your cardiovascular health. But for those with FH, it is a magnitude
or a higher risk for the average person. #2And I think it’s important
for the person with FH to realize that this
is across the entire population, that it appears that they all have this increased susceptability
to platelet aggregation. But it’s the subset then that had
the additional risk factors. Such as the high blood sugar. But you know what is disturbing to me
is that I read the reviews on FH, I read about treatment for FH, and we’re talking about 20, 30 authors
writing a massive review on FH. The word “platelet”
does not come up once. Coagulation does not come up once.
Total focus in on LDL. #1Yeah, that’s interesting,
do they just not– they just disregard that
it’s even an issue because the papers are there,
the science is there. You might say,
I don’t believe it’s such a big issue, but you can’t ignore that the science
is there, and they have to address it. #2Yeah, that’s what they do. And it’s not just one or two papers here
and there where people can’t find it, and you know, we’re talking about 50 years
of research looking at people with FH. And there’s some anomalies,
kind of interesting and people who get their FH,
it’s heterozygous so it’s either from one parent
or the other. It just turns out
that there’s a maternal influence. People who get their FH from their mother are much more likely
to develop heart disease than people who get it from their father. #1Really? I haven’t seen that. #2Yeah, it’s out there, it’s confirmed
LDL levels appear to be equivalent. It’s interesting and it says that maybe– I mean I’ve hypothesized that coagulation
factors come along with maternal FH and not with paternal FH. They may be more reactive
but nobody’s talking about this. #1Yeah, there’s no money in studying it and there’s no real benefit in studying it
because we have the bogeyman, we have the treatment,
so why complicate the issue. #2Well, that’s also the other thing. There has never been a study on FH
going back 50 years. Never been a study on FH
with a placebo-controlled trial. And there’s a lot of modeling
that you will see, no one ever– from the beginning
they thought it was ethical and we got people with FH,
we got to give them treatment, two different treatments
because we’ve got to be able to save them. And the way to look at it is there’s no evidence
that statins have any benefits or any other benefit as a treatment in FH
because it’s never been compared to placebo. #1Right, but historical data
shows in the statin era, risk of cardiovascular disease
has decreased tenfold is what you would read in most papers
since statin treatment has been instituted. Now, as we know
from epidemiological studies, there are lots of other things
that can happen and coincide with that. The relative risk drop since statins
have been introduced is impressive. I mean, when looking at data
from that standpoint, but my guess is you have
a different interpretation of that. #2Well, no, it’s just a matter of looking when is it that death from coronary
heart disease has declined, it actually began in the 1960s. Death peaked in the 1950s and you can actually see
that decline began in the 1960s, and really, the slope in the decline
hasn’t changed much with statins. And the statin research has shown
a very low effect on overall mortality. So, there’s no reason to believe that the statins have any effect on population
mortality from cardiovascular disease. So, clearly, and there are papers
to read in the 1970s questioning why is it so much fewer
people are dying from heart disease now than they did 20 years ago. That may very well be that it is better care
and it’s actually post-coronary care that may be reducing– it’s death
from heart disease that has declined
over the last 40 years or so. But probably the incidents of heart disease
may be increasing with obesity and diabetes. But actually, what it should be
potentially the use of antibiotics. It’s actually very important because
you do see a linkage of infectious disease with heart disease. #1Yeah, we hear about smoking, we hear
about blood pressure management. #2Oh, yeah, you know,
that’s so important. The decline of death from heart disease
has come with the decline in smoking too, which is again peaked
in the 1940s and 1950s. #1Could have also been treating
tooth abscesses or treating, you know,
chronic smaller infections. The point is we don’t know the answer.
We could come up with lots of hypotheses. #2But statins don’t deserve the credit
for reducing it because it preceded
statin development by decades. #1Yeah, oh, okay.
So, we just went down a little rabbit hole. I think I’m going to do a lot with you here
because there’s so much to talk about. But I was starting from the point of asking
is LDL causative of cardiovascular disease, and sometimes I do get in trouble
of making statements that make it sound like I support them when I’m really quoting the literature
and trying to play devil’s advocate. But I think there’s so much controversy
about being involved and being causative and we blur the lines far too often. So, I mean, would you agree that APO-B
containing lipoproteins like LDL lipoprotein are involved in the atherogenic process and
involved in developing cardiovascular disease? #2It’s certainly possible
and I am open to any possibility; I’d like to learn more about it. But what just doesn’t make sense to me is when you look at people
that have astronomically high LDL and they don’t have heart disease.
if we’re talking about it being causative, I mean why is it not being caused
out by itself? We’ll talk about the environment,
the metabolic environment. What you’ve got
is a harmful metabolic environment and you’ve got people
who have high blood sugar and high blood pressure,
which is causing damage to the endothelial, it’s causing damage to the vasa vasorum, and potentially one could say is then
you’ve got infection, that the LDL is found
at the scene of the crime. And again it gets to the association
versus causation. I mean, the police are always found
at the scene of the crime, and so one can make an argument
that police have caused the crime. It’s the same kind of argument. There’s good evidence that LDL works
with white blood cells, with macrophages to target pathogens… to target and be able to kill bad viruses
and bacteria and that is why, in fact,
you find LDL in damaged artery. And you also find white blood cells. Wow, this guy is saying that these white
blood cells obviously must be atherogenic. You find calcium in your artery,
well, calcium must be causing heart disease and you find lots of bacteria in these arteries,
well, bacteria must be causing. LDL is found along with other things
inside the arteries and essentially, there’s so much work showing
that LDL is a part of the immune system. And when you find
actually bacterial remnants, this is very common in the plaque,
you find bacterial remnants. Infection is often associated
with heart disease. And so, LDL is found
where you have infection. And so that helps to understand LDL’s role,
which is a part of our immune system. So, I would say at this point,
there is no evidence of causation. And, in fact, to take it to another level,
there are different kinds of LDL. And this is so important
to the low-carb community because we have to see that is so obvious is that the LDL changes
depending on the environment. And so, what you find is– and there’s
so much work by Ron Krauss and others– is that the LDL changes
under the condition of low blood sugar. So, you don’t have that abnormal LDL. I mean, natural, native LDL is large–
as I say– large and fluffy. And when you surround it by sugar
that is glycated and oxidized, well, you end up
with what’s called small, dense LDL. It has much less cholesterol in it
and it’s much more reactive. The way to think about this
is that is not the way LDL is supposed to be. That small, dense LDL is associated
with an endothelium, with the lining of the artery wall
that’s damaged. And so, what you got in conjunction
with too much blood sugar, too much blood pressure, and then you’ve got damage to the wall,
the LDL itself is damaged. So, I would actually say at this point, I think small, dense LDL is potentially…
think of it as atherogenic. But that’s because it’s contributing
to the noise, it’s contributing to the damage. But the native LDL in a healthy person
is not contributing to the damage. #1So, here we have a lifestyle intervention
that can improve metabolic disease, improve insulin levels,
improve glucose levels, can take small, dense LDL
and make it the larger fluffy LDL, can lower triglycerides, raise HDL,
lower blood pressure, it can do all these impressive things. Yet, the medical community is afraid
that it can also raise LDL. So, would you say this is a completely
different paradigm and environment than has been studied before and we’re outside of any realm of evidence
that medicine can point to? #2Right, and what I’ll be talking
about today is that there’s so little work relating
ketogenic diet to so many factors that people assume have to do
with heart disease as well as other disease. I mean, we could talk
about the microbiome. People say you’ve got to have fiber; you’ve got to have vegetables because
this bacteria must feed on the fiber. Well, no one that I know has ever looked at
ketogenic diet – the microbiome– So, we don’t know what really
a healthy microbiome looks like in someone that’s ketogenic. The same way with LDL, there’s been sufficient work looking
at LDL in people who are ketogenic. There’s no work I know of looking at statin
effects in people that go low-carb, and my guess is who wants
to fund that study, because the low-carb
will blow away statins and the benefits. So, the person who’s going low-carb
in a sense – and I say this – and you don’t know
what the outcome will be because there’s never been a study
on low-carb and ketogenic diet and coronary outcome. And sometimes people… really atrocious work saying
that low-carb actually increase mortality, people die from low-carb…
Truly awful epidemiological work. But the answer is we don’t know that ketogenic diet will reduce coronary
events because no one’s ever shown that. It’s reasonable to assume that because
the biomarkers all move in the right direction, it should all be protected
from coronary events. And the LDL will turn out
to be completely irrelevant. #1So, the argument of course
saying the LDL still matters. Let me rephrase that
because there’s two arguments. One is the one you just made,
we don’t know and we have reasons to believe
it’s going to be protective. The other is we don’t know, so we really shouldn’t treat this
as a special circumstance until we do know, and we should lump it all together. And then when you… if you go that route and that’s sort of the mainstream
medical community would go that route, they really point to three versions
of evidence to support that any elevated LDL
is going to increase your risk. There’s the Mendelian randomization, the genetic trials which we sort of talked
about with FH, but there’s also the PCSK9 gain-of-function,
which… so, PCSK9 basically is involved
in the degradation of the LDL receptors. So, if you have a higher functioning PCSK9, you’re going to actually have
more LDL receptors, you’re going to clear the LDL faster. So, there’s a population that had a lower risk of cardiovascular
disease with that gain-of-function, and thus, the development
of the PCSK9 inhibitor drugs. So, just a study like that showing benefit
from lower LDL with higher receptor action, I mean is that enough to say,
okay, there is more evidence there to say that a lower LDL is beneficial
for some people, so therefore, we should air on that side. #2Yeah, the original PCSK9 work was based
on people who had abnormal PCSK9 and so they had significantly higher
LDL receptor density therefore lower levels of LDL and
somewhat lower levels of coronary events. But that was really related to a relatively
small number of people showing no overall mortality difference between those with the PCSK9
abnormalities and the controls. Now, the reason was– and again, target is
LDL because that’s where all the money is. The recent work has targeted
the PCSK9 inhibiting drugs. The thing that’s so important to realize
is when someone takes this drug, what they’re doing is increasing their LDL
receptor density, okay, which is abnormal. There are beautiful
negative feedback systems to maintain LDL receptor
just to the right level. This drug blocks the neative feedback
so you’re increasing LDL receptors, meaning where is that LDL going to go? It’s going to buy into these receptors
and go into the cell. So, the cell will become
chock full of LDL that shouldn’t be there. The cardiologists love this because now
the LDL is taken out of the blood, so you drop LDL levels by 70%. But that LDL doesn’t disappear. The LDL is being crammed into liver cells, and ultimately – my prediction,
they’ve only looked like two years now, and there’s no real difference in cardiac
events when you look at the PCSK9 trials. My prediction is you’re going to see
a really screwed up liver. You’re going to see liver damage
in these cells that have too much cholesterol
inside them, and so 5, 10 years down the line, you’ll be looking at people
that will be harmed by this drug. #1Wow, that’s a great hypothesis. And we need longer term studies because
so far, they’ve been only two years. In defence of
the PCSK9 inhibitors, they take the highest risk patients
already on a statin, they give them the PCSK9 inhibitors…
they drop their LDL further, two big studies, one showed
about a 1% reduction in cardiovascular events with no mortality difference. One showed a 1.5% reduction
with a small mortality benefit at two years. So, the proponents say,
well, if we had this effect in two years, think of the effect
we’re going to have at 10 years. And of course, your response is what are
the side effects and the risks will be at 10 years and we
don’t know the answer to that question. #2We don’t know that answer. #1So, there’s the Mendelian study,
the genetic predisposition, and then there’s
the epidemiological studies, which we sort of touched on
but studies like Mr. Fit, like Framingham which showed the association
between total cholesterol and LDL and cardiovascular risk. Although, a small association
but an association… now what about–? #2-Can I interrupt you?
#1-Yes. #2I’m going to be talking
about Mr. Fit today. This is an amazing study because Mr. Fit showed a 400% increase
in coronary mortality based on cholesterol levels
going from the lowest to highest. And it’s actually right now at the University
of Minnesota website, you can see Mr. Fit. And this is looking at about 400,000
middle aged men and they’ve got their cholesterol levels and they had followed them
for quite a few years, seven years. The mortality rate from the lowest
to the highest man was 1%,
the actual mortality rate was 1%. And they have distorted this
to turn it into a 400% mortality rate. So, you mentioned Mr Fit.
That was an abomination of science. Framingham, I think it’s all very clear. When you look at unhealthy people,
you look at LDL in an unhealthy environment. Potentially, it’s either trying to save
the unhealthy environment or it’s a part of it. But again, it means the patient needs
to sort of take his life into his own hands or her own hands. They need to take control
of their own environment, they’re not going to find health
in a pill has been my point. And so, the person who has diabetes
and is obese thinks they’re going to be protected
by taking a statin, well the answer is still they’re going
to be very unhealthy. #1Yeah, and that’s one of the traps
we fall into as a medical community, just trying to make things
so simple for the patient. Make it easy for them,
and that easy doesn’t always work. #2Right, and so, for the person
who’s going low-carb, improving all the biomarkers, and yet
they’re still concerned about the LDL. So, when we look again, getting back to 4S,
which I think is so incredibly important. The 4S trial, again run
by the drug companies, and so even though I’m skeptical looking
at the data going wow, this is amazing. The people have the kind of biomarkers
you see with someone on a low carb-diet showed no benefit whatsoever
with statin treatment. That tells you a little something about what to predict
when we have someone that is low-carb, and therefore, they don’t need the statin
because there is no benefit. #1Right, not proving that the low carb is–
the low carb eliminates the benefit, because that wasn’t tested but you can draw
a hypothesis with that evidence if you want. #2Yeah, and there’s every reason to believe
that adverse effects don’t discriminate. There’s no reason why there shouldn’t be
adverse effects in someone on low-carb. And so the adverse effects
are just the statin effects in physiology. So, potentially, they’re looking
at the cognitive effects and the muscle damage
and the liver and kidney effects as well. #1So, what’s interesting, though, when you specifically the cognitive
effects and the risk of diabetes, I mean that’s what low-carb is purported
to be able to benefit, so I would like to think that
that would be a safety mechanism to hopefully reduce those side effects;
again, no data behind it. But it certainly makes empiric sense. So, if I have someone on a statin, I would
actually want them on a low-carb diet. One for the metabolic benefit and to help
with the LDL beyond what a statin could do but also to reduce potential side effects. Now, you’ve pointed out to me that there was actually a paper showing
some beta cell dysfunction in the pancreas, so maybe low-carb isn’t going to be enough
to help reduce the risk of diabetes. -What do you think?
#2-No, not at all. When you think cognitive effects,
the brain makes its own cholesterol and it needs the cholesterol
to make new brain cells to make memories. Well, we actually published a paper showing that the statins
that actually are lipophilic, which means they can get into the brain, are the ones associated
with adverse cognitive effects. And so that statin is going in the brain independent of whatever
the person’s diet is. It interferes with brain
cholesterol synthesis, which is essential for making memories. And so, no, I don’t think it has anything
to do with the person’s diet, this is now just simple physiology. You interfere with cholesterol production
in the brain, you’re going to interfere
with brain functioning. #1Yeah, and the critics say
it’s difficult to measure that because if statins are being used
in an elderly population, elderly people are going to get
reduced memory function anyway, how do we quantify it
without a trial, same thing. But it comes down
to what are you most worried about. Are you most worried about
developing Alzheimer’s disease and cognitive decline or a heart attack,
and as we age that may change? And age is such a fascinating topic when
it comes to cholesterol and LDL in general because whether it’s Framingham study
or whether it’s the Honolulu Heart study, there are a number of different stages. Taking it together suggests there is again
maybe a bimodal response in the 50s and younger, there’s a tighter association between
LDL and cardiovascular risk, but in the 70s and over,
that association seems to flip. And you’ve been very big
about pointing that out. So, tell us about that difference. #2Yeah, so, what I would still go with
is risk factors. What you’ve got there are risk factors
that kill people relatively young; smokers and diabetes. These risk factors potentially interact with oxidized and small dense LDL
at a younger age. You make it into your 70s and 80s, then
you basically don’t have those risk factors, you’ll much less likely have
the risk factors. And so, you don’t see obese people
typically living into their 80s and 90s. And in fact, what you do find is that people with the highest LDL–
and there’s more than 50 years of studies– people with the highest LDL actually live
longer than those with low LDL. So again, it’s completely inconsistent with
the idea that LDL causes harm on its own. And we published this paper
in BMJ Open a few years ago. We reviewed and looked at every paper that looked at mortality in relation to
LDL levels. There wasn’t a single paper
that showed increase mortality in relation to the general population
in older people, that’s over 60, with the highest LDL,
compared to lower LDL. So, that’s completely inconsistent with the hypothesis that LDL itself
is causal to heart disease. Because it’s not killing older people who are at the highest risk of death
from stroke and coronary heart disease. #1Yeah, the comeback there is that
as people get sicker, their LDL declines, so as they’re on their death bed,
their LDL is going to lower. #2That’s really the reverse causality
argument, which really completely fails because it’s not looking one year
after someone has had a blood test, which actually does happen. Someone dies and you find
the year before death, especially if it’s a cancer death,
LDL levels do decline. But these are 10, 20, 30,
even 40 year-long institutional studies. You got a blood sample from someone
in the 50s or 60s, and 20 years later you look at who’s died
and so, you’re looking years beyond and these are people
who had good health to begin with and you eliminate any people
that had died in the first couple of years. You’re still looking 20 years later. Those who had the high LDL in their 50s
and 60s are still living in the 80s and 90s. #1Yeah, so, again,
observational data doesn’t prove that the high LDL
is what is improving their health, but certainly flies in the face of high LDL
is dangerous and going to kill you. #2These are completely inconsistent
with the idea that LDL is causal. It’s so simple; essentially it relates me
also to the vegan versus carnivore diet. Vegans love to say
how bad red meat is for you. If only the people who were eating
red meat in their 40s would die of a heart attack,
it would be so simple. Well, if the people who demonize LDL and say, well it causes heart disease
and people die, well, if people with high LDL would just die,
in their 30s or 40s, it would be so simple. But they don’t. The people with high LDL are living
into their 80s and 90s and even 100; we’re going to hear that today
that the people who are 100 years old have the highest LDL of those measured. It just simply doesn’t make sense
to think of this as causing heart disease. There is an environment,
a toxic environment where you will find LDL,
especially in the younger people. A toxic environment has to do
with smoking and high blood pressure. And so again, if we think of high LDL
coming to the rescue, now, the reason why we want to think
of LDL being beneficial is that people with FH
have a lower rate of death. Again, got to emphasize, it’s not statins. People in their 70s
have a 40% reduced rate of death because they have a normal rate of death
from coronary heart disease but a lower rate of death
from non-coronary heart disease in their 70s. Less death from infectious disease,
less death from cancer. This is how you look at it;
if you live up to your 70s with high LDL, you’ve got a more
protective immune system, and no difference in cardiovascular death. #1Yeah, it’s interesting to see it’s certainly
not talked about it from that standpoint. #2There’s no money
in talking about LDL as protective. #1Right, and then there’s the concern
about time of exposure, that has something to do with it. Whether you have LDL in your 40s
or LDL in your 70s, that it’s a different… a whole different time of environment,
a different time of exposure. but more than time of exposure, is likely what else is going on from other
risk factors and metabolic health. #2The person that has FH and is in their 70s
have had 70 years of exposure. And so again, they call that
lifetime LDL burden. And if you actually look at some
of the work you cited earlier, they’re saying that FH untreated, you can expect people to be dying
in their 30s or 40s. And again it simply doesn’t happen. #1Right, right. Where else to go? There’s so much to talk about here,
so much more. You have been criticized and any time anybody goes
against the mainstream medicine, of course they’re going to be criticized. But one of the criticisms has been that you’re cherry picking your studies
and cherry-picking the data. How do you respond to that? #2Yeah, I think the people
who have criticize statins are called statin deniers
are cherry-picking the data and actually
their criticism goes beyond that. They are actually saying
that this is an internet cult and they say these people
are no scientists. I have no bias whatsoever. And again, I’m just a scientist. My first priority
was to improve my own health. I have no reason to be biased to pick the studies that would basically
make a point for me. If I want to be showing that LDL
is not harmful and I picked those studies, but ultimately
I don’t care about my own high LDL. I mean, it harms my own health. So, I have no bias. I have no interest in this
other than looking at good science. I want to look at all the science
and come to valid conclusions as a scientist. Because I get no money from this,
I have no pay, I have no funding for my interest
in cardiovascular work. It’s purely a personal venture for me. I don’t want to be biased,
I don’t want to cherry-pick the data. I’m looking at the entirety of the literature
and then coming to conclusions. #1Yeah, and so, it leaves us
as doctors and clinicians facing someone who’s improved
their health, improved their blood pressure, improved their metabolic parameters but
have a high LDL, being confused what to do. The average doctor out there
who doesn’t see this every day is going to have the knee-jerk reaction
that this is dangerous. Someone say ignore the LDL completely
and you don’t have to worry about it and some are trying
to really put it into context. But it’s because of work like you,
because of Zoe Harcombe and Aseem Malhotra and Malcolm Kendrick. People are willing to go against the
juggernaut of the medical community and Big Pharma to say wait,
we need to look at this differently, that allows clinicians the ability to say,
okay this is something different, there is something to this. You’ve put yourself out there
to really help move this forward and you’ve gotten
a lot of attacks for it. I mean, has your skin
really thickened from this? #2Actually, I’m not sure
what attacks you’re talking about. I think in general the statin advocates
have ignored to a great extent the people who have been critics. I know it came out there an article
in the UK paper recently specifically criticising Zoe Harcombe,
Malcolm Kendrick, Uffe Ravnskov. They left me out of this because I’m not
a UK person, but that article was truly awful. I mean, attacking them and saying,
you know, how wrong they are. But really, I don’t even think…
we’re not coming out against Pharma, speaking for them as well,
there is no bias whatsoever. I am not looking to praise LDL and I would grant that the small dense LDL,
which is an abnormal LDL, may be contributing to disease along with– it’s almost like LDL, small dense LDL may very well be the gas on the fire,
but it didn’t make the fire. So, I don’t take it personally. And oh, I actually do recall that there was
a cardiologist at Duke University, who wrote a note specifically about me saying that I was causing harm
to her patients, that people would all die because I was
explaining how statins have adverse effects and how overall the adverse effects
are greater than the benefits, to which I wrote a rebuttal
to that cardiologist to reply. So yes, there was one example I can think of
which I’ve personally been attacked. But then again to me, it’s all just science,
it’s not something I take personally. #1I think that’s a good perspective,
it’s all science. And actually, just to talk quickly about that
article in the Daily Mail where they compared LDL cholesterol
deniers to the anti-vaccine movement. Which I think is fascinating because
they drew that comparison to the doctor who was falsifying
data about the vaccines. And I thought that was awful, I thought
that was clearly overstepping the bounds because you are not falsifying anyt data. You are helping us see data that exists,
that other people did, that’s either being ignored
or been promoted in a different way, you’re just helping us re-see that data;
there’s no falsification there. #2Well, there’s a strategy in combat,
which is to dehumanize your enemy. And what people do is say,
they’re not real scientists, so you can call them an internet cult. You can say that they’re
just like the anti-vaccine people. And that way, in a sense,
you dehumanize them, you denigrate them and therefore they’ll have less credibility
and that’s just wrong. What we have to do is talk about science
and I’m open to any aspect of the science. From the very beginning, I just wanted
to learn how is it I can make myself healthier. And what I realize is that I did ignore
the LDL and I did ignore my LDL now, which is quite high
and what I really care about and what matters
is blood sugar triglycerides, HDL is important but it is
the canary in the coal mine. You don’t want to take a drug
that’ll raise your HDL. HDL tells you about your lifestyle,
triglycerides tell you about your lifestyle telling you you’re consuming
too many carbohydrates. LDL doesn’t tell you much. #1Yeah, and I think that’s a great point and
a great way to sort of summarize this, is are we talking about causation
or are we talking about markers of our underlying health
and our underlying lifestyle? That improves with a low-carb lifestyle. Your markers improve and then that
should give us the evidence that our health down the road improves. I hope that we get that long-term evidence
and in the absence of it there’s certainly reason
to believe it’s going to be so. #2-That’s a great summary.
#1-Okay, good. Well, thank you for joining me,
I really appreciate it, and where can people hear more about you,
about your thoughts and your research? #2Well, you know, I don’t sell books. I don’t have a book, I don’t have a blog,
I don’t have a website. This for me is still, it’s personal. I have my day job in which I still do
my neuroscience research. I will be… I actually don’t have any talks
planned for the future. For me, it’s important
to write medical publications, so I’m in the process of writing more papers
to be published in medical journals. So, I’m really approaching this
as a scientist. I don’t promote myself as anything,
I am not making any money from this, so I welcome the opportunity
to talk about it with you, thank you so much for inviting me, but frankly, I don’t have anything to share
as far as promoting myself. #1That’s a breath of fresh air,
we don’t hear that very often. -Thank you for doing that.
#2-You’re very welcome.