Diet Doctor Podcast #15 — Prof. Andrew Mente

Welcome to the DietDoctor podcast
with Dr. Bret Scher. Today I’m joined by Prof. Andrew Mente. Now prof Mente has a PhD in epidemiology
from the University of Toronto, he’s done his postdoc work
in cardiovascular epidemiology from McMaster University and he’s an associate professor of health
research methods at McMaster University and most recently he was
one of the co-investigators on the lifestyle and the nutritional side
of the PURE study. Now PURE is this enormous study
over five continents, 18 different countries,
over 135,000 different individuals, that has had some pretty profound
research evidence as it comes to saturated fats,
cholesterol fat in general and their implication
on overall mortality. It has a number of data
on salt intake and mortality. And a lot of it is contrary
to conventional wisdom and guidelines. Now all that being said,
this is an epidemiological study and we definitely talk about the strengths
and benefits of epidemiology versus randomized controlled trial and he is a good perspective on how
we really need both to further research and affect policy. So there’s a lot of data here
going over the PURE study and it has some pretty profound impacts on
the way we should make recommendations and how we should see older
recommendations and their falling. So I hope you enjoy this interview
with Prof. Andrew Mente and learn a lot about the PURE study and understand how we can use that data
in our daily lives. Prof. Andrew Mente thank you so much
for joining me on the DietDoctor podcast. It’s a pleasure to be here. Now you have really become known
as the PURE guy because of the PURE study and all the data
that’s come out of that and how that’S impacted how we see salt how we see fat and carbohydrates
and how we see lipid biomarkers, three huge concepts
that we’ve kind of been misled on. So this has been pretty revolutionary data
that you’ve come up with. Yes well the unique part of PURE is that it’s a large prospective
epidemiological study, but it’s also a global study
so it covers five continents of the world. And as a result we captured
broad patterns of diet globally from across a broad range of intake, both very low levels and very high levels of individual nutrients in foods
and dietary patterns. That’s important because that allows us
to assess shapes of relationships between dietary variables
and health outcomes. Which has never been characterized before
with any high degree of statistical precision. Yes it’s such an interesting part when
you talk about nutritional research and it is complicated,
let’s be honest, it’s very hard to do, whether you talk about randomized
controlled trials and observational study, a study in one type of population
or a study in a large swath of a population, and each have their benefits
and their drawbacks. So when you look at analyzing the data
from the PURE study, tell us what you think some of the strengths
and weaknesses are in that type of a study. Sure, obviously observational studies, we assess relationships
or associations between variables, diet and health outcomes, so you don’t prove causation
with any one observational study, but what you do is you look
for a coherent pattern of information from observational studies,
both looking at foods or nutrients versus intermediate risk markers
for cardiovascular disease and actual outcomes. Of course with a large randomized
controlled trials we can better assess causative effects. The problem with large randomized trials is
they’re very difficult to conduct with diet and it’s very difficult for people
to sustain a particular diet for a long term. And so there’s a challenge there. On the other hand
when you have weak effects, it’s harder to assess weak effects
in observational studies, because you don’t know if the result is true
or due to residual confounding. So we tend to think of different designs
as complementing one another. So not one design being the best
considering feasibility and also, you know,
what is the cleanest design. But using different designs complementary
to one another and capitalizing on the strengths of each
is the ideal way to go forward. Yeah, and then the harder question is
how to take the data you have and incorporate it into guidelines
for the entire country or the entire world to try and follow? And when is that data strong enough
to support a statement that this is the way to eat? And so far it seems like we’ve been
a little misled in that stand, haven’t we? Absolutely, so we take the issue
with the fats and carbs for instance. So the current dietary guidelines
go back obviously to where that was conducted in the 50s
that led to the adoption of a low-fat diet which we know it really hasn’t panned out and populations have gotten fatter and diabetes rates tripled, coinciding with the introduction
of the guidelines. So our data suggest that the conventional
way of thinking of diet focusing on higher intake of carbohydrates
may actually backfire, which supports what has actually
happened. And so higher carb intake, and remember many parts of the world consume
very high amounts of carbohydrates, low and middle income countries, and largely it’s refined carbohydrates
and added sugar. And we find that higher carb is related
to more cardiovascular events and mortality particularly all-cause mortality,
whereas for fats we see the opposite. We see higher fat intake
related to lower risk of mortality and saturated fat related
to lower risk of stroke. So this kind of challenges
conventional wisdom on diet, but it is consistent with the trials, because you look at the randomized trials that replaced saturated fat
with polyunsaturated fat, that haven’t really panned out. Largely neutral effects. And other observational studies too
have shown neutrality looking at relationship with saturated fat
and clinical outcomes. So our findings, if anything,
are supportive of previous studies. Let’s jump into the study a little bit. So you mentioned 18 countries,
5 different continents, over 135,000 individuals and what was
the timeframe that you followed them? So for our papers that came out last year
in the Lancet it was eight years of follow-up. This year we had a paper that came out
on dairy that was nine years of follow-up, because the follow-up is ongoing
and PURE is still during the follow-up and we hope to follow people
for at least another 5 to 10 years. So you mentioned the data
on the saturated fats and carbohydrates. So with a higher carbohydrate diet
starting at 68% of the calories there was an increased risk
of all-cause mortality. Now we need to talk about hazard ratio, because you know we’re quick to point out
that smoking with a hazard ratio of 3 1/2 is a dramatic change. The red meat leading to colon cancer
at 1.17 is a small hazard ratio. So the hazard ratio here
was small at 1.17 and 1.28. So how do you help us interpret that in terms of it was a fact because
of how many patients there were, but yet the hazard ratio was small and
it’s sort of against what the guidelines say. So how do you incorporate all that
into how we should interpret that data? Dietary effects are weak. If you look at the collective literature
whether it’s nutrients or foods, largely effects are weak up to the degree of
like 10% change in risk, relative risk change. So that’s a very weak effect,
unlike smoking, where you see a 20 fold increase in risk
of smoking versus lung cancer. So that’s a challenge with diet, studying diet
in observational studies, but if anything, you look at the data
of other cohort studies and if you focus on the studies that looked
at carbohydrates versus mortality as a percent of energy, you also there see that higher carb intake
shows an increase in the risk of mortality. Now some studies have looked
at calculated diet scores or carbohydrates scores and so what goes into that is different
coating of our carbohydrate foods. So you can select almost any food you want
to go into a carbohydrate score and you’ll get different results, but the studies that looked at percent
of energy from carbs, you see a positive association
with mortality. Now there aren’t that many
free living populations with very low carbohydrate intake. So don’t misread me, I’m not saying that
going as low as possible would be beneficial because that has yet to be demonstrated but certainly appears that there is
an optimal range between 50% to 55% of energy from carbs that appears to be associated
with lowest risk. At the low-end it’s a little more murky,
we really don’t know. And then the problem comes in
of the quality of the food that you’re eating. So there’s really no control
for the quality of carbs, because it’s free living people
like you said, in some of the poor countries,
underdeveloped countries, it’s going to be a lot of refined
carbohydrates and refined grains. So not a surprise that a higher level
of carbohydrate increased mortality risk. Now what maybe was a surprise that the higher level of fat intake
decreased mortality risk, I think that’s where the real headline is,
that is so counter to what we’re being told. And now you broke that up into
monounsaturated fats, polyunsaturated fats and saturated fats in terms
of their mortality risk; so tell us how those varied. Yes, so first of all
each individual type of fat, saturated, mono and polyunsaturated
were associated with lower risk of mortality, so they all directionally
went toward protection. Now with looking at saturated fat
we found– because remember we’re covering
low and middle income countries here where saturated fat in many parts
of the world is very low, and so saturated fat going up
to about 13% of energy was associated with lower risk of mortality. Now what this suggests is that when you go
to low levels below 10% and further do you actually see
the increase in mortality? Which is actually what the guidelines
recommend; to go to those lower-levels. Now we are not saying that our data supports consuming 20% or 25% of energy
from saturated fat, only because that’s not captured by the natural distribution of saturated fat
in free living populations. And certainly some societies you see
consumed 3 to 4 decades ago much higher amount of saturated fat. So our data is not capturing
that high level of saturated fat, but up to about 13% or 14% of energy
we see a lower risk of mortality compared to people consuming
lower amounts of saturated fat. Now interestingly the mortality also
for fat in general and saturated fat was neutral for cardiovascular mortality and beneficial for all-cause
and non-cardiovascular mortality. I mean is that one other surprise
or is it what you would expect to see? Well we look at the randomized trials, at Cochrane review by Hooper in 2015
of randomized trials, where they replaced saturated fat
with polyunsaturated fat, again a direct test
of the diet heart hypothesis, the summary estimates were neutral. So our results were consistent with that. The Women’s Health Initiative trial which compared the low-fat diet
to a higher fat diet again found no significant change in risk
for cardiovascular events and mortality. So that was another large study,
cost half $1 billion. So if anything our results
are consistent with that. Now if you look
at cardiovascular disease mortality and non-cardiovascular mortality, directionally we did see
that different types of fats were beneficial, although it wasn’t statistically significant
but directionally. And in carbs directionally was harmful versus cardiovascular death
and non-cardiovascular death. It was the nonfatal events
were as large and neutral. Now are we able to breakdown
the non-cardiovascular deaths anymore, whether it’s cancer, infection
or the various different causes? Well the main non-CVD causes right now
in PURE are cancer and respiratory mortality. So those two,
those were the main drivers of it. Now of course PURE is a large cohort
that is still ongoing, so we are following people up. We don’t have enough event rates
right now to characterize cancer
or respiratory events alone or individual types of cancer. But as the cohort gets older
the event rates will pick up and we’ll have more events. So that’s why it’s very important in PURE
to do the follow-up over the next 10 years than we can assess
individual types of cancer and diet. Right, now you with a study like this
that goes against our guidelines and goes against what you can say
that the most common dogma is now, would you say this is strong enough
evidence to say things have to change now? Or do you think this is sort of one blip
on the screen and we need more to come in order to affect policy
and make a change? Well, I think collectively looking
at our data and other studies as well we could relax a bit on the threshold
for saturated fat and given the population on average
in the US for instance, the average intake of saturated fat
is about 12% of energy. So it’s only slightly above
the WHO recommendation of 10%. So it’s not like we have a saturated fat
emergency, so I would say that’s fine. What we’re consuming else, fine,
we could even consume a little bit more. We’re not saying consume
unlimited amounts, we need data for that still, but what we consume now
appears to be right and we don’t have to put in
stringent cutoffs to get people to lower their saturated fat. Now also there’s concern about–
like we talked about earlier, data quality, so is this mostly from food frequency
questionnaires that people filled out and how often were they filling that out and
is there any concern of reliability for that? Yes, so the food frequency
questionnaires were extensively validated and developed specifically for each region and there were long-frequency
questionnaires, so captured detailed aspects of diet. So for instance we have 150 items
measuring diet in a particular population. So that’s a very in-depth analysis into diet. Now the downside with these questionnaires
of course is random measurement error. And so that adds noise but that more
dilutes associations toward the null, and that is a factor
in every epidemiological study. So it is the best tool we have at the moment
for large epidemiological studies and that’s what we use. Again that’s why I say complementing
randomized trials, focusing on risk markers
would be optimal. So the major strength however
is the fact that we cover again a broad range of intake
across different parts of the world, again characterizing those extreme ranges as much as they are represented
by human consumption and that’s really
where the advantage of PURE is. Now you mentioned comparing the trials
to randomized trials using risk markers. And that’s one of the parts of PURE
that I really enjoyed most, was looking at the risk markers. So you looked at… as they increase carbs
their LDL decreased and so did their HDL and their triglyceride to HDL ratio increased
and their ApoB went down a little bit. So their ApoB to ApoA ratio also went
down. So then you looked at outcome data
in terms of what these markers all met. And what did you find in terms of the
difference between LDL cholesterol, the ApoB to ApoA…?
Share that data with us. Yeah, so as you said
looking at the risk markers, saturated fat had an increase in LDL
with higher saturated fat, but the effects on the other lipid markers
were largely beneficial. So when you look at the ratio
of total cholesterol to HDL, which is a stronger risk marker
of future cardiovascular disease, that’s just a potential beneficial effect,
because the ratio went down and we know that that risk marker
is a better predictor of future events. And when you look at ApoB to ApoA, which remember in INTERHEART
and INTERSTROKE, two large international studies, was the strongest lipid predictor
of heart attacks and stroke, we found that the ratio goes down
with higher saturated fat, which again suggests a beneficial effect
since that is the strongest risk marker and that goes down
with higher saturated fat. And then what we did is we modeled… we said okay assuming we don’t have
any data on clinical events, let’s model and use the lipid markers to project what the effects of diet
on cardiovascular risk would be. And then we did that,
we modeled using LDL and we found a positive association
as you would expect. After all saturated fat
is positively associated with LDL. But then when we map that
versus actual events, we found that LDL was a poor
predictive marker of future events when you look
at the observed associations. On the other hand
ApoB to ApoA ratio was much better at projecting the effects of diet
on health outcomes. So this suggests that if we focus on LDL we may be largely misinforming diet
for populations. ApoB to ApoA ratio, which is a measure
of small dense LDL particles that are more atherogenic than LDL appears to be the much better
predictive marker to project the effects of diet
on health outcomes. Are you able to quantify that
to give us some sense… like how much better,
how much more associated it was? Or is that data sort of hard
to quantify that way? What we did is we calculated
the I-squared value, which generally assesses the degree to which the actual estimates
agree with one another. And so when you calculate that statistic you see that the estimates
from the ApoB to ApoA ratio, projected estimates versus
the actual observed estimates agreed and it was a good agreement. Whereas with LDL they diverged
in opposite directions. So the projected estimates
showed an increase in risk, whereas the actual effects of saturated fat
on the events go down slightly. So they diverged in different directions. It would suggest that LDL is not very good
for projecting dietary effects. It may be very good for projecting
statin effects on health outcomes, but not for diet. That’s so worth repeating; that the projected effect
would be that the risk would go up and the observed effect
was that it actually went down. That’s right. It was completely discordant. And that calls into question every
single dietary study that’s looked at LDL because the presumption is
if the LDL level goes down, this diet is therefore beneficial
and protective. And you really don’t have to look any
further than the sort of the older studies that looked at giving polyunsaturated
fatty acid oils, seed oils, which showed LDL went down
and that’s what was publicized, but then a re-examination of the data
showed that mortality actually went up, but that’s not been talked about very much. So my hope is that this study would cause
just a huge snowball effect of people realizing that LDL-C is not
the marker we should be following. Yet I don’t feel like I’ve heard enough
about that in the media and in the scientific circles. Is that just because old dogma dies hard
and people aren’t ready to hear it? Why do you think that’s the case? Well, you know, LDLs
is considered by the– You’re conventionally thinking of it
as an infallible marker. Right. And so people think of it
in a very reductionist way, many scientists. So they figured that, if anything, that
adversely affects LDL, it must be harmful. And you could ignore
all the other biomarkers. But diet is much more
complicated than that. So you take foods,
natural sources of saturated fat, that contain saturated fat but they also
contain monounsaturated fat. They also contain protein,
they contain vitamin Bs, including B12. They contain zinc and magnesium. So this is all thrown out and we treat food almost like it’s a single nutrient
saturated fat that’s infused into our veins. And that’s used to project the effects and really is an absurd way of thinking
if you really think about it deeply. So for diet we have to think much more
multidimensionally than that. Absolutely,
I think that’s a great statement, because we do like reductionist thinking, we do like to try and make things
overly simplistic and this is the mess we get into
when we do that. I know your study did not specifically look
at a low-carb or ketogenic diet, but in those circles the main concern is,
“What about the LDL?” The LDL goes up and that’s why doctors
are hesitant to prescribe it, that’s why a number of guidelines
will not include it because of that concern and yet looking at this data if the ApoB to
ApoA ratio stays the same or gets better it shouldn’t matter what the LDL does. So I think that’s why this evidence
is so powerful and we need to be seeing this
from the rooftops more to say we need to reevaluate dietary
changes and their effects on cholesterol. And quick, to point that out… It may not be the same for drugs,
it may not be the same for genetics, but for dietary changes
that’s what we need to look at. Absolutely yes and we need to study
a much wider range. So you look at the PURE study because the level of carbohydrates and fats
only cover a particular range. That’s where the randomized trials
are needed… like Virta for the work
that Dr. Hallberg is doing to capture the lower end
of the carb distribution. So it’s very important to look at that to see
what the effect on the risk markers here are for very low-carb intake. Which PURE does not capture, because it’s largely representing
parts of the world that consume from moderate to high carb. So that’s why Sarah’s work
is very important. Right and since you brought
Sarah’s work at Virta Health, you know, at their one year data mark
the LDL-C went up by about 10% with no change in their ApoB
and their HDL went up, so their ApoB to ApoA ratio improved. And so based on this
that is a net benefit for mortality and that’s what we care about. That’s right. Yeah, it’s so fascinating. The tide is changing maybe a little
too slowly, but it is certainly changing. Yes. Now this study also had
other aspects to it. So the next one was increasing fruit,
vegetable and legume consumption decreased mortality
starting at three servings per day, with really no difference between the three
and eight servings per day. Now I am curious about that, because
fruits, vegetables, legumes, they frequently do get bunch together. And I think it’s a sign of somebody maybe
being a little more health conscious, because that’s what we’re told
as a healthy way of eating, but was there any parsing out individually
of how vegetables are different than fruits and different than legumes individually? Yes, absolutely. So the beneficial effect was largely driven
by fresh fruit, raw vegetables and legumes. It’s the cooked vegetables,
when you put that end into the equation, that’s when you start
to drown out the beneficial effect. -Interesting.
-Yes. So if you look at versus CVD
and also looking versus mortality, fruit, raw vegetables and legumes
were beneficial, but when you look at cooked vegetables
that’s when you see no effect on CVD and maybe even directionally
maybe even a harmful effect. So maybe cooking methods
and what we add to food while cooking may be an important factor. Yes, I wonder if this is because they’re
cooking in Omega six seed oils or they’re cooking
in like heavy sugary sauces or something. It certainly makes you wonder
because that’s not what I would expect. So of course everybody’s got their bias. When you see something you don’t expect
you want to find out what makes it wrong and that’s part of the trouble
we get into and I need to catch myself for doing that. Because interesting,
with increased fruit intake, if somebody was diabetic
or had metabolic disease, you would think that would have
a deleterious effect, but over the whole sample,
fruit intake was beneficial. Yes, well we have to also remember
that PURE represents general population, people living in communities,
so it may very well be different for diabetics. The diabetics may need to restrict the very high sugary
or high G.I. type of fruit in their diet. But for general populations
fruit was largely beneficial. So I guess it depends on the population
that you are studying and diabetics may be different. Yeah and I think is important to point out
for the general population, fruit, vegetables, legumes can certainly be
part of a very healthy diet but in certain populations
we need to measure their effects specifically on that individual. Yes indeed. And then the other part of the study
was salt. So salt and saturated fats have to be
the two most misunderstood and misrepresented components
of our food intake. What you saw from a salt intake was that
a higher risk below 3 g of sodium and a higher risk at above 6 g of sodium. So first before we get into the details tell me the difference between
grams of sodium and grams of salt, just so we’re all speaking
the same language here. Yes so 1 g of sodium
is 2.5 g of table salt. So the WHO recommendation
is 2 g of sodium which is 5 g of table salt
or 1 teaspoon. One teaspoon! Tiny amount. Yes, very difficult for most people to
consume in the short term let alone the long-term
and that’s the recommendation. Yeah, so the recommendation I think
is less than 2.4 g, or is it less than 2 g? Now depends on the guidelines. WHO is 2 g, the US dietary guidelines 2.4, for high risk population the American Heart Association
recommends less than 1.5 g per day, which is only 0.7 teaspoons of salt per day,
very low amount. And there was a study showing only less than 3% of the population
adhered to the less than 2 g per day. Correct, and when you adjust
for random error, it’s well below 1%. And when you look at people who meet
the sodium and potassium recommendation it’s only 0.001% of the population
who meets the recommendation. Now what we currently recommend
is what nobody eats. Right, and this
completely seems undoable. So where does recommendation
come from? Well, the entire field hinges
on an assumed benefit considering the effect of sodium
and blood pressure. So given that sodium is associated
with higher blood pressure, it’s assumed that this will translate into
a cardiovascular benefit if we lower sodium. Now of course this assumes that sodium
affects only blood pressure and has no other effects
on any other biological systems in the body. But because sodium is an essential nutrient
it doesn’t quite work out that way. So we agree that at high levels you get
toxicity and increase in blood pressure, but at low levels you get deficiency. And so what that does is it activates certain
mechanisms that are built into our bodies since salt is an essential nutrient. So you get renin angiotensin
system activation at low levels. And this has been shown repeatedly
in intervention trials. And so you have
dual competing mechanisms, which is consistent
with an essential nutrient. Toxicity at high levels,
deficiency at low levels, sweet spot in the middle. And our findings reaffirm that and
other studies as well reaffirm that. There is not one single study ever that has shown that low-sodium
at currently recommended levels is better than average sodium,
that sweet spot of 3 to 5 g per day, versus cardiovascular events
and mortality. High levels above 5 g per day, certainly, we should get those populations
down to moderate levels, but there’s absolutely no evidence
to support low levels versus moderate levels and yet that’s what
we currently recommend again based on an assumed benefit,
looking at blood pressure. Right, an assumed benefit and a lot
of people will quote the DASH study, thinking that this was the end-all be-all
conclusive study on salt intake, that the DASH study really was
the moving force to inform the guidelines. But tell us a little bit about the DASH study and maybe why that wasn’t such a good idea
to use that to base our guidelines. Well, the DASH study
was a proof of concept study, it was an excellent study
in that it was a randomized trial and people were provided the food
during a 30 day period. So it was a feeding study. So it was an excellent study
in its own right in that way. However the problem is how we interpret
the data from PURE– sorry from DASH, how we interpret the data from DASH to make dietary recommendations
for cardiovascular disease prevention. Because there are a number of limitations
we have to point out. One is that we have to remember that this
was largely a salt sensitive group of people, a lot of hypertensives
and pre-hypertensives, and we also need to remember that
potassium intake was low at baseline. So when you put someone
on a very low potassium diet, lowering or changing their blood pressure
will result in changes– changing their sodium
will result in changes in blood pressure. But when you give people higher amounts
of potassium, put them on an all-around healthy diet,
like the DASH diet, that contains
many of high potassium foods, then the effects of sodium
will be largely mitigated. So that’s what DASH found. That when we consume
a low potassium diet you see large changes in blood pressure, which doesn’t surprise
really anyone given that, but when you give them
a high potassium diet then sodium becomes less important and so the important point is
DASH is only 30 days. So we look at the long-term effects,
we need studies with longer follow-up to look at the effects in the long-term. So some studies like TOPP have looked
at longer term follow-up. TOPP originally was designed to look
at blood pressure, so people were followed up
for a period of 36 months, but what TOPP found
was that people initially… they never reached the 1.8 g per day target, they lowered their sodium a little bit
to down to 2.5 g per day, but then by around a year they migrated
back to their original sodium intake. And so even though they followed
people up over time, we don’t even know what people
were eating during the course
of the extended follow-up. But there’s every reason to believe they were not even following
the low-sodium recommendation. So we really don’t have any data
from randomized trials, so we have to look at the data
on long-term clinical events and that’s where the cohort studies
come into play and there’s consistency
across a dozen cohort studies showing low-sodium is either associated
to harm versus moderate sodium or there’s no change in risk. But no study is suggesting or showing
a lower risk with low-sodium compared to average intake. Yeah, and that’s what so frustrating
about this whole concept is that it’s one thing to make a recommendation
that has a neutral effect. It’s another thing to make
an official recommendation that actually might put you in harm’s way
and that’s what this seems to suggest and that’s what happened
with the carbohydrate recommendation that sparked our diabetes and obesity crisis,
and that’s happened with the salt as well. The official recommendation
based on your studies says you should be following a sodium
intake that is going to worsen your health. Why is there not a public outcry about this?
I mean that’s unbelievable. Yes, so science works that way in that when we have a position
for a long time, change takes time. It’s always been like that
and so this is no different. And so eventually in the long-term
the truth does win out. And so the only thing we can do
is just keep publishing our science and the truth eventually works itself out. The other important point I want to go
back to about the DASH trial that we don’t hear much about is the difference between the high
and low sodium diet– sorry, high and low potassium diets and how that affected blood pressure
response to sodium, that’s definitely worth repeating. So on the low potassium diet there was a larger blood pressure effect
with increase in sodium. On the higher potassium diet was essentially no blood pressure impact
on increase in sodium or a very small amount. That’s correct. Now when we say, what examples of low
and high potassium diets, when I think of a high potassium diet
I think of fresh vegetables, when I think of a low potassium diet
I think of potato chips and pretzels and packaged foods. And so I think where the salt is coming from
and what type of diet you’re having clearly makes a huge impact. So as a supplies, the low-carb community, if someone is eating their broccoli
and their cauliflower and their spinach and they’re putting
their Himalayan salt on it and having it with their know, chicken,
meat, fish, eggs and cheese, that’s a perfectly reasonable diet where you
can be having the higher end of sodium and based on the DASH study
you would say would have no effect. Is that a fair statement? Yeah absolutely, so you need to consider
the overall pattern of the diet, which is what you’re saying, so that needs
to be taken to account as well. So it’s not only necessarily
a potassium effect, but also potassium is a marker
of the quality of the diet. So if you have a higher potassium diet you’re consuming an all-around
balanced healthy diet with plenty of foods
containing high potassium; fruits, vegetables, dairy and nuts
and seeds for instance, all are potassium foods. So we have to consider within the context
of the dietary pattern. And DASH is important in that respect because it shows that salt sensitivity
is not an immutable trait. You can mitigate it by eating
an all-around healthy diet. And when you do that we find
that salt becomes less important. So the messages just concentrate
on consuming an all-around healthy diet and you don’t need to be worried about
individual nutrients like salt and saturated fat. Yeah, and the other component
about salt I want to bring up was you also broke it down between those
with hypertension and those without hypertension. And there was a difference
between the low-end and the high-end. So for both groups,
whether you had hypertension or not, the risk increased at the low-end
of sodium intake below 3 g. But at the higher end
if you didn’t have hypertension then that risk was mitigated,
the risk did not go up as much. So would that suggest there may not be
much of an upper limit if you don’t already have hypertension? That’s right,
that’s what that data suggests. So if you don’t have hypertension there’s
no increase in risk even at the high-end. So if we take a cautious approach, would say well, still that’s aimed to get
people in the middle, which is where most people are anyway. But the people who are hypertensives,
we did see an increased risk. So this would suggest that
rather than a population wide strategy, best we target people with hypertension
who also consume high amounts of sodium exceeding 5 g per day
and get them down to moderate levels. At the low-end, what’s interesting, we see an increased risk, as you said,
irrespective of blood pressure. So whether you have high blood pressure
or normal blood pressure, you still see the increased risk
at the low-end versus clinical events, cardiovascular disease and mortality. And what that suggests is another
mechanisms that play here. And again consistent with other data, showing activation
of the renin angiotensin system, which we know is vascular damaging. And you get exponential rise in these
hormones with low levels of sodium and therefore you see the consistent results
across different subpopulations. It’s been shown repeatedly in people
with hypertension and without hypertension, people with diabetes and without diabetes and people with vascular disease
and without vascular disease. It’s a consistent finding. How about congestive heart failure?
Where are the data on that? So congestive heart failure… there was one study looking at data
from the EPIC-Norfolk that found in healthy people
there was a lower risk of heart failure with moderate sodium
compared to low-sodium. So even versus heart failure
as a primary outcome, in healthy people we see a beneficial effect
with moderate sodium rather than with low-sodium. And looking at heart failure patients there
are some trials that are ongoing right now looking at low-sodium versus average
sodium in heart failure patients so we will have to see
what the results are for that. I think it’s fairly well accepted that heart
failure exacerbations and hospitalizations increase with increased sodium intake in severe poorly controlled
heart failure patients. I have to re-examine
whether it’s a mortality effect or not or more of a symptom
and hospitalization effect. And then at what levels
you break that down, at what level
of renin angiotensin activation because most of these people are
on ACE inhibitors or ARBs, which are really angiotensin blockers, there’s definitely a lot of other factors
to incorporate for the heart failure patients. That’s right, that’s one of the bigger
challenges with heart failure patients is that they are
on all these different medications. So we need more data on what the effects
are for heart failure. Certainly there is compelling data
that again high amounts of sodium, exceeding 5 g per day is certainly harmful. So the question is whether very low
amounts is better than moderate levels. Really that’s the research question
and we need more data on that. Well, this has been a great discussion
of the PURE study and I mean for one study to upend our
common wisdom in dietary guidelines for saturated fat, for salt and
for lipid biomarkers is pretty remarkable. So I think you did a great job with the study
and in representing the results and I hope there’s more to come. I mean you said it is ongoing
and there’s more data coming. When can we expect
the next installment? Do you know? Yes, so right now we’re working
on our other dietary papers. So obviously we collected using
a long food frequency questionnaire, we’re now looking
at all the different types of foods versus cardiovascular events
and mortality. So we want to spend the next two years
to publish all these papers and then also one looking
at the dietary pattern as a whole. That would be a key paper as well. So this is what we are going to publish
in the next year or two and also we’ll do more dietary assessments
during follow-up and that also helps improve the precision
and accuracy of the estimates of diet and then continue the follow-up
as much as we can to look at effects on less studied outcomes
like cancers and respiratory events and infectious disease as well. Great… If people want to learn more
about you and more about the PURE study where can you direct them to go? There is a website online. If you go to there is a link
that takes you to the PURE study. If you want to read up more on it,
it’s there. Great, Prof. Andrew Mente thank you
so much for joining me today. My pleasure.

13 Replies to “Diet Doctor Podcast #15 — Prof. Andrew Mente”

  1. I'm trying to understand… I had an extremely high ldl 2 weeks ago 275 ldl.. but I think the hdl was a bit higher 80 and leucocytes we're low to mid 35. so I asked for a particle test of my ldl, my doctor doesn't really approve but she's doing the test to appease me because I refuse to take statins. I don't understand what I should be looking for in the particle test.. I did read there are large fluffy particle vs the smaller harder particles.. and supposedly fluffy ones are better and not to worry about but smaller ones are bad.. and these 2 size particles both total the large ldl I have?? How do I interpret the test? I honestly don't trust my doctor to look at the results from my keto diet point of view.

  2. Why do they always say to avoid salt, but don't Express their opinion in potassium chloride.

    I just bought 2 cans of No Salt brand potassium sult substitute

    What should I do with it?

  3. After 1 1/2 years keto my APOB-82 and APOA-201, which is super good .41 ratio. But I make use of a lot of supplements also so not just keto . Thanks for getting us up to date on these more relevant markers! Triglycerides at 57 and HDL at 87. chol/HDLC ratio 2.2.

  4. If we assume, that a healthy grass fed cow, contain all the nutritions,

    in the right amount and ratios, we need for for optimal health,

    it should be a simple task to figure the right recommendations 🙂
    Am i right or am i right 🙂

  5. You have be very very careful with a food questionnaire here in the USA.

    Butter is a food that many people will write down, when in reality they eat "Country Crock", "Earth Balance", or some fake butter that dominated the butter section at every single supermarket in the USA, including Whole Foods.

    And when people have a bad health outcome they write down butter, but it was really you know what, and we'll be warned about how bad butter really is.

  6. If apoB/apoA1 is the important ratio to look at, what then is a good ratio? Is it 0.5, is it 0.9? What's the best number to aim for? Also, I've seen studies too that suggest if your insulin is low, then a higher ratio does not matter as much. I would bet the studies being discussed never bothered checking peoples' insulin levels (e.g. fasting insulin).

  7. Having moved from Chicago to Atlanta I was astounded by the use of margarine instead of butter. When you ask for butter(a nectar from the Gods) they invariably bring you that processed crap instead. Makes you wonder why the xxxlg wheelchairs and hospital beds are beginning to out number the what used to be normal size ones in our medical facilities.

  8. This paper corroborates your podcast, particularly on the relation of LDL to CVD events.

  9. I recently learned thru an expensive Cardio IQ test panel that I have extremely low Lipoprotein (a) but very high small dense LDL particles and elevated Apo B. What is my best course of action with this type of results?

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