The Melanie Avalon Biohacking Podcast Episode #163 - Simon Hill
Simon Hill is the host and founder of the hugely popular The Proof podcast and blog of the same name, and a nutritionist and qualified physiotherapist. On top of his formal education, Simon spends hours and hours deciphering scientific studies so he can break down how to fuel your body to promote longevity and reduce the chance of developing disease while simultaneously achieving whatever health and fitness goals you may have. He is the plant-based food contributor to Chris Hemsworth’s fitness app, Centr, and in 2019 Simon opened a plant-based restaurant, Eden, in his Sydney neighbourhood of Bondi. In 2021 he published his book The Proof is in the Plants, with Penguin Australia, which shot to the #1 non-fiction book Australia-wide in it's debut week.
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Instagram: @simonhill and @theproof
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13:15 - simon's background
18:00 - is there one right diet?
20:20 - how plant based should we be?
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31:00 - how best to interpret types of studies
34:40 - how long is a long term study?
39:00 - Saturated Fat and Cholesterol
43:00 - an evolutionary diet vs an optimized diet
46:20 - longevity and procreation
47:10 - our inherent intuition for Nourishing foods
49:15 - liver & broccoli
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53:20 - antinutrients
1:00:20 - grains and gluten
1:04:30 - TMAO
1:08:00 - hDL
1:10:20 - raising and lowering lipids with diet
1:17:55 - forming plaques from high levels of cholesterol
1:21:30 - CAC Scans
1:25:00 - nitrates and nitrites
Melanie Avalon: Hi, friends, welcome back to the show. I am so incredibly excited about the conversation that I'm about to have. Okay, a little backstory on this conversation. As you guys know, one of the main questions in life that I'm haunted by is, what is the ideal diet for us humans? I'm really curious and perplexed by the different findings on the carnivore side and the keto side on one hand, and then the plant-based sphere on the other. So, I'm always trying to bring on people of all different perspectives and opinions. Since I tend to be more saturated in the low-carb, paleo world, even though I actually follow a high carb diet, I actually listen every single night to Rich Roll's Podcast, because a, I just find him so calming, to listen to and b, I think it's really helpful because he's very vegan and brings on a lot of perspectives in that camp and so I love to just keep my mind open to all of that research and all of those thoughts.
So, a few months ago, now, I'm not sure how long ago it was, but he had on a guest, Simon Hill, who wrote, The Proof is in the Plants. And I loved this interview so much, I thought, Simon's approach was so nuanced, and really open minded and very comprehensive and I was like, "I've got to get him on the podcast." So, I put them on my list of people to try to book. And then literally, it was very soon after that, I posted a post on Instagram from another guest about cholesterol, I think, and Simon commented on it, and said that he would love to come on the show and discuss a different perspective on things, and I was so excited. [chuckles]
So, yes, we connected. I got his book, I read it. It was after listening to the interview, it was everything I thought it was going to be, which was extremely comprehensive. Went into every topic concerning health in a plant-based diet. Tons of studies, lots of nuance, very approachable. I have so many notes in front of me, and there's so much we could talk about. So, I'll stop talking so Simon can start talking. But, Simon, thank you so much for being here.
Simon Hill: Melanie, it's a pleasure and honor to be here and with your community. I'm glad that I commented on that post. I sometimes refrain from doing that for my own personal sanity. But yeah, I'm glad that I commented there, and it's a great pleasure to be with you today.
Melanie Avalon: It made my day. And then funny enough, I think a few weeks later, I had on the Sherzais who wrote The Alzheimer's Solution. They commented-- actually, I don't know if it was-- it was something about them, or something from max Lugavere. There was some sort of discussion, and they actually mentioned you in the comments and was like, "You have to bring on Simon." And I was like, "He's coming on." Here we are, long awaited.
But in any case, so for the audience, who is not familiar with your work? Would you like to introduce yourself a little bit, tell them a little bit about your personal story, which you talk about in the book, and I've heard in the interviews, but what led you to where you are today with the plant-based diet?
Simon Hill: I'll try and keep this short so we can get into the nuance of nutrition. But I became interested in nutrition a little bit more than a decade ago. My undergraduate degree was a Bachelor of Physiotherapy. I went on and was working with professional athletes in Australia and really enjoyed that part of my career. I had a big interest in nutrition, and I realized it was a large gap in my kind of overall knowledge and was somewhat hindering my ability to help patients that I was seeing in private practice, but also athletes that I was working with, who were going through injuries and rehabilitation and whatnot. And I felt there was a big gap actually in the professional football setting that I was working in.
A culmination of that, and then also, my family's history with chronic disease. My dad had a heart attack at age 41, and I witnessed that, I was the only person with him. And following that event, I always had a bit of a limiting belief that our health was very, very much determined by our genes. I went on to discover that sure, our genes do have some, say, but there is a lot that we can do. We have a lot more control than we're often led to believe and how those genes are expressed, whether they're turned on or off, can be very much determined by the way that we navigate through our lives.
So, at some point, I decided that I wanted to go back to university and really strengthen this weakness of mine that I felt compelled to do, and I did a Master's in Nutrition Science at Deakin University, which has a very strong nutrition program, actually one of the leading nutrition schools in the world looking at how diet impacts mental health, have a very big reputation for that. So, I went back and did that.
Really, you mentioned at the beginning, we would explore what is the optimal diet, and that's obviously a big interest of yours, and that became something that I was just so fascinated by. You'd look at the bookshelf, and you find you pick up one book. It says some sort of absolute claim or it's promoting some form of diet as the best diet. And then, you shuffle just to the side, maybe take one step, and pick up the next book, and it will say the exact opposite. And you jump on social media, you're exposed to the same sort of conflicting ideas. You look in mainstream media. Again, the narrative is always changing. We know one thing today, and then tomorrow, we see something completely contradictory or the opposite. As a person in the general public, that's very, very confusing to make sense of, and I think that many people are left thinking, "Well, gosh, if experts can't agree, we really don't know anything." And they just kind of throw their hands up in the air and probably just continue doing what they've always done, which is the sort of societal norms, and we can talk about what the average diet looks like.
So, I think that this confusion is not really doing a great service to the to the general public. So, I became fascinated with, why do all of these different opinions exist? And do we actually understand what an optimal diet looks like? And if we do, what is that? And how can we go about perhaps better communicating this to people, be it online or through a book or through mainstream media, to give people a bit more confidence in the decisions that they're making, what food are they buying for their families, what does their breakfast look like, their lunch, their dinner, etc.?
Melanie Avalon: I love it so much. And yeah, I was really impressed just by the length of the beginning of your book, talking about this question of why we're so confused, and the role of studies, and funding and agendas, and ethics and perspectives and how that affects everything. I'm actually pretty curious. Now that you have done all of this research and looked at everything, have you come to the idea that there is one right diet or is it still unique?
Simon Hill: Well, that would require us to define diet. I don't believe there's a single dietary label, these labels that we kind of make up, carnivore, vegan, Mediterranean, low carb, high carb. I don't believe that a label like that defines optimal diet. I do believe there is a set of characteristics that are consistent with good health outcomes, people feeling better or more energized in their day to day, but also better long-term health outcomes. So, lower risk of chronic disease, and also lower risk of premature death. So essentially, people living healthier for longer, and we could go into what those characteristics are. But essentially, where I'm getting at with this is that I don't believe that the kind of dietary labels or brands that we've made up and sort of put into buckets, and we see the diatribes out there, I don't think that's the best way of going about things in terms of trying to come to this ultimate conclusion of what an optimal diet is.
I know that is not necessarily what people want to hear because most of us, we do want to know, what is the silver bullet, and I want it as a prescription, tell me exactly what to aid and I'll follow it. Unfortunately, it's much more nuanced than that and while that can sound like a negative thing, I think it's actually really positive because with a theme or characteristics, and once we unpack those, it actually gives people more choice, and there's wiggle room in there to find a way of eating within that that's consistent with that theme, that leaves you feeling best. It's something that you can sustain, is something that you can do not just for a week or two weeks, but for decades, hopefully the rest of your life.
Melanie Avalon: Yeah. I cannot agree more. For me, for example, the blue zones, which is something that people talk about a lot when discussing this, if I look at that I see the consistencies being heavily plant-based, but not exclusively, with the exception of Loma Linda, wholefoods-type diet, and then a lot of environmental factors, and social factors and things like that, and exercise. And it's hard to know, to what extent diet versus, environment versus lifestyle, social, family, all of that is playing a role. but something I found really interesting about your book specifically is-- so another common friend of yours is Dr. B, who wrote, Fiber Fueled. He wrote the foreword for your book, right?
Simon Hill: Yeah, he did. Yeah.
Melanie Avalon: So, a small little nuance there a difference, for example, in his book, he talks about a plant-based diet, and how it would ultimately be ideal to be 100% plant based. He's still open to people not being quite there, but ideally, in this ideal world, you're 100%, in your book, I love your thoughts on is the ideal still 100% or I think you say in your book that you looked at all the research and you walked away with an 85% plant based maybe. I was wondering what you think about that difference between the 85% and the 100%.
Simon Hill: Okay. The first part of that question, do I think 100% plant exclusive is the optimal diet? And I would just straight out say we don't have the evidence to say that. So no, I wouldn't make that claim. And in the book, I write approximately 85%, and the reason for that is when you are eating in that manner, it then becomes consistent with that theme. So, it might help if we walk through that theme. And even if we took a step back, if you're okay with it, to kind of how do I think about science and how have I come to that this conclusion of this theme, and why might there be people out there who are looking at this differently, and have a very different opinion about what a healthy diet looks like.
Something that's often, I think, lost in interpretation of research and in headlines is when we're looking at evidence, we need to understand that not all science is equal. We have preclinical data that can be in a petri dish or an animal model. We have observational research, looking at populations of people. You just alluded to the fact there with the blue zones, that in such studies, it can be hard to decipher what is leading to their good health. You can see a number of different factors. But it's impossible to be concrete and say it's 100% their plant-forward diet that is contributing to their longevity, because we're also aware that these people are not smoking much, they are quite active people, they're not sitting down all day. They may consume some alcohol, but they're not consuming a lot, they're not smoking, etc. But it's still an important piece of evidence and you can use statistical analysis to adjust for some of these what we call confounding variables. A good observational study will understand those limitations and try to as best as possible consider them.
And then, you have clinical trials, and these can be short term trials that look at what happens when people eat certain foods, and how does that affect biomarkers, so things that could change in a matter of weeks, like blood pressure, or cholesterol, or blood glucose control. Or they could be longer term, which are rare, because they're very expensive, and it can be hard to control people over a long period of time. And if they're longer term, like for example, the Lyon Diet Heart Study, which was about 4-5 years in length, often, too in order to see an effect, you have to look at a sick population, because if you've looked at healthy people for 4-5 years, you might not see much. So, these longer-term trials allow you to potentially look at not just biomarkers, but actually look at things like heart attacks or strokes throughout the duration of that trial.
Where I'm getting at with this is that not all science is equal. I made that point and when we're evaluating research, we need to be considering the quality of the evidence and also whether as you move up the evidence hierarchy towards more reliable, valid data, does what you see at a sort of preclinical level continue to play out? So, when I'm looking at research, that's exactly what I'm looking at. I'm looking at preclinical data, observational, and the interventions. But I'm not going to place too much stock in mechanistic preclinical data, if what we see in human health outcomes studies is different.
And then to add a little bit more complexity here, within a study, when we're thinking about nutrition and a particular food, we have to always think about a number of different things. If you said to me, "Are legumes healthy?", my initial response would be it depends. This is perhaps a bad example, because in most cases they are. But let's change that to something a bit more controversial like dairy, "Is dairy healthy?" Well, again, it depends compared to what. So, with nutrition, and I think everyone can appreciate this, if you are adding something to your diet, usually it's displacing or removing something. It comes at the cost of something else. Or if you're removing something like, say, you're removing dairy from your diet, usually you're going to add something back in. And so, the replacement becomes very, very important, because that often affects the net outcome.
Now, not only do we need to consider compared to what we need to consider, well, how much. You're asking me, "Is dairy healthy?" and this is actually a really good example, because we also need to consider here, are we talking about low fat, full fat? Are we talking about yogurt, cheese, milk? And then, how much? Are we talking about 30 g, a cup, two cups a day, etc.? And so, you can quickly see that there is quite a lot of nuances, and all of these things are worthy of consideration when you're evaluating research. If we're not considering this, we can really find evidence to support anything.
So, with all of that said, when I look at the overall body of research, the theme that I see that is consistent with good long-term health in particular is diets that are low in saturated fat. They're not going to be devoid of saturated fat, we can get into that, there's always going to be some saturated fat in the diet. They're low in saturated fat though. They're really, hopefully, completely excluding trans fats. They have a good amount of polyunsaturated and monounsaturated fats. They're high in fiber, and they're low in ultra-processed foods. Ultimately, when you eat in a plant-predominant manner, you automatically achieve all of that. And so, that's why we see diets like a thoughtfully constructed Mediterranean diet, or a pescatarian diet, or a well-done vegetarian diet, or a wholefood plant-based diet consistently, we do see and studies that they improve these biomarkers of disease. And in the studies that we do have, where there are clinical trials that are long enough, we do see improvements in health outcomes.
Melanie Avalon: I just want to say I'm so enjoying this conversation, because I don't think I've had a detailed conversation on this actual concept in all of the episodes that I've had. Some thoughts to what you just spoke about. So now, listeners can probably see why it can be so overwhelming with everything and potentially contradictory. First of all, even the adjusting for confounding factors and stuff, even that can be complicated, because the factors that might be "confounding" might be related to what you're testing. So, it's like by adjusting for them, it's just hard to know [chuckles] if you're correctly testing what you need to be testing with the mechanistic studies and the trials on mechanisms of action and such. So, is that too reductionistic? What can we learn from that? So, like looking at the effects of saturated fat on a cell compared to in a human being, can we still draw value from that or how can we know how to interpret that.
Simon Hill: I think we can still draw value from mechanistic sort of preclinical data. I'm definitely not suggesting that this is not an important area of science. In fact, my dad is a Professor of Physiology. He's been doing such science for 40 years publishing in cell, and metabolism and circulation. So, I'm certainly not someone that would rip into that area of science and say it's not needed. It's important, but it's hypothesis generating most of the time. Often that that deep science gives us an understanding of something and we go, "Hmm. Now let's see, does that play out in humans?" And this is where it's really, really important because we often think we're smarter than we are. And when you look at a mechanism, so you're looking at a food, certain foods, or saturated fat, you're zooming in on one pathway. Often, these nutrients and compounds effect a myriad of pathways in the body. And so, if you just look at one isolated pathway, how can you be sure that exposure to that nutrient or compound, how can you be sure of what the net effect is? Because it could be under a microscope, you might be seeing a deleterious, or what you think is a deleterious effect of one pathway. But if you were to be able to have visibility of all pathways, you would end up seeing that the net outcome is a positive one. And that's where looking at actual humans and health outcomes becomes really important, because it assumes that were seeing the net effect, we were seeing what happens to human physiology as a whole when you're exposed to a certain compound. And it means that if we have any kind of blind spots in terms of our mechanistic understanding and the mechanistic science, that what we're getting is a more complete picture.
And so often what we see is the health outcome data, we see a finding, we actually don't understand all of the mechanisms. And that's okay, because ultimately, what is more important to the average person out there is when you eat more of this or less of this, what happens in terms of your biomarkers of disease, or what happens in terms of your risk of, say, developing fatty liver or having plaque in your artery, developing atherosclerosis and having a heart attack. So, all that is to say that mechanisms are important, they help further our understanding of things, but they're not essential. They're not essential in terms of making public health recommendations.
Melanie Avalon: Yeah. I've been thinking about that a lot recently, because I recently launched a supplement line and one of the supplements I want to make is berberine. And right now, there's this whole debate about berberine versus dihydroberberine, which is an even more isolated form of berberine, and potentially having, I guess, better effects on blood sugar control. But stepping back I'm like, "Right, but maybe it's not accounting for other things and berberine." It's like the more granular you get, looking at a specific action and what might happen from it, it's just harder to know what you're losing or what context. It's like taking a sentence out of a book and trying to understand what the book said, you just can't. So, I've got another question about the timeline of things. So, like the word 'long term', for example, what actually is long term?
So, two questions related to that. You might say, for example, that the carnivore diet, that we don't have long term studies on it. So, it's hard to know at what point would we have long term, when would we cross over to that qualifying as long term? And then, the second question sort of related is, I guess the longest-term study we have is just the evolution of humanity, but even that-- it stresses me out, that is so debated. I feel we should know what we were eating for these millions of years, but even that's debated. You talk in your book about, for example, I didn't realize this that people often say that we started using fire and that allowed us to eat animal products. And that is what led to our increased brains. But you talked about how there's actually a debate that maybe it was that we started cooking starches with fiber, which I was not aware of that. [chuckles] So, long term, time.
Simon Hill: Okay, there's a lot to unpack there. I definitely think our ancestors ate meat. There's no debating that. There is a lot of debate around the contribution of meat, the contribution of tubers. And what seems to be apparent-- and I think, Herman Pontzer has done, probably one of, if not the best jobs at summarizing all of this. He wrote a book called Burn, which I would highly recommend. I think that what's clear is what's amazing about humans is our ability to survive on a myriad of diets, and 'survive' is the keyword there. But if you look across the world at hunter-gatherer diets, populations living in completely different environments, you see the contribution of animal and plant foods in terms of calories is vastly different in different areas. Some populations have an abundance of calories from animal foods and less from plant foods. Some have the opposite. It can change on a month to month, on a seasonal basis as well within those populations.
So, I think this idea from the sort of the carnivore crowd that there was one paleo diet, I think, is a massive oversimplification. And in fact, Herman in his book, he sort of goes back through how the paleo diet was formed originally from through a lot of Loren Cordain's work. He points out that the formulation of the paleo diet as a single diet that was the sort of relatively low carbohydrate, contained quite a lot of animal foods originated through Loren going through the Murdock Atlas. At least, that was the source that he cited in his formulation. And within that Atlas, there were a number of different diets documented for hunter-gatherer tribes. What Loren did was-- and I'm not suggesting that he was being disingenuous, I just think that he oversimplified things, because often, an oversimplified message is an easier message for the general public to grasp.
But today, I feel like people want more information. What he did was he looked at all of these different diets from hunter-gatherers. And it actually didn't tell you in the in the atlas, you can look at it the percentage of calories from animals and plants, it just sort of ranked them as to how important they were and he sort of took that and translated it to calories somehow, which I'm not sure if that can be done accurately. That was the first thing that's interesting.
But where it gets more interesting is, so there was a huge variance in the types of foods people were eating, he then took an average across the world to create the paleo diet. That overlooks what I mentioned at the start is probably the most important takeaway, is that the diets vary greatly around the world. And really, what this suggests is how incredible it is that humans can survive and adapt to a number of different types of diets in terms of the calories coming from plant foods and animal foods.
So, that's kind of my thoughts on the paleo diet. I'm not sure that there is a singular paleo diet and also, I think that, and Loren Cordain himself has published on this, but the types of meat that would have been consumed, based on our current knowledge of the types of animals that people were eating, were a lot lower in saturated fat than many of the foods that we see today people eating in that sort of crowd. So, that's another thing to kind of just be cognizant of. And Loren Cordain, has actually published a paper, I'll send you the reference, on this point exactly and on his thoughts on cholesterol, which I thought was really, really interesting.
In terms of long term, how much long-term data do we need on the carnivore diet, look, it'd be great to have something that shows decades of inflammation, but I'm not sure that we need it. I think this is a really, really interesting discussion around the carnivore diet, because there's no denying that people are improving their health, at least in the short term. I'm sure you would agree with that. There's enough anecdotes for us to acknowledge that people seem to be feeling better, or at least certain people that are doing this. And I think there are some reasons that can explain that. Now, one of the big inconvenient things for this group is what this diet does to lipids, and I think there are several folks who are kind of prominent in this space that want to downplay that, because it is a bit of an inconvenient truth. People are losing some weight and feeling better, but their lipids are kind of moving in the wrong direction. And that needs to be either accepted or explained the way. I think it should be accepted, and really, what I would love to see within this group is the same thing that I'd love to see in the plant-exclusive vegan group is just acknowledging that, "Your diet can work and be great, but it can still have limitations."
When you acknowledge that limitation, and if we're thinking about the carnivore diet here, the fact that it raises ApoB-containing lipoproteins, not for everyone, but for most people quite considerably, if you acknowledge that as a limitation, then you go, "Okay, well, this diet's working in a number of different ways, and there's a benefit." This is a limitation. How do we want to address that?" And in that case, that can be addressed through modification of the style of carnivore diet through manipulating things like the types of fat that are being consumed, or it could be through treatment with drugs. That we know there is a lot of evidence to show that they are beneficial. But there does seem to be some resistance within that diatribe, and it's the same in all diet tribes, to acknowledging that maybe this diet is not perfect in all ways. And rather than kind of trying to turn a blind eye to the limitations, let's look at them and work out what is the best path forward to help people within this community achieve their best health.
Melanie Avalon: I think that is a fantastic perspective. And I can hear my audience probably getting just really excited to listen to this, because a lot of the feedback I get is, "You're always bringing on people of all different perspectives, and they're saying one thing, and then I hear another. How do I know you know what's true?" And I think that a lot about what you just said about the carnivore diet, yeah, people often will go on carnivore, and like you said, have an unfavorable-- well, they would say I guess that it's not unfavorable but a seemingly unfavorable response in their lipid panel. And so, the thought I've always had as well, maybe you could, like you just said this. So, I'm repeating what you said, but I often think, you could stay carnivore, and you could adjust it and probably see a different effect and kind of have the best of both worlds.
So, here's a question as well. People often say-- and this taps into what we were just talking about with the evolution, people often say that we should eat like the way we evolved, because that would be the best diet to support longevity. But something I think about is that evolutionarily, it might inform the diet that we're most suited for to live, but our genetics or epigenetics or evolution, I don't know that longevity was their goal. It seems like the goal was reproduction, and then not so much. I actually don't have a problem, because some people will say-- I was having a conversation with my friend the other day about an entirely 100% vegan diet. And they were saying, "Well, that's not natural. It might require supplementation." And my thoughts are that are, "Okay, how is it a problem to have a diet where you actually optimize it yourself through a manner that you might not have evolutionarily naturally followed?" if that makes sense. Does that make sense?
Simon Hill: Yeah. I mean, there's something called the naturalistic fallacy, which assumes that kind of what whatever is natural is always best for us. And this kind of weaves into this conversation and I would agree with you, I think that evolution and anthropology is interesting, and it adds to the overall body of evidence for sure. But I do think we need to be cognizant of the fact that Homo erectus, he or she was not eating to maximize their health span and lifespan. We just kind of went over this, the fact that humans could adapt to many different environments. Homo erectus was very much eating to survive and as you say, the goal being to get to an age where-- or the primary goal, I should say, there is a little bit of nuance in this, but the primary goal being to get to an age where you can procreate because that is going to be beneficial to Homo sapiens from an evolutionary perspective. The goal not being to select foods that are going to lower your risk of chronic disease and that's a very, very different question. And that's why thinking about the optimal diet, today, we have to broaden our lens. We can't just look at the data that we have from the foods that our ancestors ate. It's interesting and important, but we have to include all the modern datapoints that we have. There is really no reason why a diet with certain supplements might not be the best diet, the most optimal diet. It might turn out that a diet with the addition of certain isolated supplements is the key to longevity. And the kind of that remains to be fully understood but I think it's an important point that we need to be open minded about the fact that might be the key forward.
Melanie Avalon: Do you know-- I actually don't think I've looked this up. Have there been studies on longevity and if you've had-- I guess this might just be for women, if you've had children are not? Talking about confounding factors you would have to control for people who have a child and then maybe become metabolically unhealthy after that. So, somebody who regains all of their metabolic health pre and post child, I wonder if their lifespan is shorter because they had the baby.
Simon Hill: That's a great question. Yeah. that's something I'd have to look at. I would not be able to give you an accurate answer right now. But I agree, it's very interesting,
Melanie Avalon: I have to add it to the research list. So, if we have a baby, and we put them in a room with access to-- and I'm trying to decide if this thought experiment should include processed food or not. When we're born, do you think it's a blank slate as far as having an intuition as to what foods nourish us or is there genetic factors, gut microbiome factors? I just wonder at what point do our cravings and desires become learned versus intuitive?
Simon Hill: Also, a very, very good question. So, if you had a child and you surrounded them with a whole lot of different foods, would they make the right choices? would they automatically balance out their nutrition and achieve nutritional adequacy?
Melanie Avalon: There's actually been a study on this.
Simon Hill: Yeah. The guys from The University of Sydney, who wrote a book called Eat Like the Animals, Stephen Simpson, one of the authors, he's looked at this but more looking at animals. And they do tend to balance things out when they're in an environment that's not manipulated. That's the key. So, our environment today has been heavily manipulated and 42% to 60% of the average person's calories are coming from ultra-processed foods. I would argue that nature cannot compete with these foods. So, if you were to expose a young child to an environment with those foods, I think their radar, their intuition would be off. Essentially, their appetite would become-- or their regulatory system that controls appetite would become hijacked. So, I think there is enough evidence for us to kind of conclude that. And yeah, if a child, on their own accord, was able enough to select their foods and access them, I think they would make fairly decent decisions if they're in a sort of "natural environment," for their development. I'm not sure whether they would be making the best decisions for their longevity.
Melanie Avalon: Something I often think about related to this question is, for example, at least in the animal sphere, they'll often say that liver is like the superfood that it has all of this nutrition. And my question is it's very rare that I meet somebody who-- even people in like in the paleo world, who the taste of just plain raw liver, and why is that? Especially, people who aren't eating "processed foods"-- So, me, for example, I eat all whole foods, I even went through a period where I was very anemic, which is maybe something we can talk about. And at that time, I was like, "You know what? I'm anemic. There is no reason that liver shouldn't taste amazing to me," and it just didn't. And I'm haunted by like you said completely cultural, where did my intuition go with that?
Simon Hill: Well, I think the same argument could exist on the other side of the spectrum, in that there would be many kids and probably adults that have an aversion to, say, broccoli or certain green vegetables. So, it kind of works both ways. It's an interesting question. Is that a result of what we've been exposed to and the hyperpalatable foods, but also the way society thinks about certain foods? I'm not sure I have the perfect answer, but I would presume if you have someone who is not exposed to our current environment, where there is just so many delicious foods available, then foods like broccoli and liver are probably more palatable.
Melanie Avalon: Actually, I'm glad you brought up the broccoli because that is something that the carnivore sphere people will say a lot as an example, they'll say that or is "evidence". They'll say that all kids basically don't like green vegetables, and it's not until later. So, they say we accustom ourselves to this taste, and that's due to the antinutrients and such in broccoli. Where do you fall on plant antinutrients?
Simon Hill: There are certain foods if overdone, for example, if you consume too much spinach, you could end up with kidney stones. You'd have to consume a lot though. A lot of this comes down to exposure. For example, lectins is one that gets thrown up a lot, right?
Melanie Avalon: I've had Dr. Gundry on the show twice. [chuckles]
Simon Hill: Yeah. So, how should I phrase this? I think Dr. Gundry has some really great things to say. So, I don't want to come across as kind of just having a go at him generally. We would disagree on lectins a bit though, and where I think he puts a lot of his emphasis is on the preclinical mechanistic data. So, what happens if you put lectins into a cell that's been removed from the body in a petri dish kind of thing. That level of evidence we need to be thinking about very critically, and there's a few reasons for that. I mentioned how important exposure is before, whenever we're looking at something. If we're talking about whether our food is healthy or not, critical to that is how much are we being exposed to. And in this mechanistic level of science, what's really easy to do is to expose a cell to something like lectins at a level that it would never be exposed to in the human body through a human diet. I could expose the cells to the amount of lectins magnitudes higher than what you would ever be exposed to through eating legumes, for example. And we see that many, many mechanistic studies that show that lectins could be problematic, the exposure level is astronomical.
Now, what I like to explain to people here is that you can have a compound like lectins, or any compound that can be healthy at a certain level of exposure, but then it can also be harmful at a certain level of exposure. Let's take oxygen for an example. I think that most of us would agree, breathing in air that contains oxygen is a good thing. We require it, it sustains us, it's critical to the production of energy and the maintenance of life. But if I was to give you 100% oxygen, you would soon pass out and eventually you would die. The oxygen concentration in air, I think, is 21%, maybe 26%, but if I expose you to 100%, oxygen, it becomes deleterious. That same compound that's healthy for us ramped up at a certain exposure level becomes harmful. Now, with that in mind, the fact that 100% oxygen is harmful to us, none of us are going around saying. "Don't breathe air." Are we? [chuckles] The common-sense approach is, "Okay, 100%, oxygen is bad, but 21% in air is beneficial for us. I'm going to breathe today." Now, with lectins, we see this extreme exposure in mechanistic petri level science can cause some deleterious effects to cells, can increase markers of inflammation, etc.
Now, what about in humans? Well, if we look at population data, and you look at populations who are consuming foods that contain lectins, and sure they're cooking them and soak beans and cook them, which does remove or minimize, reduce some of the lectins but there's still lectins in these foods, these people have very good health outcomes. And if lectins were as kind of poisonous as they're often portrayed to be, then we should expect to see these cultures and populations who eat a lot of lectin-containing foods, we should expect to see higher incidence of autoimmune conditions, or conditions related to gut barrier breakdown, we should expect to see poor health but in fact, we see the opposite.
So, I think that alarm bells go off for me when a lot of this is derived from mechanistic data, where there is a very, very extreme exposure amount. I think we just need to be careful over extrapolating from that to human health. So, we started this, I guess, thinking about antinutrients. I would just posit the question to everyone with regard to antinutrients is, if a claim is being made, and it's based on something that's mechanistic, that's interesting, but remember, your food is a matrix. It's not just a single nutrient that a cell is being exposed to or a compound. It is a combination of nutrients and compounds, phytochemicals that all then together create a net outcome, a net effect on your physiology. So, we have to be careful not getting too reductionist. There are certain compounds in foods that could be considered antinutrient. But again, what I'm most concerned with is when you eat those foods, sure, they might contain those, but they contain a number of other things as well. What's the net effect on your physiology and your health? And so, I ask to kind of remember to zoom back out.
Melanie Avalon: Yeah. I love that so much. I developed an app called Food Sense Guide, and it actually looks at 11 different compounds in foods, and shows their levels in different foods. I was researching lectins for it because it has lectins, and I was actually very surprised by the overwhelming lack of studies that I could find on lectins. And then also, the fact that lectins are in everything, including meat, and on the flip side, sometimes linked to health improvements. So, I was like "Okay, well, that's complicated."
But also in the same sphere, there have been a few different categories of food that I've actually changed my perspective on pretty intensely. First-- well, back in my standard American diet days, I didn't really give credence to anything being necessarily good or bad. But when I first went paleo, I went to this world where some foods I thought were just really bad. But now I've stepped back and try to objectively look at some of these things and it's a little bit different than what I've been thinking. For example, like grains, if you just go to Google Scholar and type in 'grains' and 'health', and try not to be biased in your interpretation, it's hard to make the argument that grains are as bad as I think we make them out to be. And that was a big epiphany I had relatively recently actually. Gluten is a whole another issue. You do talk about gluten in the book. What do you think about gluten? And are we being reductionistic with it? Is it a problem? It's a big hot topic for people.
Simon Hill: I think it's certainly a problem for those with celiac. Outside of a kind of wheat allergy or celiac, I think there probably are a number of people that are removing gluten that perhaps don't need to. I guess where I sit on this is that if you, for whatever reason, feel you want to remove gluten, I have no problem with that. I would just suggest that you really consider what you're replacing that with, because this is where people run into problems. If you're going gluten free, and then buying a lot of the ultra-processed gluten-free foods that have a bit of a halo effect, these are really not health foods, then I think you might be shifting your overall dietary pattern in an unfavorable direction. If you are replacing these gluten-containing foods, however, with gluten-free wholegrains, like buckwheat or brown rice or black rice, then I think that's perfectly fine. So, really comes down to personal preference. I'm okay with someone who say, "I want to adopt a gluten free diet." I just think that some thought into the replacement is probably important.
But I would side with the kind of idea that gluten I think has been a little bit unfairly demonized. I'm not sure that it is the cause of all of the gut inflammation that perhaps some have kind of thought. But certainly for certain individuals, it could be an issue and we haven't spoken about the microbiome here or personalization, but I'm a very big advocate of personalized nutrition and I do think the microbiome is central to that and it would be foolish for us to think that each of us are going to respond to the exact same food in the same manner.
Melanie Avalon: It's interesting with the gluten because it's like there was this whole movement of gluten free, then there was like an anti-gluten free movement, which I'm so glad you said this that you're okay with people being gluten free because now, there's sort of a backlash where they'll say, "Oh, you shouldn't be gluten free because gluten is not an issue at all." But some people seem to genuinely feel better on gluten free, so it's nice to just be open to people, like you said, finding what works for them and paying attention to how it affects them and making sure that they're getting what they need.
Simon Hill: Yeah. Look I see that kind of some of that rhetoric online and around really trying to hammer home this point that, "No, gluten has been demonized and you shouldn't worry about it, you should change your diet." But I also just kind of take the position that look, gluten is not necessary it's not essential so if you if you want to remove it there are some great substitutes and options and you can certainly achieve optimal health and a healthy dietary partner without gluten in your diet. I just don't think we need to demonize it at the same time.
Melanie Avalon: It's funny. I was gluten free for years before I actually tested to see if I was celiac or whatever it maybe. I tested negative for celiac, but I've been gluten free for so long, I'm not sure if it's accurate, but I did test for wheat allergy, so I was like, "Okay, [ laughs] I can do this and not have to make it and make an excuse."
Speaking to the microbiome, such a frontier of stuff that we just don't even remotely understand. I was reading, this is a kind of a nuanced random rabbit hole of the microbiome, one of the things that I'm really fascinated by is TMAO, for example. You talk about that in your book, and I was reading one of the studies that you referenced, and it was so fascinating because it was looking at-- So, for listeners who are not familiar, or maybe you can tell us a little bit about TMAO and what it is, but high levels are correlated to health issues. One of the studies that you referenced, they actually had people on a plant based-- or I think it was a vegan diet, it was a plant-based diet compared to an animal diet and testing TMAO levels. The animal diet increased TMAO levels, but not if it was the arm that ate it after having done the plant-based diet first. So, it was sort of like, "Oh, maybe changes in the gut microbiome are actually playing a role here." That's an example of a context, I think-- we don't take in the whole context of things like TMAO, for example, the role of other foods. Any TMAO thoughts?
Simon Hill: Yeah. And I mean, the good the role of other foods and I guess, complementary foods and overall diet, this is a really interesting conversation. Particularly, one thing that, and we can come back to this if you want, but now or in a future episode is red meat and risk of cancer and how potentially the inclusion of plants may modulate that risk, which I think is a fascinating thing. But in this instance, we're talking about the production of TMAO through the microbiome and then that actually goes into circulation in the liver you produce TMA, which is, as you say, is associated with this increased risk of cardiovascular disease, type 2 diabetes. Now, what we see is that people who have been eating plant-based, more plant foods, they have a reduced capacity to produce TMA, which means less TMAO in circulation.
Now, I must say, I didn't expand on this in my book, and one of the reasons for that was, I kind of was sitting on the fence as to how important is this marker. And since the book was published, I've read some published, Mendelian randomization studies, which look at genetics. And they're really, really, these are really fascinating studies in the same applies for elevated levels of LDL cholesterol or ApoB-containing lipoproteins, there's a bunch of these studies looking at that. But in this instance, looking at genetic studies, looking at people who have genetically elevated levels of TMAO, we don't see increased risk of cardiovascular disease. And so, for me, I think the jury is still a little bit out in terms of TMAO, is it just associated with cardiovascular disease, but it's not actually involved in the causal-- in the development of it? I'm leaning towards that right now, which doesn't mean it's a marker that we shouldn't look at. I'm just not sure whether it in and of itself is causing or contributing to cardiovascular disease.
And an example, that I would use that similar to that is HDL cholesterol. We know that people who have elevated HDL cholesterol have lower risk of cardiovascular disease. However, we've had a bunch of trials that have used drugs to raise HDL that have failed. They haven't lowered risk of cardiovascular events in those people. And so, what where we are currently with HDL is that it is certainly associated with cardiovascular disease, but we don't think it's causal, we don't think increasing HDL is directly lowering cardiovascular disease. It seems to be more of just an association.
All that to say with TMAO, and this current conversation, I think that research, what you pointed to which I put in the book, it's very interesting association. But I am somewhat reluctant to say right now, that people that are eating more meat and producing more TMAO, that is directly causing cardiovascular disease, I'm just not sure about that.
Melanie Avalon: And fish that's preformed TMAO. Is there a difference between that? Like taking it in preformed versus creating it yourself?
Simon Hill: Not really, but that also, I guess, adds weight to this idea that maybe it's not causal. And I say that because fish consumption is associated with reduced risk of cardiovascular disease. So, that's another thing that's a little difficult to explain if you take the position that TMAO is directly causing cardiovascular disease. It's another kind of finding that would be hard to reconcile. It's another piece of evidence that sort of just leaves me thinking, "Hmm, I think TMAO, certainly the association is there, people with elevated TMAO, higher risk of cardiovascular disease, but I think it might be an innocent bystander, I'm not sure that it's actually involved in the kind of pathology."
Melanie Avalon: Then speaking to the HDL piece, I find this really interesting, at least in my own panel, because I like to do either high carb low fat, or low carb-- not really high fat, but like low carb, higher fat, but I don't like to do high carb, high fat at the same time. What's interesting is I monitor my blood lipids pretty regularly. And if I do the lower carb, higher fat approach, my HDL will raise but so will my LDL, and then if I switch to the low fat, it's like the HDL drops, but so does the LDL. [laughs] So, it's like, I don't know how to make the HDL go up and the LDL go down. So, I'm very, very fascinated, there's so much research. This could be an hours and hours' long conversation, and there's so many opinions, but I'm very haunted by the correlation versus causation and the role of both LDL and HDL and health. It's just a lot. I think people are very confused.
Simon Hill: Yeah. I would say I just mentioned the HDL. I think that HDL right now, if you look at all of the guidelines, and the latest evidence on HDL, I would say that the absolute amount of HDL, or any sort of ratio to do with HDL, we really can't use that as a way of determining risk of cardiovascular disease. And that is off the back of we had this hypothesis. Observational studies showed high HDL is associated with lower risk of cardiovascular disease. That hypothesis then went on to lead to the development of certain drugs that would raise HDL took people that were at risk of cardiovascular disease, jacked their HDL up did not see any protection. What that tells us is that maybe the amount of HDL is not actually as important as we thought it was and now there's a bunch of researchers looking at HDL function. It's going to be a whole another topic to come in future years.
Whereas with LDL, it's a different story. I should say, I'm going to talk about LDL cholesterol here, but really, I mean ApoB-containing lipoproteins for any of the kind of lipids specialists out there, I'm simplifying this a little bit. But LDL cholesterol, we have genetic data. So, we know very clearly that over 50 different genetic variants that increase LDL cholesterol through different pathways, depending on the extent of that increase, the magnitude of that increase, there will be an increase in risk of coronary heart disease and it's linear. The higher that LDL cholesterol goes up, the greater the risk. And in fact, if you look at folks with familial hypercholesterolemia, whether it's heterozygous or homozygous, particularly homozygous where someone could have an LDL cholesterol 500 to 700, if left untreated, they will often develop severe atherosclerosis and heart disease in their teenage years.
So, those are genetic points that we have and then we have the observational research, which shows the association higher LDL cholesterol, higher risk of coronary heart disease, and then it's further strengthened by clinical trials that lower LDL cholesterol through different pathways, PCSK9 drugs, we've got statins, ezetimibe, there's a whole bunch of different drugs that work on different pathways to reduce LDL cholesterol and you see a reduction in cardiovascular events and you see regression of plaque once you get down to a certain level. So, when you add all that up, it becomes a very compelling case to kind of lead you to believing or concluding I should say, "That LDL is causal. " And more specifically, that a ApoB-containing lipoproteins are necessary for the development of atherosclerosis. And certainly, that's my position, I would find it hard to come to a different position today.
And I do think also, one thing to add to that, I think it's really, really important is often you could look at a drug trial and you could to look at the kind of risk reduction, and might think it's not a huge risk reduction, but we have to keep something in mind here. When we're talking about LDL cholesterol, increasing risk of coronary heart disease, or we're talking about ApoB, more specifically, lifetime exposure is really, really important. So, what we actually see is the kids that have these genetic mutations that increases their LDL cholesterol, their increased risk of coronary heart disease is magnitudes higher than what you see in an observational study. And also, their benefit of reducing is magnitudes greater, because you can get them earlier in life. Whereas if you take someone in a drug trial, who's, say, 65 years old, and you run a four-year drug trial, they've had 5-6 decades of exposure to high LDL cholesterol already. You can only do so much when you intervene so late in life, and this plays back into this idea of just preventative lifestyle medicine and trying to make these changes to our nutrition and our lifestyle as early as we can in our life because lifetime exposure to things like LDL cholesterol is really important.
Melanie Avalon: So, if you had a person who had a lifetime exposure, and it was high, and then magically, you just made it low, like with a magic switch, is there damage that's been done?
Simon Hill: Yeah, they have significant residual risk through the development of that plaque. It doesn't just go away. So, atherosclerosis is bubbling away underneath the surface for decades. Sure, it'll become symptomatic, perhaps when someone's in the 50s, or 60s, but we know that the actual pathophysiology of that is occurring, even in the fetus, depending on the mother's cholesterol levels and health. But certainly, during the teenage years- and some of the early evidence for that was looking at Korean War, looking at American soldiers, and the postmortem sort of analysis of the soldiers who were killed by a gun wound, looking at the condition of their cardiovascular system, these were on average, 21-year-old males from America, and saying that many of them had substantial atherosclerosis. That was one of the landmark studies that got people thinking, "Wow, here's a group of people that we thought were fit and healthy." And they certainly looked it on the outside, but they were on the road to developing symptomatic cardiovascular disease.
Melanie Avalon: Can you have-- because I guess this is what an argument that carnivore people make, can you have these really high levels and no plaque?
Simon Hill: Yes, you can. So, remember, what we're looking at in these studies is typical average response. There will always be outliers, 100%. But just because those outliers, that doesn't mean that what we're saying and what we're recommending to the public is wrong. Do you want to take the punt that you're an outlier? You know, it's possible that you are, but it's not probable. So, just sit on that for a moment. Are you really-- by the off chance, are you one of these outliers or are you more likely to have the typical response that we see?
Melanie Avalon: I guess the tiny nuance there is, can there be a contextual environment where you would have that situation, but because you're not in inflammatory state, you're not even forming-- I don't know, to what effect is that genetics versus the environment that you create with your diet, the creation of plaque from the high levels.
Simon Hill: Yeah. Certainly, and I think this would-- again, it would be foolish of us to zoom in just on ApoB and LDL cholesterol. Because, as you just mentioned, then inflammation is important, there are other blood pressures, another one that's really important. But what we know is that those other risks tend to stack upon each other and increase your risk. However, what's absolutely necessary to develop atherosclerosis is elevated levels of LDL cholesterol, more specifically ApoB containing lipoproteins. And if those levels are not elevated, we essentially do not see atherosclerosis. So, my position and a position in the guidelines is why take the risk and elevate them to a level where you have increased numbers of these floating around entering into the arterial wall greater chance for retention, greater chance for plaque buildup. When there are very simple ways for most people, not everyone because some people have genetically elevated levels, but there are very simple ways through lifestyle to shift them into a favorable direction.
And if we look at a study like the PESA study out of Spain, which looked at subclinical atherosclerosis, so they took a group of people that were otherwise healthy, and they looked at their LDL cholesterol levels, and then they used ultrasound to look at subclinical atherosclerosis. So, they were looking at plaque buildup in these healthy individuals. And what they saw was what your doctor would describe as normal, say, 110. I think 110 mg/dL, might be 100 mg/dL or 115 mg/dL, I can send you the graph. But what your doctor would say is normal, about 50% of people had subclinical atherosclerosis. And it wasn't until you got to 70 mg/dL of an LDL cholesterol level, where there was virtually no atherosclerosis. And that piece of study finding, which came out a couple years ago, is consistent going back to the earlier part of our conversation with Loren Cordain, Paleo Diet author, who published a paper with Eaton and a few other colleagues that also went through and looked at cholesterol levels in babies, in chimpanzees, in humans that do not develop atherosclerosis. And the conclusion of that coming from the guy who wrote The Paleo Diet was that the optimal level of LDL cholesterol is 70 mg/dL. And so, there's quite an extensive body of research that would suggest that if we could target that level at a population, we'd see huge reductions in cardiovascular disease.
Melanie Avalon: Yeah. That's the perspective I've had, which is it just seems like playing with fire to have these really high levels, even if you think it's fine and like a clear calcium artery score, whatever that may be, it just seems dangerous.
Simon Hill: Yeah. And with the coronary artery calcium scan, again, I think one of the important things to consider is what's the utility of that. And when you're young, and you haven't had many years' exposure to elevated LDL cholesterol, let's say you're in your 30s and adopt a carnivore diet or early 40s, and you've been eating it for two or three years and had elevated levels for that period, there's not enough time to see calcified plaque. So, getting a coronary artery calcium score of 0--
Melanie Avalon: Like it should be 0.
Simon Hill: Yeah, it should be zero. So, it's not that helpful for that individual at that point in time.
Melanie Avalon: Yeah. Great, I'm glad you pointed that out. I want to be respectful of your time. I might take you up on your offer if you want to come back in the future and touch on climate and environment, and I would love to do a show on that. One more just food-related question, because you've talked about this, and I've heard you speak about it, and I don't think I've talked about it on the show before, nitrates and nitrites. I was wondering if you could just talk really briefly a little bit about that. I'm so fascinated by the difference in those from plants versus animal products.
Simon Hill: Right. So, I guess in animal products, nitrites are often used in the preservation, particularly in the kind of ultra-processed meats, deli meats and whatnot. Whereas in plant foods, like let's say rocket or arugula, depending on where you're from, or beetroot, these are naturally rich in nitrates. What's interesting is that tactually the way that they're packaged and within this food matrix affects how the body metabolizes them and the pathway that they go down. So, in short, when we're consuming these nitrates in plant foods that are packaged next to antioxidants compounds like vitamin C, also polyphenols, we see the nitrates go down this pathway where they are acting as a precursor to nitric oxide. And nitric oxide is a really wonderful compound for our physiology. It helps lower blood pressure, improve vasodilation. We know that it increases blood flow to the brain and may have effects on cognition and the development, or lack thereof, of neurodegenerative diseases.
Whereas the nitrates that are in these sort of more processed animal foods-- and I don't think there's a lot of debate out there about ultra-processed meats being something that should be limited, if not avoided. But the nitrates in those foods go down this other pathway mostly because of what they're packaged with. And what I'd love to see, and I have asked a few researchers about this, and I haven't seen much, is one about if you're eating those meats with, for example, rocket, or with beetroot? I think that's an interesting thing for us to kind of look at. But what we see is that at least when you're consuming these meats by themselves or within a diet that doesn't contain a lot of antioxidants, that those nitrates end up being converted to N-nitroso compounds, which are thought to be carcinogenic. And this is kind of one of the proposed mechanisms that may help explain why we see an association between regular consumption of ultra-processed meats and colorectal cancer, for example. So, all that to say is it's just a neat part of physiology, I guess, that similar compounds, depending on the food that they're in, can go down different pathways and affect our physiology differently.
Melanie Avalon: Yeah. It's so fascinating. Now, they label things as nitrate free, but it'll technically be the same compound just from celery, basically a reductionistic approach. But in any case, this has been so amazing. I could talk to you just for hours and hours. So, maybe if you would like to come back in the future, and we could tackle the climate stuff, that'd be amazing.
The last question I ask every single guest on this show, and it's just because I realize more and more each day how important mindset is, so what is something that you're grateful for?
Simon Hill: Ooh, the ocean. I'm currently up in Byron Bay. I spent a bit of time up here. It's sort of the north part of New South Wales on the northern coast there. I've been spending a fair bit of time surfing. So, yeah, the ocean is certainly something I'm very grateful for. Always feel great coming out.
Melanie Avalon: I love that. Well, thank you so much, Simon. I cannot thank you enough. This conversation was like a sigh of relief. I think people are going to feel so empowered and feel a lot better after listening. I cannot thank you enough for your work. And you have you have a restaurant, correct?
Simon Hill: Yeah, I have a restaurant in Bondi, which is in Sydney, in Australia, and that's called Eden Bondi. So, if you're ever in the neighborhood, we'd love to have you in there.
Melanie Avalon: That's amazing. What links would you like to put out there for listeners to best follow your work.
Simon Hill: So, if folks want to listen to more of what I have to say and my guests, they can listen to or tune in on The Proof.
Melanie Avalon: To your podcast.
Simon Hill: Yeah. The Proof Podcast, on Twitter. I'm @theproof and on Instagram @simonhill.
Melanie Avalon: Awesome. Well, we will put links to all that in the show notes. Thank you so much for your time and everything that you're doing. This was incredible and I hope you have a wonderful rest of your day.
Simon Hill: Thank you, Melanie.
Melanie Avalon: Bye.
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