There are plenty of supposed “anti-cancer” diets out there, but what does science say about the relationship between nutrition and cancer?
Dr. Evan Lien, an assistant professor in Van Andel Institute’s Department of Metabolism and Nutritional Programming, gave an illuminating talk on this topic March 20, 2024, as part of the Van Andel Institute Public Lecture Series.
Rewatch the lecture below:
Video transcript
Note: The following transcript has been edited for readability. Click a timestamp to jump to that part of the video.
Maranda [0:03]:
Good afternoon. Welcome to the Van Andel Institute’s Public Lecture series, the Science Behind Cancer and Nutrition. My name is Maranda. I’m from WOOD-TV8, and I’m so excited because today is one of our largest crowds, this conversation. We have all of you gathered here, but we also have several hundred joining us online. And this tells me it’s a very important topic. I was just speaking with our presenter, and I said, “I think we’re all here hoping for the silver bullet,” right? We want those five things I can write down and do. I don’t know if we’ll get it or not, but I’m excited.
As you know, the disease we call cancer is actually a group of diseases with hundreds of types and variants. The scientists at VAI are hard at work solving the mysterious — or the mysteries — of many of these cancers, looking for better ways to diagnose and treat them.
There’s a lot to unpack as cancer can be affected by a variety of factors, from our genetics to our environment. But have you ever asked yourself, how does our diet affect cancer? And if we have a better understanding of this relationship, can we use it as a tool to fight this disease? There are many so-called, anti-cancer diets in popular culture today.
Unfortunately, many of these follow unproven or outdated science, ignoring the countless unknowns about the relationship between nutrition and cancer. Lucky for us today, our speaker is working to change that, using the latest technologies. Dr. Lien investigates how certain nutrients affect cancer growth. He works to identify evidence-based dietary strategies to enhance current and emerging cancer treatments.
Today, he is going to guide us through what we know, and what we don’t know, about nutrition’s impact on cancer, and how new breakthroughs could inform tailored diets to combat this disease. At the end, we’ll have time for questions and answers, so I ask that you hold those questions until the end. Also, if you are online, please use the chat function to post your questions. Now, join me in welcoming Dr. Lien.
Evan Lien [2:29]:
Thank you, Maranda, for the kind introduction, and good afternoon, everyone. It’s my pleasure to welcome you to the first installment of the VAI Public Lecture Series. I’m really excited to be here with all of you today and hopefully we’ll have a thought-provoking discussion about the science behind cancer and nutrition.
So, I am currently an assistant professor at Van Andel Institute, and I’m in the Department of Metabolism and Nutritional Programming. As you might be able to tell from the title of the department, many of us here work on how metabolism contributes to various diseases. And so when I say the word metabolism, I think there can sometimes be some confusion about what metabolism actually is. And I think we all have heard this word thrown around in various contexts and places, and many people mean many different things by it.
I think the most common thing that, the first thing that we all think about when we hear the word “metabolism” is diet, right? The food that we eat every day. And this is obviously a major part of the metabolic processes that happen in our body. We see it do its work, right? As we eat, the nutrients that the cells in our body take up are used and converted into the energy to support growth and development. And we can watch a child grow up into an adult as they eat more and more food.
And so I don’t think I need to convince any of you that diet is a really important part of human health. At the same time, I think all of you probably recognize that it’s really difficult to know what types of diets and what factors in your diet can actually help improve your health.
There certainly are dietary recommendations out there, but even these recommendations have changed over time. So when I was a child — I grew up in the 90’s — I saw this image everywhere. I remember sitting at the breakfast table as a child and eating my bowl of cereal. And on the back of that cereal box would be this food pyramid. And looking at this food pyramid, you know, I felt really great about myself, right? It told me that I needed to eat a lot of grains. And so with that bowl of cereal, I was being healthy. What I didn’t know as a child is where these recommendations actually came from.
Now, certainly some of these recommendations were based on our scientific understanding at the time. So during this time period, it was thought that fats and oils were bad for you. And so the recommendation was to avoid — minimal fats in your diet.
But what I didn’t know is that some of this was also based on outside influences. And so it turns out that a major reason for why there was such a heavy emphasis on carbohydrates and grains, breads and pastas, was in part due to the grain lobby and the government at the time.
And so over time, these recommendations have actually changed. We now know that fat isn’t as bad for you as we once thought it was. And it turns out that this emphasis on carbohydrates might have contributed, to some degree, to the obesity epidemic in our country today. And so, in 2011, the USDA revised these dietary recommendations. They came up with this thing called MyPlate, where now, instead of a pyramid, you split up the plate into four quadrants, and different amounts of vegetables, fruits, grains, and protein. And like I was saying, some of this is based on scientific evidence because we know that carbohydrates are not as good for you as we once thought.
Some of that has changed. Now, it is interesting to me to note that perhaps some of this might still be based on some outside influences. So it’s, there’s something that, that dairy, part of the reason that it’s there might be due to the dairy lobby. But regardless, the point I’m trying to make here is that it’s really hard to make good dietary recommendations. And if it’s hard in the context of a regular, you know, just our daily lives, you know, it’s hard in the context of disease as well. And so there are a lot of diet plans that are out there that are very popular for doing things like losing weight, preventing disease.
I pulled this from the U.S. News and World Report best diet rankings, right? There’s five best diets, five worst diets, and there are many, many options out there. It’s really hard to filter through all of them. Some of them are easier than others to do. It’s hard to know which of these diets are actually based on good scientific evidence. And it’s really even harder in the context of cancer, right? There’s a question of how these interventions can be integrated into cancer treatment.
If you’re interested, after the talk, you should just go online, go on Google and search diet and cancer, and you’ll find all sorts of things, all sorts of books, websites, that push these so-called anti-cancer diets that might be able to help you prevent the disease. And I don’t wanna, I don’t want to kind of discredit all of that, right? I think there are general, there’s general dietary advice out there that’s good for, for your general health. But what’s really clear is that much of what’s out there is not based on good scientific evidence.
And so what do we do about that, right? Like, what is out there and how can we understand it better? So I’m gonna give you an example here. One of the most popular ideas out there is that these low glycemic diets — these are diets that lower your blood sugar — that these diets are supposedly good for fighting against cancer, for preventing the progression of the disease. Things like, you might have heard the ketogenic diet, which is primarily fat and very little carbohydrates.
And this idea is not entirely based on fiction. There is some scientific backing to it. So over a hundred years ago, there was a scientist named Otto Warburg, who found that tumors consume very high amounts of sugar, right? And based on that, many proponents of these diets argue that if you lower your sugar in your blood through the diet, you can inhibit the growth of tumors.
However, this diet is really difficult. These diets are really difficult to maintain. It’s very difficult to test in humans. What we can do, however, is test how these diets affect tumor growth in our experimental models of cancer that we do in the lab. And under those conditions, we can very tightly control the diets that these animals who have, that are bearing tumors, are receiving.
And so here is some data that’s out there. What I’m showing you on the top are three different graphs. And what we’re looking at is the growth of different types of tumors. And so on the y-axis, I’m showing you the volume of the tumor in these animal models. On the x-axis is time. And so as time goes on, the tumors grow bigger. And what you’ll notice is that a ketogenic diet, one of those low glycemic diets, it has varying effects, right?
In this model of glioma, a brain cancer, that ketogenic diet blocked the growth of these tumors. On the other hand, in a pancreatic cancer model, no effect at all. And then, kind of scarily, in a melanoma model, it actually even enhanced the growth of those tumors. And so this kind of data makes me scared, right, about making any kind of dietary recommendations, because what you then run the risk of, is if you broadly apply recommendations to everyone, you might end up harming some. And so we should be very cautious about making dietary recommendations for people with cancer without solid scientific evidence.
And therein lies a problem, right? There isn’t a lot of good scientific evidence. There’s a lack of rigorous and systematic scientific studies that examine this question of how diet impacts cancer progression. And a big reason for that is because, simply put, this is a really complex question.
There are many factors that go into how diet interacts with the disease. And so as scientists, what we want to do is we wanna take a complex question like this, how does diet impact tumor metabolism and progression? And we wanna take a complex question and break it down, break it down into something a little bit simpler, some simpler questions, some simpler hypotheses or predictions, that we can then go into a lab, do a very controlled experiment to answer that question, and that then might potentially inform us, give us some insight, about the complexities underlying this.
And so here at the Van Andel Institute, we are fundamentally a basic science institute. We do studies in the lab using different models, whether they’re cellular models or animal models, and we ask questions. For my lab, we ask questions about diet, and we hope to find something fundamental about what is happening at the molecular level in these dietary models. And we hope that through these fundamental discoveries, that down the line, these discoveries can be used for some sort of translational application and hopefully be applied towards patients.
And so how are we approaching that? How is my lab approaching that? I want to come back to where we started, what is metabolism, right? And we talked about how we generally think about it as diet. For those of us scientists who think about biology at the cellular level, metabolism — we’re gonna zoom in a little bit — metabolism involves the thousands of chemical reactions within cells that allow cells to take nutrients from our food and transform those nutrients into useful things, right? Whether that’s energy for the cells to function and survive, whether that’s biomass or biomolecular components that allow those cells to grow, as well as the generation of waste products from those nutrients.
And so many of you probably remember if you have to, you reach back to your studies in high school, maybe in college, maybe you took an introductory biology class, you probably learned some of these pathways these metabolic pathways in class.
Hopefully, I’m not triggering any traumatic memories here of these pathways. Now, when I was in, when I was in school, I really, I loved learning about these pathways. They were really fun to think about. But I do acknowledge that for many of us, maybe it was a little bit boring to learn about these. And I would say a big part of that is because these pathways are often taught as static processes. They’re just processes that are going on in your cells all the time. You don’t really have to think about them. They just happen. But it turns out that these metabolic pathways are very dynamic. They’re constantly changing. They’re regulated in different ways in different contexts.
And so, let me give you an analogy to illustrate this. So I moved here to Grand Rapids a year and a half ago to start my lab. And one of the things that I have really loved about living here is that it seems like everything’s 15 minutes away or less, right? Anything, I want to go to, it is 15 minutes away or less. If anything is over 15 minutes, oh my god, that’s too far to go to. So here’s a map, right, illustrating that.
Now, before I was in Grand Rapids, I did my training in Boston. So here’s a map of Boston. And it was a very different situation there. So here’s a static map where you can think of the roads as different pathways that help you get from point A to point B. And so for me, according to Google Maps, to get from my home to work, it should take me 20 minutes driving on the highway. But because this is a static map, it just shows you the pathway is connecting different points.
It doesn’t actually tell you how these roads are being used, right? And so the situation is different. If I show you something like this, right? On a Sunday morning at 8 a.m., indeed, takes me about 20 minutes to get from home to work. But if I attempt the same route on a Monday morning at 8 a.m., it all of a sudden turns up to an hour, and it would indeed take up to an hour. And perhaps under these conditions, there might even be alternative routes that would get me to my location faster.
And so the point here is that these pathways are altered by context, by environmental context. So in very much the same way, metabolic pathways in our cells and our tissues and our body, they also change depending on the environment that the cells are in. A really easy example, a simple example of this is just thinking about our different tissues.
One of the factors that regulates these pathways and how they work is determined by the function of the tissue, right? So our liver, our liver is one of the organs in our body that stores nutrients, right? So when we eat food, our blood sugar rises, and because there’s more sugar than we need, that excess sugar gets stored in the liver, in this molecule called glycogen. When we stop eating and fast, our blood sugar drops, and our liver responds to that by taking that stored sugar and turning it back into that sugar called glucose, which is then released to the rest of your body for use. The liver’s function is very different from the muscle function. Muscle function helps you move, walk around and do exercise. Therefore, muscles need a lot of energy to do their work. And therefore, muscles take sugar, like glucose, and use it primarily to make energy in the form of this molecule called ATP.
And so these metabolic pathways shift, and they’re dependent on the function of the cells and the tissues that they are in. And so what about cancer? And what is the function of a cancer cell and how is that different from normal cells? What we have come to appreciate is that normal cells in our body, they take up nutrients like sugar, like glucose, and really their primary priority with that, with those nutrients, is to make that energy in the form of ATP.
You think about most of the cells in your body, they’re not growing in number, right? We have what we have for the most part. And those cells just need to survive, maintain viability, maintain homeostasis. So their primary goal is to generate energy. A cancer cell is very different from a normal cell. What a cancer cell does is its function is to grow, it grows uncontrollably.
That is fundamentally what cancer is, right? These tumors that grow uncontrollably within our bodies. And so in order for a cancer cell to grow from one cell to two cells, what it needs to do is it needs to first double in size, right? It needs to make an extra copy of its genetic code, of all of its DNA. It needs to make extra membranes. It needs to make extra proteins until it reaches roughly double its size, before it can then split off into two cells.
And so the metabolism that supports this is very different from what I just described for normal cells. These proliferating cancer cells have to take those nutrients and not only generate energy, but also generate all of the other components like proteins and DNA needed to grow to double. And so over the past 15 years, this area of research has really just exploded.
There’s been a lot of work in understanding how these metabolic pathways are different in cancer cells to support this proliferation program, versus normal cells that don’t have to do this. And the reason why there’s been so much interest here is because that there is a difference here. Potentially you could target, you could inhibit these pathways in cancer cells and block their growth while leaving your normal cells relatively intact, right? ‘Cause normal cells aren’t doing the same thing.
And so how does this all apply back to diet? My lab’s vision, and the vision of many labs in the cancer metabolism research field, is to take everything we’ve learned about these chemical metabolic pathways in cancer cells and try to apply those principles — what we’ve learned — to this complex question of what diets might be beneficial for patients. And the approach that my lab takes specifically is a somewhat simplified approach, right?
If you think about it, the food that we eat influences the levels of nutrients that end up in our blood, right? And therefore, that would then change the nutrients that are within tumors. And what we know is that by simply changing those nutrient levels in tumors, we can alter the activities of these pathways within these tumors to influence their growth, right? And so if we could understand this process by which a dietary change leads to a difference in nutrient levels within the tumors, we can potentially understand at the molecular level how these diets are mediating their effects.
And here at the Van Andel Institute, we have a bunch of technologies and, you know, some of the latest instruments that allow us to make these measurements and to do this work. And so I wanna just give you a flavor of some of the work that is coming out of my lab right now.
I want to come back to this idea about low glycemic diets, these low-carbohydrate diets that lower your blood sugar, like the ketogenic diet. And I’m gonna show you some data from the lab that is based on two different types of low glycemic diets. One of these types is what’s called caloric restriction, limiting the number of calories that you eat by simply reducing the number of carbohydrates that are in your diet, in this case by about 40%. And then the second diet is the ketogenic diet, which I’ve referred to. It’s basically all fat, 90% fat, no carbohydrates, some protein. As you might imagine, not a great thing to do by yourself as a human. But we can do these diets in mice. In animals, in animal models of cancer, we can very strictly control what they are consuming.
And so we did a very simple experiment with these two diets. We took some mice, some animals that are bearing pancreatic tumors, and we just put them on these two diets and asked, “How do the diets affect the growth of these tumors?” And what we found is that they’re not the same, right? Caloric restriction, limiting calories, reduced the growth of these tumors. The ketogenic diet does nothing.
However, both of these diets are great at lowering your blood sugar, right? And so this began to really tell us, “Hey, it’s not just about the sugar,” right? If it was all about the sugar, then both of these diets should impair tumor growth, but it doesn’t. So there must be something else going on. There must be some other nutrient that is important.
And so we began to ask, does caloric restriction change the levels of other nutrients in tumors? And what we found is that there was a major impact on fat within tumors. So these molecules called fatty acids are derived from the fat in your diet. You’ve probably at least heard of them and they’re categorized in many different ways. But the most common categorization is what are called saturated fatty acids, monounsaturated fatty acids and polyunsaturated fatty acids.
The reason why they’re called this is because the chemical structure of these fatty acids have different numbers of these double bonds in the chemical structure. So saturated has zero double bonds, mono has one, and poly has two or more. And so what we found in our studies is that when we measured the levels of these fatty acids in our tumors, which I’m showing you here, again, categorized into these three types of fatty acids, what we found is that caloric restriction really reduces the levels of monounsaturated fatty acids in these tumors. Those fatty acids with one double bond, the others, not much of a change. And so we began to ask, well, maybe the way that caloric restriction is inhibiting the growth of tumors is by depleting tumors of this particular fatty acid type.
So to try to ask, to try to determine if this is the case, what we wanted to do was alter our caloric restriction diet to boost up monounsaturated fatty acid levels and see if the effect of the diet disappears. The way we did that is we took our diet and we not only made it a caloric restriction diet, but we doubled the amount of fat in it. We just raised the amount of fat in the diet. And then what we found is that it’s not only the amount of fat that matters, but the type of fat that matters as well.
So here, again, we are looking at these growth of tumors. The caloric restriction diet in the red lowers, inhibits the growth of these tumors. But then if we took our high fat diet and used palm oil in it, palm oil has a lot of those monounsaturated fatty acids I was just talking about. So if we boost up the levels of monounsaturated fatty acids within the diet, all of a sudden the tumors start growing faster again. Right? We lose the effect of caloric restrictions, which really tells us that by giving tumors these types of fatty acids, they grow faster. And if we take it away, they grow slower.
On the other hand, if we put soybean oil in our diet, soybean oil has high polyunsaturated fatty acids, they have low monounsaturated fatty acids. This diet, the soybean oil diet has no effect, right? It doesn’t change anything because we’re not providing those monounsaturated fatty acids.
And so it turns out it’s really these monounsaturated fatty acids and how they’re affected by the diet. That’s important. The takeaway message, I think, here, is that the amount and types of fat in our diet play a big role in how different types of diets influence the growth and progression of cancer. And we don’t totally understand everything about it yet, but the lab is doing a lot of work in this area using this framework I just shared with you earlier. We have many projects in the lab where we’re manipulating the amount and types of fat in the diet and trying to understand how those changes influence how those metabolic pathways are functioning within tumors.
And I, what I want to finally end on is this idea that we’re also pushing in the lab, which is that, you know, Maranda was saying that everyone wants that silver bullet. And maybe some of you today came hoping that I could tell you a list of five things that you could write down and change your diets with.
Unfortunately, I can’t do that because a lot is still unknown in this space. But I also want to point out that there’s very unlikely to be a silver bullet diet of diet for cancer treatment. There isn’t gonna be some diet that a cancer patient can just go on and prevent their disease. And a big reason for that is because we have many great cancer therapies that have been developed that extend patient lives. They’re used as standard-of-care therapies for cancer patients, whether that’s chemotherapy, targeted agents, as well as immunotherapy, which has really transformed cancer treatment in the past several years.
And so one of the ideas that we are pursuing is that, well, it’s not just about the diet. It’s about how diet might interact with the therapies that patients are already receiving. Perhaps we can understand how we can, for each patient, target a specific dietary change that will enhance, that will improve the efficacy of the therapies that they are receiving. And if we can find those synergistic combinations, that will probably be the best opportunity for integrating diet into cancer treatment.
And indeed, there has been a fair amount of work amongst researchers in the field already. There have been several combinations that have been identified that may be effective, at least in our experimental models, and are now being tested in clinical trials and within cancer patients.
And so with that I, I want to acknowledge all of the people that have contributed to this work. Of course, my lab right here, we just opened up the lab a year and a half ago, we’re at eight people in the lab and they’re doing really great work every day, advancing the research and science. And then also at the Van Andel Institute we have many people who support the research that’s going on here every day, from core facilities that allow us to make our careful measurements to people in facilities and operations and logistics that really help us get our work done. And so with that I just wanna thank you for your attention. We’ll be here for another 20 minutes or so. And during that time, I will be happy to take any questions you might have. Thank you.
Maranda [29:05]:
How exciting. I’m sure we have a lot of questions. We have some friends who will have microphones here and, if you have a question, I just ask that you please raise your hand. And once you get the mic, go ahead.
And then also, if you are joining us online, I would encourage you to use that chat function and we’ll try to get to as many of those questions as we can as well. I love seeing a room with hands up. We’re gonna have some fun. Let’s get started.
Audience member [29:28]:
You talked a lot about cancer treatment, but what about diet as far as cancer prevention? So does diet, like, maybe that decreases body fat and reduces inflammation, help prevent cancer in the first place? And then, also, maybe, thanks to our friend [Dr. Andrew] Huberman, a lot of talk about alcohol.
But you know, what about the presence of alcohol in our diet, and your thoughts on that as far as cancer prevention or causes? Or also while you’re, you know, currently battling cancer, does that have an impact if you’re using or ingesting alcohol?
Evan Lien [30:00]:
Yeah. so in fact, a lot of the work that is out there has more to do with prevention than it has to do with treatment. And so there are many epidemiological studies that have been performed in the human population to try to make these associations between dietary intake and cancer risk. And some of that, some of that is solid, right?
So there’s, for example, very high association between obesity and various types of cancer. And that is coupled with more mechanistic laboratory studies that begin to really tease out why that link exists. And so some of that is solid, but a lot of it is also associations, right? So there are things that we observe in the population that are associated with an increased incidence of cancer. And there might — as many of you probably know, correlation does not mean causation.
And there are further studies that would then need to be done to try to understand, are these factors actually causing or preventing cancer? Or is it just an association that we see? And so there are many of these associations out there. There’s a lot more work that needs to be done to understand whether there are actionable things that you can do to actually prevent cancer risk.
Regardless, there are, you can find recommendations from, for example, the American Cancer Society and other organizations that try to integrate this data into certain recommendations that can generally be helpful. But again, right, not necessarily rooted in solid scientific evidence.
As far as, you know, alcohol, that’s an interesting question. You know, I think there’s a lot of studies on alcohol and other aspects of health. I am at least not aware of really careful studies and, kind of, animal models of cancer that have really tested how alcohol influences progression of tumors. And so, you know, that’s something I, that’s probably worth looking into. Yeah.
Maranda [32:22]:
Great. Next question.
Audience member [32:26]:
Hi. I was interested — so I’ve been looking into some different studies, specifically with Dr. Eric Berg. He talks about it a lot. Fasting has been kind of a trend that a lot of people have been interested in. And I know that a lot of people talk about autophagy when it comes to fasting. That could be either cancer prevention or cancer-reducing that could kind of go along with fasting. I’m curious your thoughts on the use of fasting with cancer?
Evan Lien [32:54]:
Yeah, great question. So there is a lot of work on fasting and fasting-type diets. In fact, caloric restriction, that data that I showed you, that is a form of fasting, right? Because you’re reducing 40% of your caloric intake.
So I think there’s a lot of pretty interesting data out there, again, in our experimental models. Caloric restriction by far, across many different animal models of cancer, has been shown to very robustly prevent cancer progression. There are few, very few cases, where it doesn’t. And not only that, there’s actually really fascinating work from a couple labs that show that fasting type regimens can really enhance cancer therapy.
So if you take an animal with a tumor and you, and you do a short-term fast, for example, the day before, right before giving chemotherapy treatment, that really enhances the effects of the chemotherapy.
There are many examples like this, but I have to emphasize that all of this is in animal models, in animals. Mice are not humans, right? And to really know that these effects will translate over to humans, we need to do careful clinical trials that test whether these diets, these types of fasting regimens really have that kind of effect in human patients.
And that’s, to be honest, that’s what’s lacking in this type of research, and even integrating diet into cancer treatment, is that there for a long time, there just have not been clinical trials that involve dietary interventions as one of the perturbations to study. That is changing.
So, for example, the fasting-plus-chemotherapy combination I just described, there are ongoing clinical trials testing that idea right now. And there are a few others as well. So people are coming around, clinicians are also coming around to realizing that if we want to, if we want to effectively implement diet into treatment, we have to treat it with the same level of rigor that we give towards drugs that we develop. We have to test them in trials.
Audience member [35:17]:
Has any of your work been done with respect to preservatives in like proteins, nitrates, nitrites. Any correlation between that and cancer?
Evan Lien [35:31]:
We have not done anything in that space within our lab. There are, again, I think, epidemiological studies that link those two, right. But I am not familiar with any laboratory mechanistic work looking at that.
Audience member [35:55]:
Great work. I wonder in terms of lipid metabolism, how can you flush out the bad fats with the good fats in these cells? Because we’re storing a lot of bad fats. Can we get rid of them?
Evan Lien [36:09]:
Yeah. That’s a good question. One of the things that my lab is really trying to work on right now is, like I was saying, as we change the fat types in the diet, how does that even affect the levels of fat in the blood and in various tissues? And you would think that maybe this should be known, but not a lot of close careful work has been done with it, right?
And so I think that is an answer that we hope to answer in the future as we do our studies, as we characterize changing the fat type in our diet. How fast does it take for the changes to occur if there are fats that are detrimental to tumor growth stored in our fat tissues in our body, can we somehow replace that? Can we somehow change the composition there by making a tweak in the diet? We don’t quite know the answer yet, but maybe if you come back in a few years, I can tell you.
Maranda [37:13]:
I have a quick question for you. You are the father of two children. Are there certain foods you do not allow your children to eat?
Evan Lien [37:21]:
I thought I would get a question like that.
Maranda [37:23]:
Well, I just thought I’d throw that out there, but I’m very curious.
Evan Lien [37:25]:
Yeah, yeah. So you know, I think, I think in the lack of any other, any, you know, solid evidence, moderation is good, right? Like I think we want, we want our children to develop healthy eating habits and eat a variety of different foods. We do avoid things like processed foods and sugar. We’re not giving our 2-year-old candy all the time.
But in general we try to expose her to many different things so that she hopefully does develop a healthy relationship with food and learns moderation and can be equipped to make decisions about her diet in the future that will benefit her health.
Maranda [38:10]:
Good. Next question.
Audience member [38:12]:
Thank you very much for your presentation, it was excellent. Along the lines of that earlier question, toxins in our food chain, do you have an opinion on that? And then also specific foods that we should be eating that have anti-cancer properties in them, do you have a feeling regarding that?
Evan Lien [38:27]:
Yeah, so my lab doesn’t quite work on environmental toxins, but there are many labs that do do that, including a lab here at the Institute. So there’s a lab here, for example, that works on arsenic exposure and, of course, that gets into water that might get into some other routes of ingestion into our bodies. And that can have an influence on cancer risk as well as cancer progression.
Of course, you know, we’re still, they’re doing, they’re trying to do laboratory research to try to understand that link. And so there is work in that space and it can have an effect for sure. Your second question was anti-cancer foods. At this stage, I would say in the absence of good scientific evidence and good clinical trials, there’s very little that I would kind of hold up and say, like, “This is the food, this is the list of foods that, that you should be eating.”
I will also, I think there is an interesting anecdote around this, though, which is that things that you think might be anti-cancer and that are promoted by people to be anti-cancer, might not always be the case.
So the clearest example of this is that many people think antioxidants should be great for you, they should prevent cancer. And this was a big idea 10 or so years ago, right, that antioxidants would be beneficial. And because this was an idea, there were clinical trials that were done with this, giving cancer patients antioxidants to see if that would impair their growth, the growth of the tumors. They had to cut the trial short because the antioxidants made tumors grow faster.
And so there are things we do not understand and they just need to be tested better. So that, and there need to be trials like this to be done so that we can understand how to make better recommendations.
Maranda [40:31]:
Interesting. We have something coming in online.
Moderator [40:34]:
One of our virtual attendees wants to know, “Are you considering, or how are you considering, the state of the gut’s microbiome on the development of cancer?”
Evan Lien [40:46]:
That is a fantastic question. There, in the past several years, have been many studies beginning to try to explore this question about how the microbiome interacts with diet to generate microbiome-direct metabolites that might have an influence on cancer. My lab is not personally doing, we’re not personally doing anything in this space. You do need very specialized equipment and facilities to do these types of microbiome studies, but this, I would say is one of kind of the frontiers, the next steps, of diet and cancer research, is trying to understand those interactions.
Maranda [41:29]:
Next question.
Audience member [41:31]:
Hi, thank you so much for your work. I appreciate it. I am currently in treatment for — I just came from there, and so I’ve been trying to do my own research, specifically with the microbiome and nutrition. And so I don’t know if you — it would be any different, but I’m already past chemo, but since I’m in radiation, I have been just naturally restricting my calories because the medications I’m getting also make me gain weight. So there’s this push-pull.
But one of the last things you had up on the screen about, like, what diet you might correlate while you’re going through treatment. I don’t know, I’m my own experiment right now, so I don’t know if you have anything that you would suggest.
Evan Lien [42:20]:
Yeah. I’m sorry to hear that and I hope treatment’s going well for you. I do have to, I think, I have to continue to emphasize, right, we are basic scientists working on experimental models, and I’m not a medical doctor, and for that reason, I try to avoid making any specific dietary recommendations to patients.
I would definitely encourage you to continue to do your research and talk to your doctor about that. And unfortunately at this point, without good data, it’s very hard to make a recommendation that I could tell you with certainty that would help. So unfortunately, we just don’t have all the answers yet, but we’re certainly hopeful that there will be a point as we continue this work that we can actually give doctors advice to actually act on.
Audience member [43:13]:
Yeah, absolutely. It’s well-needed. ‘Cause they’re going on old models and that’s not helpful. I mean, respectfully.
Maranda [43:24]:
Next question. Yes.
Audience member [43:27]:
Could you perhaps elaborate a little bit more on the caloric reduction? I mean, you mentioned 40%, and it’s basically coming from carbohydrates, so I’d imagine that’s, I’d imagine that’s probably from, kind of, breads and sugars. I mean, where would you target if you were trying to say, you know, here’s where you find the 40%.
Evan Lien [43:46]:
So in animal models, we can control — we don’t feed our animals bread or grains. Everything’s kind of — if you go to the pet store, you kind of like see these food pellets. That’s what we give our animals, and we can formulate very precisely what is in those pellets. For, again, with the caveat that, you know, I have not, I would not be advocating that we all go out there and do caloric restriction, right, and try to limit our daily caloric intake, necessarily.
But yes, right, like the carbohydrates would be things like bread and grains and things like that, right? I think the, one of the things that we’re hoping for, you’ll probably, you can probably recognize that many of these diets are tough to do, right? So even if you wanted to calorically restrict yourself by 40%, that’s very difficult to maintain. Even something like a ketogenic diet, which has gained a lot of, you know, popularity in our culture.
To do that correctly, it’s essentially like eating butter all the time, right? And that’s not, that is not a happy lifestyle, it is very difficult to do. One of the perspectives that we have from a basic science perspective is that, if we can understand how these diets mediate their effects at the molecular level.
So, for example, if caloric restriction influences these fatty acid metabolism pathways to mediate its effects, then could we potentially target, just target the fatty acid pathways without the diet, right? The diet ends up being a way for us to understand how the metabolism of these cancers, of these tumors, are being altered in beneficial ways, and can we mimic that without needing to do an extreme diet? And so that’s another perspective from the lab.
Audience member [45:57]:
Thank you for your work. You started off with saying that, you know, there, I believe, a hundred, hundreds of different types of cancer, and then the graph with how sugar impacts the three, with pancreatic cancer, I believe, in the middle, not impacting melanoma. Definitely, I don’t know how to pronounce the other one, so I won’t do that.
But do we have, so that’s three of a hundred, let’s do, how many more do we know? Is it just a couple or is it…?
Evan Lien [46:26]:
It’s a handful. It’s a handful. And that’s been a challenge in studying cancer is that, you know, it’s not one disease. It’s many different types. And even within a cancer type, there are many subtypes, right?
So breast cancer is not one disease. There are many subtypes that all behave differently, respond to treatment differently. And one of the limitations of doing some of these experiments in the lab is that we don’t have models for every type. So in fact, a big part of cancer research of what’s been happening in this field over the past 10 to 15 years, is trying to develop models for different types of cancer of cancers that are out there. And as that continues to develop, then as we continue to study diet, we can apply these diets to those models as they get developed. And so it is currently a handful, but hopefully we’ll continue to progress.
Audience member [47:30]:
As an oncology nurse, I’ve seen a lot of patients who — they end up losing weight and we have to get whatever calories we can into them. So my question is, is your research centered on specific stages of cancer knowing that that changes those things?
Evan Lien [47:48]:
Yeah. So our, our research is centered on progression. So once tumors are established in our models, we then look at the effects of the diet, and that is distinct from incidence and risk, which would be models where there are no tumors to begin with, and you study the effect of diet on risk and the development of cancer. Yeah. So that’s what we’re focused on. Hopefully that answers.
Maranda [48:18]:
What excites you about the work you are doing here at Van Andel Institute?
Evan Lien [48:23]:
Yeah, so I think to have the opportunity to be at a place that gives us the resources and the necessary, from all the equipment and technologies, to do this type of work and to really pursue the lab’s research vision and to pursue interesting questions in this space. And that’s really exciting to me, right? I get to come to work every day and think about interesting research questions, interesting hypotheses, and then have the ability to actually act on that, to direct a lab and direct a team of people to conduct experiments to try to answer those questions. So that’s.
Maranda [49:07]:
Are we making progress?
Evan Lien [49:09]:
I think we are. I think we are. It’s slow. It’s very slow, as it is with, you know, we’re at very early stages, right? I showed earlier this translation of basic science to discoveries to translational application. If you think about a drug, drug development, that takes many, many years, right? From conception of the idea to development through a company and then doing all the trials necessary, it can take up to, you know, 10, 20 years to get drugs approved. And I do think it’s going to take the same level of rigor to truly understand the effects of diet and how we might use it to best help patients. But I do think progress is moving along and I’m hopeful that we’ll improve that.
Maranda [49:57]:
Right here. Yes.
Audience member [50:00]:
Van Andel Institute is one of many on a national or international basis. Is there a coordination of the research that’s being done, or is each lab independent and then you take the work and try and correlate it after that?
Evan Lien [50:18]:
Yeah, so at this point it is many, it is for the most part, many labs at their own institutions who do — each lab’s doing their own work. And there is communication between labs, either personal communication or we have conferences where we come together and present our work and we draw from each other’s data and experiences, and that helps us further our own research as well.
So there is that kind of informal community that works around this. There isn’t necessarily, I would say, like a formal, coordinated effort that links many different institutions together to ask this question. And certainly I would hope that is something that begins to develop as more and more basic science researchers get interested in this question.
Maranda [51:13]:
Yes.
Audience member [51:15]:
Yeah. Thanks for your work. One question. So looking at caloric restriction as something that, in your basic research, has shown, “Hey, this can be effective.” It prompted in my mind — we’ve all seen over the past year the rise of GLP-1 drugs and seemingly every other week, Novo [Nordisk] or [Eli] Lilly are publishing, “Hey, it’s useful for this, it’s good for this, it’s good for that.” I’d imagine it’s only a matter of time until someone’s running the clinical trial with semaglutide married with a cancer therapy. Yeah, you’re nodding your head. So I’m assuming that that’s something that is ongoing or in progress.
Evan Lien [52:02]:
Yeah, there’s, I do believe there’s a fair amount of interest in that, both from the basic research side as well as the clinical side. And in fact, I was talking to a colleague here who knows a surgeon, an oncologist, who has begun treating some of his obese patients with the drug just so that they can lose enough weight so that the tumor becomes resectable — visible and resectable.
And so people are thinking about it, right? People are trying to figure out, are there ways to use this in the cancer context? We’re still very early. There’s a lot we don’t know, but there’s definitely interest.
Maranda [52:46]:
Good. As we wrap up today’s conversation, we are all about 100% hope here. Every dollar raised goes directly to scientists like you and to research. Give us some hope. Come on!
Evan Lien [53:00]:
Well, you know, I think … I think there are many, there are many researchers, both basic scientists and clinicians who are very invested in studying cancer. And we hope that what we discover will lead to benefit for patients. Like I said, it is a slow process and we have to be patient with it. And knowledge, especially when you’re pushing at the edge of what’s unknown, takes time. Right?
But hopefully, with our coordinated efforts amongst researchers here at the Van Andel Institute, as well as other institutions, as we continue our work, we kind of continue to push at that edge of what we know. And I do think that together, there will be a point where we will see a lot of this work translate to something that helps patients. And so the Institute is doing great work in that and we definitely appreciate everyone’s support in helping us get our research done. And yeah, we are hopeful that it will lead to benefits in the future.
Maranda [54:20]:
Thank you for the work you do. Let’s give Dr. Lien a round of applause.
You can find out more about his work and the other work taking place here at the Institute. Just visit vai.org. For those of you that are here in person, we have an exciting opportunity for you. Our two mic handlers are available and they will be giving tours of the first floor of the work being done here at the Institute immediately following when we dismiss. So if you’d like to take a quick walk around, I think you’ll be very impressed and excited about what we are doing right here at the Institute.
In addition to that, I’d like to remind you that we have a few more of these Public Lecture Series. I would encourage you to tell your friends about them, bring them down. Some of the topics we will be looking at in the future is navigating AI in the classroom — that’s a big conversation — the link between inflammation and depression, and then also the crossroads of immunity, metabolism, and cancer.
Those are just a few of the things coming up and we so appreciate your engagement and your excitement. There are so many things you can do and that you chose to be with us today certainly means a lot. Once again, thank you. We appreciate the work you’re doing, and thank you for joining us today. Have a great rest of your day.