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Patrick Hanaway:
Well, it just seemed like the most natural connection because so much, as we know, happens is mediated through the effects of the gut microbiome. And so it’s not surprising at all that the circadian rhythm that we see with intermittent fasting would also be mediated, at least in some way, you know, through the gut microbiome. And, you know, we’ll talk about how that actually happens and what gets affected, but I have been a champion of fasting. It was first introduced to me by my son about 10 years ago. He was an athlete in high school at the time, and he was learning about it. And I began to dive into the literature on it and it’s like, oh, it’s actually really quite effective. And of course, it makes sense when we look at, at what people have done, you know, over cultures, over long periods of time, that fasting and having periods of less food are going to be a natural part of being human. So maybe we need to re-look at that. And we are, and the data is pretty impressive.

 

Kalea Wattles:
It’s certainly exciting to see more and more literature supporting the use of fasting as part of a therapeutic treatment plan. And research is showing that therapeutic fasting might benefit multiple body systems. So in functional medicine, we would translate that to the functional medicine matrix. In general, will you tell us, what are some of the areas that have shown positive associations with fasting treatments? How is the matrix affected?

Patrick Hanaway:
Well, first I’ll talk about it more from a disease state, and then I’ll talk about it from the matrix. And that is, you know, I think first and foremost, the effect on cardiometabolic syndrome and insulin resistance and weight loss and dealing with obesity, you know, certainly that’s where it’s gained its first major effects. And through those mechanisms, we see changes altering CNS function.

But in addition to those things, you know, we can see the effect of fasting on the immune system and decreasing inflammatory biomarkers. We can see fasting’s effect on energy production pathways and the mitochondria. Probably some of the most important effects are mediated through the mitochondria and the whole energy production system, which, of course, is going to affect, you know, things not only like fatigue but brain fog and central nervous system issues. Because the brain is the largest user of energy in the body, you know, so we also can see that a normal diurnal variation is necessary to be able to deal with environmental sensing and detoxification as well.

I haven’t seen so much on hormonal aspects that have gone on, but certainly on the cardiometabolic aspects, there are critical factors. And then, and of course, within the structural zone, you know, we do see changes in the structure of the gut microbiome itself from fasting. And so in a lot of different areas, and I do hope that we can have a chance to talk about some of those aspects around fasting and cancer treatment, that’s also a passion for me, something that is up close and personal.

Kalea Wattles:
Absolutely. Well, we’ve established that the benefits of fasting reach across several body systems. And I’m curious to know, what are some of the high-level known mechanisms that help to explain these positive associations that may be seen between fasting and health in all of these different clinical imbalance areas?

Patrick Hanaway:
I think one of the areas first is when we begin to look at, well, what happens with fasting in and of itself? And we know that decreased caloric intake by 30% will affect longevity, but we know that’s also not possible to be able to do. And so we have fasting mechanisms of intermittent fasting or time-restricted eating, you know, that has come forward that is probably very similar to what our ancestors for hundreds of thousands of years experienced. They didn’t have food all the time. And so they moved in a way where there were circadian rhythms that developed. And those circadian rhythms, actually within the gut, they get mediated through or kind of, maybe I could say governed by or conducted by a part of the brain called the suprachiasmatic nucleus, SCN. And that acts to be able to set the diurnal rhythm, the circadian rhythm in the gut, which is then when food is introduced, and this is a great word that I’ve learned recently, but, you know, food acts as the zeitgeber. The zeitgeber, what that means is that’s a rhythmically occurring natural phenomenon that sets the regulation of the circadian rhythm. And so food is actually one of the things that sets forth the circadian rhythm that goes on. And in that process, you know, we see changes in the gut microbiome that occur. We can talk more about that both in terms of the structural makeup and the functions that are going on.

And so we do see changes, as I said earlier, in insulin sensitivity and insulin resistance. Of course, that’s going to have an effect on cardiometabolic syndrome. But all the aspects that we see insulin resistance having issues with, as we’ve talked about within our cardiometabolic module for a long period of time, be they related to weight and obesity, cardiovascular disease, heart disease, dementia, other forms of mood disorders, all of which, and cancers, all of which can be regulated through insulin resistance. And so that interface of what’s going on is a key piece that’s occurring.

Kalea Wattles:
|It’s really interesting how you’re starting to take circadian patterns beyond just light and darkness cues and introducing now food is also one piece of information that’s feeding into those patterns. And I think that’s fairly new to many people.

Patrick Hanaway:
It’s true, and what’s interesting is that, you know, the light and darkness cues that we think about within the circadian rhythms, you know, what we find is that in the dark period is actually when the functional energy metabolism pathways are maximized. It’s when it’s down, that’s when the body gets to sort through what’s going on metabolically. And so having a break point from any food during that process to be able to deal with apoptosis and mitochondrial death and regulation of the system makes perfect sense because it’s during the light, you know, that we have to deal with those issues of, you know, detoxification and motility and sensing of the environment. And so it just makes sense that, well, how about if we have a period where we’re not introducing food into the system during that time, you know, no late-night popcorn, you know, or munchies, or something like that that’s going to disrupt that process. Not unlike, you know, what we see with sleep patterns, you know, where the deep sleep that happens early in the sleep pattern is crucial, you know? And so we need, and that’s so important, you know, for the brain and for our mental function with sleep to have that downtime, so too, it’s necessary to have that with food. And, you know, it’s, again, it makes perfect sense when you look at how humans have evolved and what our food stores, what’s been available and how we’ve moved with that.

Kalea Wattles:
Right, here in the Pacific Northwest where I am in the wintertime, even in the fall, it might get dark at 4:30, 5:00 pm, and I’ve had patients ask me, should I try to stop eating right around the time that it gets dark? And I’m just so curious to hear what you think about that.

Patrick Hanaway:
That’s a really interesting question because I think that when we look at climes that are farther north, and as you may recall, you know, I lived on the Bering Sea, Alaska, for a couple years and, you know, we’d have two hours of daylight in the winter and two hours of darkness in the summer. And so I think that it’s not quite like that because I do see the data that we have on time-restricted eating, you know, that’s been looked at like through the year, seeing changes in immune function in one wonderful study that was done, you know, I think it should be applied throughout the year.

Now, one of the interesting questions that’s been raised, and I’ve seen different answers around it over time, is does it make a difference if you do a time-restricted eating where you only eat in, let’s say in the morning time from 8:00 AM until 4:00 pm or only in the evening time, in the pm time, say from noon to 8:00 pm or something like that? And the data actually hasn’t shown significant differences metabolically, but some of the more recent studies actually show that those people who do early time-restricted feeding, that is, you know, eating in the morning time, actually have greater changes in the composition of their gut microbiome than do people who use a later period of time-restricted eating. And so that to me says, there may be something to really be able to create a foundational difference in following the sun. And again, with the light and dark cycles that are involved with retinoic acid receptors and things like that as well as light receptors, it makes sense. But we haven’t seen data, and in fact, the papers that look at what they say ETRE, early time-restricted eating, haven’t actually related that to what the time of the year was or where the sun was. And now that’s an interesting question to ask. I think if the patient came to me and said that it’s, I would say, if you’re going to do time-restricted eating, it makes sense to follow the sun.

Kalea Wattles:
Yeah, that just makes sense. That makes sense to me too, especially all of our traditional Chinese medicine and Ayurvedic colleagues who have been telling us to follow those circadian patterns. That just makes a lot of intuitive sense. Now, Patrick, I feel like we have to address autophagy in a conversation about fasting. Maybe that term is new to some listeners. Will you just give us a brief overview of what the term autophagy means?

Patrick Hanaway:
Well, when we’re talking about autophagy, we’re really, the simple way I think about it is house cleaning. And that is that we have cells that are dying, but they’re hanging on and there needs to be a cleaning out of those cells that are not able to perform at their highest level of function anymore. And so we see what happens within time-restricted eating or a fasting-mimicking diet, there’s really great data, you know, from Valter Longo’s group at USC around a fasting-mimicking diet, you know, that is restricting in calories and restricting in particular amino acids that helps to promote autophagy, that helps to promote that cleaning to be able to occur. And so we see that with time-restricted eating. We see that actually more so with longer fasts, like with, what’s it called? A Buchinger fast, where it’s five days of fasting that’s occurring, or even, you know, with alternate-day fasting, you know, we can see higher amounts of pushing that cleansing process of autophagy to be able to occur.

I don’t want to spend a lot of time going into all the pathways around that, it’s very fascinating in the way that it works. You know, we also see the aspects of, I’ve already mentioned, you know, fasting before chemotherapy, you know, which gives a differential stress response and that actually helps those cells of ours that are susceptible to go through autophagy or to move into a quiescent state, and those cancer cells that are really in need of glucose, and support in order to be able to continue to grow, move into a state that makes it much more susceptible. And so I find these things to be, you know, fascinating aspects of the same conversation about looking at the role of food and fasting and autophagy.

Kalea Wattles:
Very approachable explanation to a somewhat complicated subject. I had a patient once who was doing some fasting and she was telling me she was combining this with some visualization exercises in which she pictured little scrubbers inside her cells doing their house cleaning. So maybe that’s becoming more common practice. We’re doing our fasting and our mindfulness exercises at the same time.

Patrick Hanaway:
Well, I think then, you know, in that setting, it’s an interesting idea, but the scrubbing should be done, you know, kind of when you’re 12 hours into it, you know? Not just right away after you finish dinner at 5:00 pm and are going to eat next again at 8:00 am the following morning or 9:00 am the following morning. You know, and it also begs a question of, what is it? I think that the data shows that, you know, 16 hours of fasting is significantly better than 12 hours, of have patients start at 12 hours and then move to 14, and then move to the 16. You know, and for some who are more interested in doing that, I’ll move them to a 5:2 fasting cycle with five days of eating and two days off eating. But that two days off of eating ends up really being more like a 32 to 36 hour fast, which actually optimizes the autophagy.

Kalea Wattles:
Right. Well, I would love to direct us toward all of these benefits in the gut because that’s what we’re really focused on today. And recently, there’s been studies that have explored this benefit of fasting on the gut microbiome specifically. I wanted to talk about these various benefits and starting with one that I think in functional medicine we love to talk about: inflammation, we’re inflammologists. Can we impact intestinal inflammation with therapeutic fasting?

Patrick Hanaway:
Well, there’ve been some studies looking at inflammatory bowel disease that do show that using a time-restricted eating pattern will decrease the overall production or decrease the degree of severity of inflammatory bowel disease. It doesn’t get rid of it, but we do see a decline in the inflammatory biomarkers. I’ve not seen one that specifically looks at my favorite inflammatory biomarker yet called calprotectin, but you know, we have seen other measures that have been done.

And then we also see studies that have looked, I mentioned one study that’s actually talked about in this insight from The Institute for Functional Medicine on fasting and immune health, you know, that talks about decreases in inflammatory cytokines throughout in patients who are using a time-restricted eating pattern of eight hours over a one-year duration of time. And so in comparison to their before levels of cytokines and to control, we find that there’s improvement. And we recognize that, as you say, as inflammologists, that much of what’s happening in that low-grade inflammation in the gut that drives insulin resistance that can drive systemic inflammation is actually, the driving of initial cytokine production occurs through the pathways in the gut, not only in diseases like inflammatory bowel disease but across many other states of low-grade inflammation.

And of course, we see this in our, you know, autoimmune patients. We see this in many patients where there’s a low-grade inflammation that’s happening. And in my sense over a long period of time is that’s being driven by alterations in the ecosystem of the gut microbiome. And we do see changes in the ecosystem of the gut microbiome happening from time-restricted eating. Those can be changes that will lead to increases in Ruminococcus and butyrate producers. They can be changes in mRNA transcription factors that relate to, you know, sirtuin 1 that’s associated with longevity or to, you know, foxhead proteins that are involved in inflammatory processes or also in several other transcription factors, one called CLOCK and one called BMAL1, you know, that have an effect on inflammation itself. So we are seeing that time-restricted eating will change transcription factors, it will change the overall composition and diversity of the gut microbiome, all of which are factors that help to decrease the overall inflammatory process. And then again, like I said, and we see that manifesting in a study on inflammatory bowel disease and we see that manifesting in a study looking overall at cytokine production.

Kalea Wattles:
Patrick, do you have a sense of the timeline here? Let’s say someone begins doing time-restricted eating. How long until we might see a shift in their gut microbiome?

Patrick Hanaway:
Well, it’s interesting, you know, when we… you know, and I have been doing, talking about the gut microbiome for a long time, right? So probably now almost 30 years. And what we thought early on was that there weren’t significant changes in the gut microbiome when we changed the dietary patterns. Now what we found is, well, yeah, that’s true, if you keep eating the same thing. Now when you start to change both the types of food and the frequency of food that you’re eating, we begin to see changes in the gut microbiome, really within 24 hours, but certainly within three days. Now those become more, let’s call more institutionalized within two to four weeks period of time where there’s the new mix that’s there. But you know, one other thing to note is that when you stop intermittent fasting, the changes go away. You know, so it’s there as a function of that process of that resetting of the circadian rhythm and the changes that then occur, you know, where there’s a modulation of the abundance of particular bacteria, then there’s a change in the diversity. The diversity actually happens first and then the abundance happens over time.

Kalea Wattles:
I imagine with this shifting in the microbial composition that we also might notice some changes to metabolites like short-chain fatty acids. Is that something you’re seeing in the literature?

Patrick Hanaway:
So again, the literature is very early at this point in time. And so there are some studies that have been done, some of which do show increases, as I said, in things like Ruminococcus, you know, that’s a butyrate producer that do show improvements or increases in overall butyrate production that’s going on. But there’s some mitigating factors. What was your diet before you started? What gender are you, what type of eating pattern are you actually doing? Is it alternate-day feeding? Is it a time-restricted eating of 12, 14, 16 hours? Is it a 5:2 process? Is it Buchinger or is it Ramadan? You know, there’s lots of different studies that have been done to look at these, and they get some different results. And one of the interesting things to me is they get different results, you know, based upon not only gender but also upon body types. So the effect on people who are overweight and obese is different than people who are not overweight in terms of the metabolite changes that we see going on. We do see some changes that relate to the short-chain fatty acids to butyrate itself. We see some other changes.

What I think is going on, Kalea, is in relationship to the postbiotic effect. It’s not just what’s happening with the microbiome. It’s happening with the metabolites that are produced by the microbiome that act as antioxidants. And so they’re stimulating, they’re stimulating antioxidant enzymes, you know, whether it’s glutathione S-transferase or superoxide dismutase. And we see some interesting data in C. elegans in a longevity model that actually shows that a postbiotic milieu or mixture can actually shift the overall oxidative stress that’s going on in the gut through shifting not only the products that are there but changing the activation of antioxidant enzyme systems that are present. And so I think that’s what we’re going to begin to see.

But now when we talk about this, recall that, you know, we may say, oh short-chain fatty acids, of which there are three primary ones, you know, butyrate, acetate, and propionate. You know, there are short-chain fatty acids that come from insufficient digestion of proteins that can cause that are more fermentation byproducts, you know, but so even naming just those six various short-chain amino acids are six of more than a thousand different metabolites that are produced by the gut microbiome. And so I think we need to actually be able to look at a systems approach to see what’s going on.

And that’s what, I like to look at changes in insulin resistance patterning, you know, so on a clinical basis when I’m working with patients, you know, I’m looking at what’s happening with your fasting insulin. I’m looking at what’s happening with your hemoglobin A1C, what’s happening using a continuous glucose monitor to be able to see changes of how your glucose metabolism is occurring as you’re working with tools like a fasting-mimicking diet and an intermittent fasting or time-restricted feeding pattern. Those are the things I think are the ways that I can see clinically what’s happening. You know, also look at something like an NMR insulin resistance score that helps me to see what’s actually happening with insulin resistance. So those are the tools that I’m using clinically to be able to help determine, are we moving in the right direction and is it effective?

One other side note that I’m curious about, and I haven’t seen enough data on yet, and maybe you know something about this is that, you know, we see that with other kinds of dietary patterns, like a ketogenic pattern. And I’ll often combine a ketogenic diet with intermittent fasting, you know, for my patients, but I don’t see as good of an effect in women as I do in men. I don’t know why that is. I’ve seen it described by others. I’ve talked with colleagues who’ve noted a similar thing. I don’t understand why that is. Do you have any thoughts on that?

Kalea Wattles:
No, but that’s fascinating. Do you mean you don’t see as… the metabolic changes, for example.

Patrick Hanaway:
Yeah, right. As significant of metabolic changes or even that kind of reset. I don’t see it to the same degree in women as I do in men.

Kalea Wattles:
Fascinating, if any researchers are out there listening, we’re going to need you to conduct this research so we can do a follow-up episode on that.

Patrick Hanaway:
Exactly.

Kalea Wattles:
But, Patrick, you’ve mentioned the systemic effects, so insulin resistance, you’ve talked about the exacerbation of autoimmune disease, you’ve talked about, and I think in my mind, I often relate these back to intestinal permeability. And so that leads us into this conversation about gut endotoxins. Do we see an effect on endotoxins with fasting? And then we can talk about how that influences intestinal permeability.

Patrick Hanaway:
We do, and now this is more bench-top research and animal mouse research where they’ve actually been looking at LPS, lipopolysaccharides that are generated from gram-negative bacteria, which we know will have an effect on increasing zonulin levels and increasing, you know, paracellular/intracellular permeability that’s going on. And that we do see that the production of LPS is decreased when there is time-restricted eating patterns and intermittent fasting that goes on. And so, again, I don’t know if that relates simply to the presence of gram-negative bacteria or if it’s related to some other kind of quorum-sensing phenomenon because we we’re not seeing, you know, huge shifts in the overall distributions. You know, some of the studies we’ll say at the phylum level, we have an increase in Bacteroidetes relative to Firmicutes, but we’re not seeing huge shifts in the overall distribution of what’s going on that would necessitate or that would correlate with a huge drop in lipopolysaccharides, or a huge drop in gram-negative bacteria. So we can describe that. We see that in the literature, yes, there is a decrease in LPS, and that means there’s going to be a decrease in intestinal permeability that occurs. And certainly, there’s a benefit that will occur across those disease states as specifically, like you said, the autoimmune conditions where we’re particularly worried about intestinal permeability. But whether that’s manifesting itself through changes in the composition of the microbiome, again, or due to the metabolic, the metabolomic production of what’s going on by the bacteria that are there as it moves into a different circadian pattern that’s going on. I don’t know if I’m making sense with this. I want to just try to state it simply, you know, it may have more to do with what the metabolic functioning is that’s going on that’s causing changes in the LPS than it is the actual composition of the gut microbiome.

And this leads me into an important point that I wanted to focus on, and that is that while, you know, we can look at research that says the new family called Christensenellaceae and the genus of Christensenella, and the species of Christensenella minuta, you know, have, have been associated with centenarians. And there’s one study that says, oh, we see an increase in Christensenella, but I think that we’re making mistakes when we think that there’s going to be one keystone species that we’re going to put in, and it’s going to change everything that’s going on in the gut. I don’t think that’s the way in which we want to approach this. We want to approach this through, you know, whole food dietary approaches with reasonable amounts of food at good timing, using time-restricted eating and intermittent fasting as a means of being able to reset the circadian rhythm of light and dark that our bodies have been using for the past, you know, 500,000 years. You know, so how do we do that rather than thinking we’re going to take an Akkermansia or a Christensenella and drop it in and it’s going to make a big difference? We do use probiotics therapeutically, you know, but I’m much more focused on the prebiotics and the foods of helping to bring balance back to the system and having those foods be at the right time.

Kalea Wattles:
Very well said, lifestyle factors, nutrition, that’s what we’re really focusing on, those foundational pillars of health. I’m going to make a connection here, another matrix connection, because we’ve been talking about the gut and we just talked about endotoxin, and in the research, we see this hypothesis about an endotoxin-neurodegeneration connection. So now we’re kind of linking like the assimilation node and the energy node together. I mean, are you seeing this in the literature? Is there a gut-brain axis response to fasting?

Patrick Hanaway:
Absolutely. And you know, we’ve been spending more time talking about this gut brain microbiome axis going on because we’re finding, again, I believe it’s because of the metabolites, you know, so we can look at the short-chain fatty acids, we can look at neurotransmitters, we can look at, you know, inflammatory cytokines and what their effect is on the brain, you know? So that information goes along with the afferent portion, the part of the vagus nerve that’s going back into the brain, you know, and looking at the anterior insular nucleus that acts as an aggregating factor that then brings all of those pieces together. And we also see kind of parallel to that what’s happening with echoes of what occurs in intestinal permeability is mirrored by what’s happening with permeability of the blood-brain barrier. And so we see two different phenomena that are going on. And so the LPS-mediated neurodegeneration that you talked about may be manifesting itself primarily through alterations in the blood-brain barrier that lead to glial cell activation and inflammatory processes that are occurring in subsequent neurodegeneration.

But we also find that there are, as I said, metabolic patterns that go on. So if we were to take something like Parkinson’s disease, it’s like, oh, well that happens in the setting of constipation. And we see shifts that are going on in the overall distribution of the gut metabolites that are occurring that are having an effect on the anterior insular nucleus that then has an effect on the basal ganglia and the ability of movement or the effect on movement disorders.

So there’s two different pieces that are going on that I see. I’m sure there are more, but, you know, we know and we can even find through, you know, to just take a chapter from, you know, what’s going on with COVID and long COVID, you know? We see alterations in tryptophan pathways and kynurenic acid pathways that are stimulating inflammatory changes and degenerative changes in the brain. And so we know that the metabolites have an effect on neurodegeneration, and we know that alterations in the blood-brain barrier that parallel what’s happening in the gut lining will have an effect on neurodegenerative processes. So we’re beginning to see both of those emerging in the literature. And I don’t separate them from each other because they’re all mediated through what’s happening with the gut microbiome.

Kalea Wattles:
Well, I’ll layer on another piece to this that you might say, this is all connected, it’s really all the same thing, and that’s the immune system. You’ve touched on how our gut health can impact our immune system, but let’s link that to fasting. Do we see impacts to our immune health when we start a therapeutic fasting plan?

Patrick Hanaway:
Yeah, I’ve mentioned that, you know, a couple times already in relationship to a really excellent study that was done that looked at people over a year period of time and could show changes in inflammatory cytokines, decreases in inflammatory cytokines. And part of the way in which I think that it’s also important in the process that we see is that this interrelationship between the gut microbiome and the immune system, and the mitochondria, and they’re actually working in concert with each other as part of the metabolic pathways that are occurring. And so we need to have a balance between all three of those that are going on. That, to me, forms the basis of health is working on the gut microbiome, supporting the immune system, using, you know, foods that are anti-inflammatory in nature. And that helps to balance the energy production pathways, you know, as well as the overall electron transport chain within the mitochondria to be able to optimize its efficiency for energy production that goes on. So I like to think of all three of those together. But, you know, to come back to your question specifically, there’s no doubt that time-restricted eating and intermittent fasting will have an effect on the immune system. And some of that may be mediated through that apoptosis that we spoke about earlier.

Kalea Wattles:
There are so many clinical applications for fasting, and you mentioned earlier that you might be willing to share a little bit about this connection between fasting and the gut microbiome changes and benefits to cancer treatment. So I thought we could spend a few minutes and I would love to hear your thoughts on this topic.

Patrick Hanaway:
Well, as you know, this is a personal topic for me. So if I have some emotions around it, that’s, it’s related to that. I began really looking at intermittent fasting and fasting-mimicking diet and relating that to other cultures and working with insulin resistance about nine years ago. And in that timeframe, I found it to be really potent. And I was aware that much of the work that Dr. Valter Longo at USC had done was actually started with trying to do a fasting before chemo as a way of being able to optimize a differential stress response. You know, that is, how do we make the cancer cells more susceptible and the healthy cells less susceptible to chemotherapy? So that was the research that he had done, and, you know, then moved that into more anti-aging apoptosis, insulin resistance, you know, kind of promoting fasting-mimicking diets in a broader context. But the genesis of it was from his work on cancer and fasting before chemo. And he showed initial data in 2009 through his lab of the benefits of it, and they carried that forward.

And so it was in the back of my head when I got cancer, you know, stage four cancer of the neck, in the aryepiglottic fold with lymph nodes on both sides. And I was doing a ketogenic diet at that point in time, which I later found helps to expand the therapeutic range of the radiation therapy. But what I also chose to do was to, as I went into the literature, I’m like, well, what does it exactly say? How long do you need to fast? You know, and they did fasting that looked at, you know, 24, 48, 72 hours. A lot of the data is on breast cancer, and it’s been published in, you know, Nature Communications and, you know, and they’ve been able to demonstrate an increased effectiveness and a decreased toxicity from the chemotherapy. So, you know, I said, okay, well, it looks like it’s about 48 hours is the timeframe. You don’t get a big bump out between 48 and 72 hours, but having weekly chemotherapy and choosing to not eat, or 400 calories or less for two days a week. And my oncologist wasn’t very happy about that idea. He is like, “I’m worried about you losing weight and you’re going to not eat for two days?” But what I found was I was able to move through the chemotherapy, you know, without, you know, because I was on a ketogenic diet without steroids, you know, without having the need for antiemetics like Zofran, and did really well. And they were like, “You’re acting differently than the other patients who get this kind of treatment.” And I didn’t lose significant weight during that period of time. My weight stayed pretty stable. I think I lost five pounds through the eight weeks of treatment.

So I’ve worked with cancer patients around this, and I find that when they work with fasting before chemo, it’s much easier to do when there’s a Q2 or Q3 week chemo process that’s going on. It’s harder to do when the chemotherapy is over a four-day duration period of time. But for those who are receiving chemotherapy, and again, to be clear, the data has been demonstrated of its efficacy, increased efficacy, and decreased toxicity in breast cancer. That’s where the studies have been done. And there are several studies, and they’re well done and well conducted. And so if you’re looking to do this, but I do, you know, I do talk with my patients who have cancer about the importance of doing this. Not all of them are able to do it. And the data in the studies that have been done is 400 calories per day, and I usually focus on a bone broth as a means of being able to do that, you know, in terms of that overall caloric intake during that period of time. But yeah, it is important and meaningful to me, and I think it made a big difference in my ability to move through, you know, chemotherapy is toxic by nature. It’s meant to be. How do we focus that toxicity differentially on the cancer cells and not on the beneficial cells of our body?

Kalea Wattles:
Well, Patrick, your experience and your story is so powerful and so compelling, and those of us who have heard you speak about your entire journey, I mean, it is really heartfelt, and I think we take away so many incredible insights from your experience. Do you think that the application of fasting and the ketogenic diet will become more standard in oncology moving forward? I mean, when are we going to see this take foot?

Patrick Hanaway:
There’s two different aspects of what you’re speaking to there. So the first is around intermittent fasting or fasting before chemo. And I think that we have a lot of great opportunity to be able to do that. I think that is something that interestingly, and if you read the literature, the oncologists will say, “Well, that’s ridiculous. No one will ever do that.” But do you ask the patients and they do it, you know? And so the number of dropouts in the studies that have been done are actually quite small, even though it was thought that no one would want to do it. So I think that we’re learning how to begin to be able to do that, and I don’t think we know which cancers it is best for and which ones it may not make a big difference for. I’m not talking about this in relationship to immunotherapy. I’m only talking about it in relationship to chemotherapy.

And then the other part of your question, which was about a ketogenic approach or, you know, a cellular metabolic approach as we see, you know, a number of our colleagues talk about, but that is for specific cancers that are more insulin sensitive. Not every cancer is going to be affected the same way as, you know, glioblastoma multiforme or the radiation-sensitive cancers like mine and ENT or rectal cancer. You know, we see breast cancer and colorectal cancer and pancreatic cancer all being in a range that they may be more susceptible for a ketogenic diet, you know, and certainly for a low-carb diet, but other cancers, it’s not been demonstrated for in the same way. So it’s not a global one size fits all. Prostate cancer is another one where, like early prostate cancer is much more insulin sensitive than are later prostate cancers, you know?

So we have to really personalize the treatments that we use. And, you know, that’s part of what we’re doing within our functional medicine approach is we’re personalizing and individualizing it so that we can give the person the best opportunity for their milieu to be optimized. And I think time-restricted eating is one great way to do that, is to reset the circadian rhythms that go on. And for me, it’s a lifestyle at this point in time, you know, so probably, you know, 320 or 330 days out of the year, that’s what I’m doing. You know, there’s times where I may, you know, go to the beach or have a brunch with my mother, you know, where I’m like, okay, you know, I’m going to do this. I’m not rigid about it, but, you know, that is mostly what I do is a form of time-restricted eating of 16 to 18 hours without food during the day.

Kalea Wattles:
Well, you have shared so many groups that could benefit from fasting. We’ve talked about autoimmune disease, inflammatory conditions, metabolic disorders, patients going through cancer treatment. I mean, is there a fasting regimen for everyone? Can any person find some type of fasting or time-restricted eating that will be appropriate for them?

Patrick Hanaway:
You know, I think the answer is yes, but you know, as we know, it’s working with individuals. So, you know, generally, I’ve started when I’m bringing this idea to someone, I’m bringing it to them at a 12-hour timeframe. Oftentimes, if there’s any significant metabolic issues that are going on, you know, I will start them off with using a fasting-mimicking diet for five days to kind of jumpstart and get them into a good cleansing, a good metabolic reset that goes on that then makes it easier for them to move into, you know, kind of starting at 12 hours per day. I’m like, look, eight of the hours you’re sleeping. And so do you need the popcorn before dinner or do you need to have, you know, the cream in your coffee in the morning, right? You can drink coffee black, you can drink tea, you can drink green tea, you can drink water, liquid, you’re just not eating anything that’s caloric in nature. There’s a whole question about, well, what about these, you know, ketogenic supports, you know, that just have fat? Do they really count? And I don’t think we know the answer to that. So I just err on the side of, well, I’m going to be clean about it. I’m not going to be adding stuff to, you know, my morning coffee and, you know, if I don’t like the taste of it, then I’ll find a tea that works for me. Usually it’s a green tea or matcha is my favorite. But I do think that there’s a way that everyone can benefit from this kind of thing because that’s how we as humans have been created over time.

Kalea Wattles:
Everyone who just learned they can have coffee and tea and still be fasting now, it seems so much more realistic. Well, Patrick, we have so appreciated hearing all of these clinical insights today. I think you’ve inspired us to keep our eye on the literature and see what emerges in terms of fasting and our gut microbial composition, our immune health, our brain health, so much to chew on. And I want to extend my gratitude for everything you’ve shared with us today.

Patrick Hanaway:
Thank you, Kalea, for asking me and for the work that you’re doing to bring these ideas out to our patients, our friends, our families, and to the, you know, the greater public at large. Appreciate your work.

Kalea Wattles:
To join the conversation on this topic, visit IFM’s pages on Facebook and Instagram. For more information about functional medicine, visit IFM.org.

Show Notes

The IFM-authored article that Dr. Hanaway discusses in this episode can be found here: Fasting and Immune Health.