Written by Christopher Kelly
Oct. 21, 2017
Tommy: Hello and welcome to The Nourish Balance Thrive podcast. My name is Tommy Wood. Today, I’m joined by Dr. Ben Bikman. Hi, Ben.
Ben: Good morning, Tommy. Thanks for having me.
Tommy: Thanks for joining us or for joining me. So for those of you who don’t know, Dr. Bikman is an associate professor of physiology and developmental biology at Brigham Young University. He has a PhD in bioenergetics and did his postdoctoral work in cardiovascular and metabolic diseases such as obesity.
Ben, I know you’ve been really popular on podcasting recently which has been really nice to see. So you probably have a really great short introduction about you and your work that you can maybe give us to sort of set the scene.
Ben: Well, I’m not sure what constitute as really popular. But let’s go with that. Yeah. I’m a prairie born Alberta, Canada sort of boy and just long had an interest in exercise. And when I started my schooling as a bachelor degree student, an undergrad, I was fascinated how the body was adapting to exercise and pursue that through master’s degree.
But then began to be more interested in obesity. How the body is adapting to obesity. And that’s what put me on the path I’ve never gotten off looking at insulin and its role in metabolic health. Other than that, I mean that’s my professional career but I always have to mention first and foremost I’m a husband, father, three mostly pleasant little children and a delightfully patient wife.
Tommy: Fantastic. That’s a perfect synopsis. Being able to balance both professional side and the family side I think is something that academics do tend to struggle with just because of the workload that comes from doing basic research and all the things that go along side that. I was actually just wondering. So you became an assistant professor in 2011. You’re an associate professor now. So that means you must have gotten tenure pretty recently.
Ben: That’s exactly right. Yes. Thanks for noticing it. This is the first year of my advancement. So over the summer I learned of my tenure and then rank advancement, which is quite wonderful frankly because as you know my research has taken me into this sort of academic black space where I’m looking at the benefits of high fat low-carb diets.
And that has earned me some naysayers here and elsewhere. I was a little anxious about that part of it where am I going to be blacklisted because I look at the research with regards to low-carb high fat. Its funny tenure once existed to help professor have security to then go into this unknown regions and more provocative research. But it’s funny cause I’ve already been doing it. So it’s just another day at the office for me.
Tommy: Can you tell us how the process works for those who don’t know in terms of academia and the process of tenureship?
Tommy: You sort of touch on what that means but sort of how that works.
Ben: Yeah. So most institutions, most universities, it’s fairly similar. You just have to show a record of productivity in a few different areas. So for us here at BYU it’s productivity and efficacy in research. So we’re meeting a sort of minimum area of how many publications we are getting published per year and the quality of those publications. How many graduate students we’ve mentored.
Here there’s a unique placement on number of undergraduates that we mentored and whether undergraduates are involved in research to prepare them for professional schooling, you know, medical school or what have you. And then service on committees across university and then just teaching. Adequate output with teaching.
This school is a little unique in that they actually really scrutinize student feedback. So at the end of every semester every class on campus the students are surveyed to basically say how was the class, how was the professor. That’s looked at for better and for worst. The unfortunate part is if you have student who didn’t do very well they’re going to hate the professor.
But on the good hand it does make you a better presenter and teacher. You do have to find ways to talk about boring things in a provocative light to keep them awake for an hour or two however the long the classes.
Tommy: We met at Low Carb Breckenridge this year which was when you exploded on to the low-carb scene. You can put it that way. One thing that I distinctly remember from your talk, which was definitely my favorite in the whole conference, was clearly teaching is something that you’re very good at because your presentation made perfect sense but it was also at the right level for the audience.
Your slides it wasn’t just death by bullet points. You had some nice animation. Just a sort of covering the important things rather than stuff a lot of stuff onto a slide or just like the people who just stick up the abstract from PubMed or something to illustrate their point. I think it’s clear that that’s definitely you’re really good at.
Ben: Thanks. It is a challenge and every time that I’m giving a talk or teaching a class I’m always asking myself what’s the story. I try to look at it as if I’m telling a story. I don’t want to read a story. I want to tell a story and so I can tell it best by you know it’s basically like a picture book. Not to insult any audience.
Tommy: That’s true and we just had a podcast now it’s about a conference that I hosted in Iceland. One of the speakers there was Satchin Panda. You might know his work on circadian biology. He was exactly the same. He’s this tenured professor. He’s been doing this for decades now and again his slides were simple. They told the story. There was almost no text. There was sort of picture. So you’re definitely on the right track.
Tommy: Going back to your transition onto the more sort of public social media side of health particularly the low-carb keto space. Was there anything that prompted you to do that? Because we have lots of doctors, we have some system scientist, we have lots PubMed warriors who are very good at reading abstracts and trying to create a story that they feel sort of fits what they want to talk about. But there’s very few real academic out on the scene talking about the work that they’re doing. What prompted you to come out and start doing that?
Ben: It’s interesting. I never realized how unique it would be. But I do have before explicitly answering the question. I have been incredibly impressed. I like how you describe the PubMed warriors, the people that do this out of just pure passion. I think of guys like [0:06:26][inaudible]. These are guys who are deeply familiar and in touch with the science. And by all accounts they’re just as much scientist as anyone.
In the end, a scientist is a seeker of truth and you don’t have to have a PhD to do that. I really have just gained a lot of respect for this community. I got into this public domain in order to get a book published. A couple of years ago I’ve written a manuscript that I intended to publish as a book all about insulin resistance. I was so naïve to the process I thought I would just submit my manuscript to a publisher and they would say yup, we want to do it. We’ll publish your book.
But little did I know. You have to find an agent and then the agent has to pitch your book to a publisher. And so I got an agent fairly quickly, a book agent. And the agent said, hey Ben, if you want to get this publish, you’ve got to get out there and get into this. You have to establish a platform for yourself. That was the beginning of it. Just about two years ago. And then someone locally in Utah had heard me give a talk about insulin resistance.
Every few months, I give just free talks to the public about insulin resistance and what to do about it; a local physician and I. And someone had heard me and then they wrote the organizers Jeff Gerber and Rod Tayler for Low Carb Breckenridge and said, hey there’s a guy here in Utah. You ought to have come present at your meeting. Then Rod Tayler and Jeff just wrote and said hey Ben, could you make this work? Colorado is just a few hours drive from Utah.
So that was the very beginning. It was such a neat experience. I’m used to presenting research at meetings where it’s just a handful of scientist. Maybe a hundred people in the room sort of thing. And most of them already know what you’re doing. It’s almost, I hate to use this word, incestuous. We keep the science in the family. The only person who knows my work is a handful of other scientist and I’m the only one who really knows their work. It would never really leave the room so to speak.
And so the idea of being in an audience and presenting to an audience not only in the room but through social media that had an interest in metabolic research just for the sake of knowing more and being better physically healthier, that was a very delightful transforming to go from the dry purely academic side to all of the rich colors that come with the more public domain. Just an informed audience that really wanted to hear what was being said.
Tommy: That’s such a cool way to describe it. I’ve done the dry academic conference, done the more public conference. That’s definitely the case. You actually get much better engagement from the audience, right.
Tommy: It’s not just your competitor trying to shoot down your work for whatever reason. It’s actually someone who is genuinely interested in what you’re doing.
Ben: It’s been delightful.
Tommy: So that on line I wanted to ask you whether – so obviously you found way to do this. How do we remove that invisible barrier between scientist and the public? Cause obviously most scientist do their job (a) for the love of knowledge but (b) because they also think it will help some group of people or the population at large in some way.
And previously the scientists were these untouchable founders of knowledge who was hidden in dark room and we have to trust everything they said because they were so smart but now it’s sort of going the other way and we tend to sort of think they don’t know what they’re doing. They published all this stuff that we don’t agree with.
So almost scientists have in certain respect become sort of well revered and people are less likely to trust them. How do we bring those groups back together to help scientist show the public, engage with them in terms of how their work is beneficial?
Ben: Right. I think these are great topics, great points of discussion. To me, as I’ve looked at this sort of global phenomenon in what’s going on with science and public perception of it, my hope is that it’s not so much as evident I should say in the life sciences. It seems like it’s more physical sciences and climate science and all that stuff, which I’m thrilled I don’t have anything to do with it.
But in life science, I’ve gotten that perception that it’s quite as much antagonistic. But nevertheless there is controversy. As anyone knows who dips into the realm of diet and metabolic science, it is remarkably controversial. That is somewhat understandable but someone has to, when they start to dive into this what I always tell my students when I show them data comparing low-carb to low fat as sort of therapeutic interventions for disease state for different pathologies in the body.
I tell them that whenever they hear something that they are skeptical of. Nowadays so much of this is available, so much data. So much information. They go into Google scholar or to PubMed and once they get a little savvy with searches how to do various searches to find the outcomes they want, they can really be incredibly well informed in very little time. But even still they might find some controversies and so I tell them they need to scrutinize number of publications and type.
For example, an intervention a clinical trial will always trump an epidemiological study. Always. Always. It’s interesting in the realm of low-carb research the epidemiological studies will typically have a negative light or negative finding and then the clinical interventions show no such thing. And so they need to appreciate that. So that’s of course, what anyone is capable of doing nowadays. Like I said before, becoming a scientist themselves and seeking truth rather than just being told it’s tremendously liberating.
It’s been gratifying to see people start that journey on their own to a large degree come to the same conclusion that I came through cause that’s what I had to do. A number of years ago I decided to stop letting the American Diabetes Association or American Heart Association tell me what the best diet for a person to avoid diabetes and heart disease. And I thought I’m a scientist literally. I’m going to find this out on my own and that’s when the whole house of cards started to fall apart.
Tommy: Yeah. Absolutely. I guess you came to this through obesity research and you mentioned the controversies. Obviously, the two broad areas that we have, the energy balance theory and we have guys like Kevin Hall doing these very complex metabolic ward studies, doing some complex mathematical calculations.
And then you have the hormone theory sort of the low-carb type people, you know, people talking about managing insulin and there’s definitely a possibility on both sides that people are sort of oversimplifying and maybe ignoring some of the better stuff that the other side is saying when in reality they’re both right in various aspects.
Do you have a good way to reconcile the two sides and give an explanation of what we think is really happening with obesity and weight gain and then also weight loss.
Ben: Right. That’s it. There are two theories of why we get fat. As you noted both of them have to be considered. We have to appreciate both and appreciate that the advocates of the caloric theory they’re just in a way adhering to that vey purist idea that we are perfect thermodynamic machines. That every calorie is going to be stored or used and there’s nothing in between.
And that was my talk at Low Carb Brackenridge of course. Just trying to impress upon the people the idea that even yes calories will be accounted for in one way or another and then we embrace the endocrine side of the coin. It ends up introducing novel ways in which calories are in fact actually regulated in the human body. All of which are relevant in obesity.
So in the end, I encourage people to always take note calorie number matters but so too is calorie type. I would in fact submit to calorie type a more important because of this so called metabolic advantage that if you’re scrutinizing the calorie type and being cautious with calories that are increasing insulin then you actually have a little more wiggle room so to speak where you don’t the sort of hard line above which everything is stored as body fat.
That line can sort of shift a little bit and we see that in studies. David Ludwig at Harvard found that while in ketosis humans have a higher metabolic rate. Kevin Hall’s research is interesting and certainly I think it has a place.
It’s also just really short term in way like you’d said accurately is trying to bring in a mathematical model which is admirable because if we could mathematically predict how a human is going to respond to a diet, well boy, we could really get a lot of research done and that would facilitate research in the future and make it more cost effective. But even that has limitations of course.
Be that as it may the endocrine theory is the one that I think people need to appreciate more simply because most people aren’t aware of it. They’re still counting calories and trying to exercise more, eat less and do that to get themselves to a better weight level. That’s a paradigm that overwhelming often will fail. The person just can’t sustain the sort of chronic degree of mild starvation.
On the US they have this TV show called the biggest loser where they have these people exercise themselves to this incredible weight loss. I sort of tongue and cheek joke how many times have we seen the reunion tour for these people.
Tommy: I mean that’s one of the things that’s slightly disregarded I guess by the more calorie focused group. Obviously a caloric deficit of one degree or another is important. But if you’re just eating less of the same food that got you in trouble in the first place like it’s really hard to maintain that, right.
Ben: Yes, it is.
Tommy: You got to make it easier somehow.
Ben: That’s right. That’s when scrutinizing calorie type that makes it easier. All of a sudden you don’t have to be starving yourself.
Tommy: You mentioned David Ludwig’s work and one of the notable things in the study that I think you’re talking to in terms of energy expenditure on a low carbohydrate diet was that those guys were eating a lot more protein sort of maybe double the amount of protein that the other group was eating. Do you some thoughts on the importance of protein?
And there’s definitely a school of thought currently that protein is going to give us cancer cause of too much mtor. People are avoiding protein cause it will kick them out of ketosis. Do you have some kind of thoughts on the importance of protein particularly in term of weight loss?
Ben: I do. Yes. The whole phenomenon with regards to cancer and protein I just don’t buy it. I really don’t. It’s just so hard. This is a case of me earlier claiming I’m only going to let the data dictate what I think. But there is also just a subjective personal opinion component to it as well when you have to interpret the research and the sum of it on one hand or the other. And to me the data just don’t add up.
But nevertheless with regards to protein and obesity, there’s no question protein is a relevant macronutrient. One of the concerns in this general space of low carb, high fat are the maybe I called them like the keto purist in a way, the people that anything that kicks you out of ketosis is to be strictly avoided. And that has led some to developing a fear of protein because protein, different protein have a different effect, but protein is insulinogenic. And if insulin comes up that puts the [0:18:04][inaudible] and ketogenesis in the liver quite quickly and quite readily.
What people are ignoring, in fact, I’ve just started a blog post about this. Hopefully, I get it done in the next week. But what people ignore is what protein does to insulin’s opposite which is glucagon and protein increases glucagon about as much as it increases insulin. The reason that’s relevant is not only does that mitigate insulin’s affected body fat. You know insulin lipogenic and ketones are lipolytic.
And so it’s sort of cancelling each other out at the level of the adipose site. But the same thing is happening to a degree at the liver with regards to ketones. And so insulin is inhibiting ketogenesis but glucagon is activating ketogenesis. And so the end sum isn’t as substantially negative on ketogenesis and ketosis as many people would like to think regardless of what it may be doing to insulin.
In fact, in the end that’s quite a magical mix, these macronutrients that’s increasing insulin and glucagon. Like I said earlier that’s cancelling each other out at the level of the adipose site. But muscles cells end up with a net positive effect. Because muscle cells have insulin receptors so it’s getting that anabolic signal of the insulin. Muscles cells do not have glucagon receptors. And so there’s no sensitivity to glucagon’s normally catabolic signal. And so the muscles just grows. The fat cells don’t.
I mean I’m oversimplifying it but it does represent an interesting paradox of promoting a generally more lean phenotype because of what protein is doing to insulin and glucagon. My thought is protein is absolutely necessary. The people that are afraid of it, I don’t think that fear is warranted. My philosophy is you just eat protein from real food and nature usually has protein coming with fat so that’s a pretty nice combination. So don’t eat a protein powder necessarily but just eat meat or something with protein. And if it has fat in it well then wonderful.
Tommy: Anytime you can get this stuff from real food and like I would say in general protein and fat tend to come together in nature. Just the same as may be isolating out the protein could be problematic in its own way. Isolating out the fat and having just that again could cause some issues. So just eat them together as they come. They’re pretty packaged.
Ben: I think so. Yup.
Tommy: Let’s talk about some of your own research. So what you’ve been talking about a lot recently and what you mentioned at Low Carb Breckenridge was you work on insulin and ketones and how those affects the physiology of fat cells and the differences between why adipose tissue and brown adipose tissue. So maybe you can tell us what you’ve been working on there and what you found out.
Ben: Right. That has been a fun new area of research. That’s part of the fun of being a scientist. If you get an itch, you can scratch it. This was a question that I had come to with some students wondering about what insulin and ketones were doing at the level of the fat tissue. There were certainly some research out there already on this. So I wasn’t the pioneer necessarily. I wasn’t the pioneer. We were just sort of flushing it out a little more.
We just submitted the insulin part of this manuscript and what we found in the insulin case in rodents people need to be cautious in studies that looked at rodents as fed diets and try to make extrapolations to human’s responses to diet. Those are always problematic. But when it comes to hormones and physiology within a mammal, that’s a much more robust and relevant model to human physiology. So I say that to defend what I’m about to say now.
We found that when induced hyperinsulinemia in the mice but kept their diet normal, we found that there was this very selective transition in how the mitochondria were working in various depots or various sites of fat tissue. Just like humans, mice has mostly white fat and it is in fact literally white. When you pulled out a little bit, you know, when we do a fat biopsy of someone’s fat from their subcutaneous fat or their fat right beneath their skin it’s quite yellowy milky white.
In contrast, we have just like a rodent a few spots on our body where it’s a brown fat. It’s brown. It is in fact much more brown because it is enriched with mitochondria. So it looks a little bit more like red meat because red meat has a lot more mitochondria of course. So it gives it a distinct color. More than just mitochondria number, these mitochondria, all mitochondria to a degree they’re in a spectrum on being very tightly coupled.
In other words the mitochondria would only be breaking down nutrients or using the products of breaking down glucose or breaking down fat. It would only break that down as much as it needed to produce ATP to get cellular work done. That’s a couple process. However, some mitochondria are uncoupled. They’re breaking down nutrients not because we need molecule to do work but just to create heat.
And so that’s very wasteful but it’s also essential to survival in a cold climate and it’s also very helpful in an environment such as ours which is an environment usually of excess. We found that insulin was stopping mitochondrial uncoupling. It made the mitochondria in brown fat act more like the mitochondria in white fat.
In other words, it was telling the brown fats which would normally want to be chewing through energy just to create heat and increase metabolic rate. It was making them start to slow down. Literally slow the mitochondria down and start storing energy rather than using energy. Ketones are doing the opposite.
Ketones are not only allowing the brown fat to continue to act in this wasteful sort of high metabolic rate way but it helps the white fat, a particular type of white fat, the subcutaneous fat, the fat right beneath the skin, it also began to act a little more like brown fat. It had more mitochondrial uncoupling than was likely that was causing the increase metabolic rate you see in our rodents with ketones.
Tommy: Was there a difference in terms of the absolute mass of fat or is it just the physiology of the fat that’s changing?
Ben: Excellent question. Yeah. The fat itself, the white fat went up in mass relative to other fat pads but the brown fats did not. It stayed the same.
Tommy: Yeah. The reason I asked that question is I was talking about your work with our scientific director, Megan, who did her masters work on low-carb and keto diets in mice. Her paper just came out in Cell Metabolism show the increase longevity in mice using – you probably read it.
Ben: Yeah. I saw it. Yup. Good for her. That’s a great study. Good for her.
Tommy: Yeah. Absolutely and brilliant work and a great journal as well. She mentioned that her in ketone mice, they actually had less brown adipose tissue or at least that was within they looked at it that’s what they saw. So are we looking just at the physiology? Is this something that’s only relevant if you have lots of white adipose tissue and maybe doesn’t change your absolute levels of brown adipose tissue? Is there sort of way to tie that all together?
Ben: That’s a great question. I’m interested to hear her report on that. We didn’t see a change in brown fat, the interscapular brown fat and that’s where the mice put their brown fat, right between their shoulder blades. We didn’t see a difference in mass there with ketone or insulin. We just saw differences in the white fat in either case. In retrospect, I’m not surprised to hear that in so far as low-carb high fat of course diminishes insulin and insulin is what’s maintaining body fat.
Jim Johnson who just moved to [0:25:36][inaudible] he has done a lot research looking at insulin and insulin receptor expression. If I remember correctly they found an effect that when insulin receptors were knocked out, the mitochondria were more uncoupled in brown fats. So more uncoupling which supports what we found but there was less brown fat by mass which supports what you just said how Megan found.
Tommy: That makes perfect sense to me. You have less brown fat but you have great mitochondrial uncoupling and then those balance out. We maybe even end up with more, overall you have more active brown fat or more ability to uncouple even though there’s less fat there.
Ben: Yeah. That could be it. Mind you that is a relevant feature of brown it. It’s never humming along 100% all the time. Brown fat will be activated or not. We can turn it on and have it really start chewing through glucose with mitochondrial uncoupling or it sort of slows that. So that might be just what we’ve seen here is that the lack of insulin results in the relative reduction in brown fat. Yet that same lack of insulin and the relative increase in ketones stimulates the brown fat to be more active than otherwise.
Tommy: It makes perfect sense. Thanks.
Ben: Well we’ve convinced ourselves at least.
Tommy: Yeah. Absolutely. I mean I guess there must also be a point where there’s a negative feedback mechanism right because you can’t just keep chewing through energy. If you’re starting to lose mass and you create a deficit, you know at some point your body is going to say okay, we need to start conserving more than just uncoupling.
Ben: I’m not sure where that point is. Because you think of untreated type 1 diabetic, someone who is skipping their insulin injections or they’re undiagnosed, they waste away. I mean their body fat just goes away completely. There is a delightful old report. Once upon a time old research it wasn’t published as individual little journal articles like we have now. It was sort of big stacks. Almost like a book.
And Elliott Joslin like the Joslin Diabetes Center in Boston. Elliott Joslin and Francis Benedict were these two early scientists that looked at metabolic rates and metabolic responses in diabetes. They found that these people, untreated type 1 diabetics, their metabolic rate was higher than when they were treated with insulin. And yet it continued to this very pathological state of just physically wasting away.
So you think maybe that’s just too extreme of an example because there’s an absolute deficiency of insulin and so maybe that’s just too artificial. But I don’t know where the normal check point, where the physiological check point would be to say this has got to stop. I suspect it would just come from a person continue to eat food and always producing some degree of insulin, always keep ketones never going above 4 or 5 mmol.
And so that’s just its natural inherent check and balance where there’s always a fasting basal state of insulin. There’s always in a normal healthy person with healthy pancreatic beta cells, there always an inhibition on ketogenesis. But they can never get too extreme like it is in an untreated type 1 diabetic, you know, when ketones get up to 15 or 20.
Tommy: Yeah. That’s a great point. So we know that ketones can be insulinogenic in the right scenario. If your ketones keep going up you’ll stimulate some insulin production in the pancreas. There is some data that suggest that ketones can inhibit hormone sensitive lipase so you could almost feedback and stop lipolysis. But then in your example of the type 1 diabetic, that’s clearly not happening so maybe that’s not enough of a stimulus to get complete closure that feedback loop.
Ben: Yeah. That untreated type 1 diabetes is just too extreme of an example. But your point about ketones being insulinogenic, love it. So this old research, I say old, it’s my time frankly. In the mid 70s there was a couple really interesting studies where they perfuse rat pancreas and they would just see what they were controlling with the pancreas and then looking at what was coming out of it.
They found that ketones alone were having little to no effect. Just like palmitate. Just like a pure fatty acid, little to no effect on insulin. However, when you mix that with glucose which of course is always present but there was a threshold. It was something like if glucose was 5 mmol and above then it exaggerated the insulin response of that glucose. Below which it wouldn’t have any effect on it.
That becomes relevant to someone who is taking exogenous ketones for the purpose of weight loss and improved metabolic healthy. If esterthey’re taking pretty much anything with the ketones they’re potentially exaggerating the insulin response of whatever they’re eating.
So it ends up being a pretty cautious or caution is warranted when we start to orally consume ketone which may have its case. I’m not trying to poo poo exogenous ketones in general. I think they really may have a therapeutic role. But when someone is just doing it for metabolic benefit, I think it’s not quite as magical as many probably believe.
Tommy: Yeah. You’ve stumbled on my favorite topic of exogenous ketones which is exactly that.
Tommy: Absolutely. I think there’s going to be a place where they have essential therapeutic benefit. They can certainly have a performance benefit. Probably the ester rather than the salt at least based on the research that’s out so far. But there’s on research study, again this is in athletes, where they gave them a ketone ester and then submitted them to hyperglycemic clamp. So they infused them with glucose to look at their insulin responses. If it had ketone as the first they basically had doubled the insulin release.
Tommy: If you have blood glucose plus ketones for your insulin I mean that’s really bad.
Tommy: And where that becomes important I think and absolutely to the point that you’re making is that some of these supplements are being promoted for people with metabolic disease. So if you are somebody with Alzheimer’s disease or type 2 diabetes or obesity and you think that just taking the ketone is going to be enough if you’re not changing the diet and removing or reducing the carbohydrates or refine carbohydrate aspect of your diet, you could actually make things worse, right.
Ben: I’m waiting for that study to come out. But it something that someone has to consider, the person who is doing this. They have to evaluate this. Mind you, there’s something profoundly unnatural about that. I mean in the whole course of human history, we don’t eat these ketone bodies or these ketones, beta hydroxybutyrate or acetoacetate. We don’t eat them. We’re not meant to eat these. These are molecules that the liver makes.
And so we’ve really created an artificial situation. I’m not saying that it’s going to cost the end of the world. But there is something fake about it. There’s something artificial. Then someone maybe could make that case of any number of interventions these days. But in this case, there’s just something obviously wrong about it in the sense that we’ve never eaten these things before. Now to try to start throwing them into our diet as some magic pill, boy as we’ve already been discussing, it likely will have consequences to the uninformed.
Tommy: Yeah. There’s also a due diligence thing, right.
Ben: Yeah. They’ve been tested in athletes and the athletes have good metabolic health. They have a good amount of muscle tissue. If you then extrapolate from there or extrapolate from the rodent studies and say this will be great for people with metabolic disease then you have to do that study before you can start telling people that.
Tommy: I agree. Completely. I know you mentioned that you’re planning to do some work with humans. You’re going to do some clinical type studies. Can you tell us anything about what you have planned or what you would like to do?
Ben: Yes. I’ve just started to venture into the realm of humans. In fact, you’ve kind of touch on this or my thinking right at the very beginning of our discussion. You talk about the relevance of interpreting studies correctly. I’ve been doing all of my findings have been in cells and rodents. That’s relevant but it should only ever be used as a justification for them progressing to human research.
That’s where I find myself now is I’m increasingly frustrated with the limitations inherent to rodent models. So I’ve just submitted protocol for humans and we’ve been able to collaborate with the local physician, a local clinic a bariatric surgery clinic to get fat samples from humans. What we’re looking at now is determining this immediate study is to complement the large amount of cell in rodent data that we already have specifically with ketones and brown fat.
We want to look at the role of ketones in fat tissue mitochondrial regulation in humans and confirm this result. And so that’s the initial study. That’s just underway now and we’ll the data pretty quickly because it’s a good cohort of patients we have access. But it’s just whether or not the human is in ketosis or not, whether they’re in ketosis or not and then looking at the degree of mitochondria uncoupling in their fat tissue. So that’s the immediate study.
And then future studies are in fact I want to do that exogenous ketone study and look at the outcome of someone just adding ketones to their diet. Just saying here once a day just drink this solution of ketone or however much. You know we’ll control for it. There’s a control group. And then just see what is actually happening metabolically. Is there a deleterious effect or is there none. No effect or is there benefit.
Tommy: You’ll be incredibly popular once you do that study.
Ben: Yeah. I’m sure someone will beat me to it but it’s on the horizon.
Tommy: Obviously, you talk about translating stuff from rodents to humans. And based on all of the interactions that you have, social media, all these conferences you’ve done. Do you have some good principles that people can use to sort of, you know, this podcast probably they have a low-carb diets, ketonic diets. Some of them have tried them. But if they’re trying to help others make simple changes, do you have any recommendations, things that people can do?
Ben: Yeah. Now are you asking specifically what could someone actually implement into their lifestyle or how could they get informed.
Tommy: Both would be fantastic. I started off in terms of just what people can actually do by become better inform. And sometimes that’s the only. If you’re trying to help somebody else, they need to become informed themselves first because they become interested. You can’t just force tell them you have to eat this or do this. They need to move along the stages of change themselves. So both parts of that is very important.
Ben: Yeah. Right. So with regards to becoming informed, it really just a second kind of warning. The second time I make this warning. A person needs to scrutinize what is the model in the research. And if it’s any study that’s using a rodent, you cannot make comparison to what the rodent is eating. You can give a rodent 90% fat diet. I don’t know of a single human who eat that’s. That will be just pure butter. I mean not even butter. That’s too much protein. Pure ghee and coconut oil. It’s so artificial.
But you can give a rodent 95% diet and they barely get into ketosis. I mean their ketones are like 15% higher than the rodent eating the standard chow. I mean these are just such a phenomenally different response to macronutrients. So the person always has to be cautious in that regard. And then even be cautious in human studies and we can’t look at studies that just say high fat diet because a high fat diet is not the same as low carbohydrate diet. And so a person needs to make sure they’re evaluating or appreciating those differences.
So the actual actionable items I am not the kind of person despite my genuine appreciation for ketones, I am not an advocate for someone being in ketosis all the time or even ever depending on the person. I’m not a ketone poster child here. But I am an advocate of just controlling insulin and one of the consequences of controlling insulin will be increased ketogensis and the potential for being ketosis. But too many times we too fixated on whether I’m in ketosis or not. Again, that can be beneficial. It may have its place depending on the person. But a person just needs to scrutinize the composition of their meals.
For me as a busy father and my family is my whole life and what I do here at work is just a hobby pretty much, for me it’s how can I make these changes and have minimal impact on the wellbeing and happy home life of my family. For me, my kids are certainly more low-carb than most kids are and that just means that you eat fewer crackers and no cheese and pepperoni and whole fat yogurt with berries. That’s just more of staple in my home. We’ve just been able to set that culture earlier in their childhood so you don’t have to make that fight when they get older.
But for the person whose family isn’t coming on board which is how I started this myself I change my own breakfast and lunch and then dinner is whatever the family is having. If my daughter, my 10-year-old wanted to make dinner for the family a few weeks ago. And she made grilled cheese sandwiches. I’m not going to push away the plate at dinner and apologize to my sweet little 10-year-old and say daddy is just going to eat the cheese from these grill cheese sandwich. I’m not going to do that.
I’m going to be really practical and I will knowingly eat a meal that’s going increase my insulin and I’m going to love every bite and enjoy laughing and being with my family. And then I’m just going to get back on the wagon. And so breakfast and lunch are easy to change because those are meals that don’t impact other people as much. It doesn’t create a particularly awkward social environment.
And so for breakfast it ends up being something like for me a staple is bacon and eggs frankly. Or I don’t drink coffee. I know it’s shocking. I’ll drink herbal tea and I’ll put a little bit of coconut oil or a little bit of butter or something in my herbal tea because I want the energy because I know I’m going to be working out that day. And I don’t fear the calories.
Anyway breakfast will always be a low-carb breakfast and lunch will usually be the sort of eclectic mix of low-carb but real foods. It’s not foods that come out of a bag or a box. So it might be a couple of hardboiled eggs, a half of avocado and a handful olive and stick of full fat cheese or something like that.
I would encourage someone actionable items don’t worry about ketosis. Just look at your meal and ask yourself is this a meal. Am I getting fat and protein in this meal? Usually that’s the way real food come unless it’s fruit or vegetable which is great. That’s fine as well for the most part depending on what the person’s goals are.
But the actionable items I would say if there’s one takeaway is change breakfast tomorrow. Stop eating toast, bagels and cereal and go back to the way we used to eat 50 years ago which would be more meat and egg based or just more fat and protein based whatever that might mean for any individual.
Tommy: Yeah. Absolutely. I’m suddenly reminded of this brilliant quote. I assume you saw the pure study that came out recently.
Tommy: So the one epidemiological study that shows that basically having a large portion of carbohydrate in the diet or restricting fat maybe detrimental to health, and that saturated fat was associated with improvement in some cardiovascular diseases. They advocated just a more balanced diet as you might call it. Just not try to overly restrict fat.
Salim Youssef who run the study he told his mom about the results and she said why did you bother doing the study. That’s just common sense. That’s what our grandmother had been telling us to do for centuries. I just thought it was so brilliant that she sort of cut through everything and just come up with that immediately and she’s probably not even interested in the whole field at all itself because she does know what to do.
Ben: Yeah. It’s something that I think people need to be more appreciative. We raved about the Mediterranean diet and yet 50 years ago that’s how we eat in the America and the UK and Canada. We ate a higher fat diet. The macros it was about 45% fat, about 20% protein and 30ish% carbs. And even if someone just shift to those macros, they’re going to be so much better off than the average American is which is around 30% fat. Almost 10% or 15% less of the calorie are coming from fat now and of course that’s all been shifted to carbohydrates.
We have never eaten that way. So yeah like his mom claimed and any of our grandparents would also likely remember we used to eat more fat. Really it was just because we used to eat real food. It was this shift from the 1930s-50s where we started eating out of bags and boxes and that just became exaggerated with the dietary guidelines in the 70s. It’s sort of eliciting this fear of fat and this really overblown shift to carbohydrates which inadvertently resulted in less protein as well. We just need to go back to eating the way we used to.
Tommy: I think that’s probably the best possible summary that you can put together of everything that we’ve talked about. Is there anything else that you’re interested in that you think people need to know that you’d like to mention? Any soapboxes you want to jump on?
Ben: No and we’ve covered them all. It’s just people need to eat real food and be smart about what they’re eating and be very deliberate about it too. If obesity control is the goal, every time the person needs to really say what’s my goal? But I appreciate. Our dictions are not that easy to control and carbs whether people want to believe it or not, they are addictive. No one is sitting craving fat and protein. Craving a hotdog or a slab of meat. That’s very rare. The average person is craving a cookie or a bagel or something.
Tommy: Yeah. Absolutely. I mean this had been fabulous. Truly fabulous. I want people to follow you on social. Actually go to a lab and read your research. How can they find all those things?
Ben: Yeah. Thanks Tommy. The easiest way is Instagram and Facebook. I have a Facebook page and that’s just my name Benjamin Bikman and Bikman is no C in Bikman. And then my Instagram is benbikmanphd and the same on Instagram and Twitter I should say. Twitter also benbikmanphd.
I simply use that as a platform not to push any of my own agendas but just to share the latest research. Usually once a day or once every two days I will just share some of the most recently published metabolic research. Just so that people who don’t have time to be scouring the literature can very at a glance get the latest report on health and nutrition.
Tommy: You know I definitely take advantage of you in that arena if I can say it that way. Because how I find social media best works for me is I basically just stalk people that I trust and then I look at the research that they post because I know that’s something interesting worth listening to. So I definitely do that. I’m hiding in the shadows even if I’m not saying very much on Twitter. So thank you very much for doing that.
Ben: Great. I’m glad you’re using it. You’re welcome.
Tommy: Again thanks so much for joining us. It’s been a huge huge honor.
Ben: Thank you, again, Tommy for the invitation. It’s always such a treat to talk all things metabolic.
Tommy: Cool. Thanks so much.
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