Insulin Resistance in Alzheimer's, Infertility, Migraines and More – with Dr. Ben Bikman

Bret: 
Welcome to the Metabolic Mind Podcast. I’m your host, Dr. Bret Scher. Metabolic Mind is a nonprofit initiative of Baszucki Group where we’re providing information about the intersection of metabolic health and mental health and metabolic therapies, such as nutritional ketosis as therapies for mental illness.

Thank you for joining us. Although our podcast is for informational purposes only and we aren’t giving medical advice, we hope you will learn from our content and it will help facilitate discussions with your healthcare providers to see if you could benefit from exploring the connection between metabolic and mental health.

A BYU professor specializing in insulin resistance suggests that metabolic dysfunction is the common thread that unites cancer, heart disease, type 2 diabetes, neurodegenerative diseases, such as dementiand mental illness. Maybe that’s a good thing? Today, I am joined by Professor Ben Bikman, who’s a professor of cell biology and physiology at BYU and the author of Why We Get Sick. And you can find him at InsulinIQ.com.

Professor Bikman has dedicated his entire academic life to understanding insulin resistance, and he’s suggesting that insulin resistance and metabolic dysfunction is the common thread of the most common chronic disorders that we face as a society. And maybe that’s a good thing because it empowers us to make changes to improve them.

So, let’s hear what Dr. Bikman has to say. But first, please remember this channel is for informational purposes only. We’re not providing individual or group medical or healthcare advice or establishing a provider patient relationship. Many of the things we talk about, whether it’s changing your diet or changing medications or whatever the case may be to treat certain conditions, can’t be dangerous if done without proper supervision. So, please always consult with your healthcare team.

So, with that, let’s get on with this interview with Professor Ben Bikman.

All right, Dr. Ben Bikman. Welcome to Metabolic Mind. 

Ben: 
Hey, Bret. Thanks so much for the invitation. Glad to be with you. 

Bret: 
Yeah, it’s such a pleasure to connect with you again. I’ve I’ve interviewed you so many times before, I think, for for each of the podcasts. And now it’s a pleasure to have you on Metabolic Mind to talk about this connection between metabolic health and mental health. But first, let’s lay the groundwork, you as a professor at BYU, the author of Why We Get Sick.

You’ve devoted your intellectual and academic life to understanding insulin resistance and how it relates to so many chronic diseases. And on the surface, someone could say, wait a second. How could cancer and bipolar disorder and heart disease and type 2 diabetes, how can one thing weave those together in insulin resistance when they’re so different? So, it’s a such a big question, but how would you summarize that underlying connection? 

Ben: 
Right, it is a testament to the fact that all of these seemingly distinct disorders do share a common metabolic core. If you will, it’s this sort of idea of a common soil hypothesis. That we look at all of these noxious weeds springing from the ground as distinct disorders, as you mentioned them, and in fact, it’s not that each, rather than continuing to go in and try to trim down or kill each individual weed, we acknowledge that perhaps it’s the ground itself that has the problem, that is continuing to bring forth these noxious weeds that we’re so bothered by or these chronic illnesses that we’re so scared with and we devote so much time and money to trying to correct.

But it is very important to note that certain cancers or type 2 diabetes or fatty liver disease or certain forms of infertility and heart disease, et cetera, they all absolutely have a distinct stimulus or stimuli that they wouldn’t share with the others. And it’s, and it’s not those that I’ve wanted to devote my career to. It’s rather maximizing the returns on effort in that if we can identify that they do, despite whatever they don’t have in common, they have one thing in common then let’s really focus our efforts on that one thing in common.

So, Imagine the person who’s opening their medicine cabinet every morning and taking out their diabetes medications, and their blood pressure medications, maybe their migraine medications, thinking that because there’s a different pill bottle for each different disease that they are totally unrelated. But in reality, with a little bit of education and then some implementation of some of these ideas that we’ll discuss, and and you have already discussed amply before I know, then they realize that by simple, if not always easy, dietary changes they can improve their metabolic health, specifically insulin sensitivity.

And you know improving their insulin resistance, which to me is the penultimate definition of metabolic health, and happy to explore that. But then they begin reducing the risk and reversing these other chronic diseases. Then, all of a sudden, the diabetes medication, the the migraine medication, and the blood pressure medication stay in the cabinet in the medicine cabinet because they simply realize that they don’t need it like they used to. 

Bret: 
I like how you said that that there’s a lot that these conditions don’t have in common, and you can focus on those to treat each individual one or focus on what they do have in common, and get the added benefits of maybe reducing the risk of all these different conditions. So, you talked about the definition of metabolic health, metabolic dysfunction and that’s something a term that’s thrown around a lot.

And you said it comes down to insulin resistance. So, if you were to sum it up in 60 seconds what is Insulin resistance and metabolic dysfunction that we can put our hands around? 

Ben: 
Yeah, any version of the term metabolic dysfunction, you know, like poor metabolic health, metabolic dysfunction, metabolic syndrome, metabolic inflexibility, each of those have a unique aspect to it or a precise definition that would be used. But every one of them is simply another way of saying the body has insulin resistance. And for the sake of time, I won’t elaborate on that.

But defining insulin resistance is very important because it’s commonly misunderstood, not even understood at all, or at worst misunderstood, including within a community that you and I are very synced with, which is the low-carb community. So, insulin resistance is really a pathology of two problems. On one hand, or the first part of it is what the name suggests, which is that the hormone insulin isn’t working very well at some cells of the body.

Emphasized, italicized at some cells of the body because some cells of the body are responding as well to insulin as they ever did. They’re not compromised at all. If insulin comes to the door of some cells and knocks on the door, some cells aren’t responding. They’re not opening the door, they’re not opening it very well. Insulin knocks on the door of another cell type, and that cell’s responding perfectly well. Opens the door right up, and does exactly what insulin wants it to do.

Now, that’s the first part of the insulin resistance problem. But within the body, if we go from the level of the cell and expand to the level of the entire organism, now we have another problem that is inseparable, namely hyperinsulinemia or the chronically-elevated insulin. This is an absolute essential component. Anyone who’s attempting to define insulin resistance and is invoking that term in a scenario where fasting insulin levels are low, they’re not talking about insulin resistance.

It is incompatible for all but one situation, which is starvation. But that’s so rare in any other instance, whether it’s a low-carb ketogenic diet, whether it’s someone who’s approaching type 2 diabetes or full-blown type 2. If they’re using the term insulin resistance, then insulin must be high. If they’re trying to say that a situation is insulin resistance but insulin is low, it is not insulin resistance by any definition.

But that first part, in fact, when we combine those two ideas that insulin isn’t working well everywhere and that insulin levels are higher, it’s those two converging phenomena that explain how insulin resistance contributes to virtually every chronic disease or these plagues of prosperity. It’s that that explains the heart disease risks. Some combination of those variables.

Maybe it’s one, maybe it’s the other, maybe it’s both? It’s that that’s explaining the increased risk of certain cancers, like breast and prostate cancers. It’s that that it’s explaining most of the metabolic aspects of neurological disorders. 

Bret: 
Yeah, so you mentioned the different cell reactions, that some cells are going to react normally to insulin and some are not. So, is it as simple as fat cells are still going to respond and muscle cells are not or what are some examples of that with pathologic insulin resistance? 

Ben: 
Yeah, I’ll start with fat cells then I’ll transition to a beautifully divergent pathology in men and women as a perfect example. But yeah, fat cells manifest with a somewhat selective insulin resistance. Insulin is still able to pull in fats, for example, even the most insulin resistant fat cell. It becomes compromised with its ability to pull in some glucose, albeit not totally but a little, but its ability to activate lipoprotein lipase, which will pull fats in from any triglycerides circulating molecules, like LDL or VLDL.

That continues to work very well, but insulin very powerfully starts to lose its lipolytic inhibition. So then, you have the fat cells dumping free fatty acids, which contributes to ectopic fat deposition, or the body storing fat and tissues that are poorly suited for that fat storage. 

Bret: 
But so, that would be like visceral fat like the fat storage around our organs? 

Ben: 
Or liver fat, for example, liver fat or the accumulation of lipids within muscle. You need like a fatty muscle, or very relevant to metabolic problems, fatty pancreas so which starts to disrupt pancreatic function. But the kind of most elegant example is infertility. When you look at the most common form of infertility in men, it is erectile dysfunction. Most common form of infertility in women is polycystic ovary syndrome PCOS.

And each of them is a perfect example of the one of the two parts of insulin resistance. Specifically and briefly, erectile dysfunction is a problem of insulin not working well at the blood vessels of a man. One of insulin’s largely overlooked effects is to induce the production of nitric oxide in capillaries and in arterials inducing vasodilation. And of course, vasodilation and the change in blood flow is essential to normal erectile function in men.

But as the blood vessels become insulin resistant, the blood vessels stay constricted and the man now has compromised erectile function. That is a consequence, again, just almost purely of the insulin resistance. Now, in contrast, the theca and granulosa cells of the ovaries, which are jointly responsible for the production of sex hormones, they don’t become compromised.

They still respond to insulin perfectly well. But now, in this insulin resistant body, insulin levels are much higher than they used to be. So, whatever insulin was doing at the cells of the ovaries, it’s now doing too much. It’s doing it too well because there’s so much insulin. And one of insulin’s very strange and unexpected effects is that it tends to gently inhibit the enzymes that transition or convert testosterone into the estrogens of the body, like estradiol.

It is a little known fact that all estrogens were once testosterone in men and women. It’s just ovaries convert the testosterone much more rapidly than testes do in men, but insulin tends to keep that in check. And when there’s too much insulin, it’s keeping that enzyme, that conversion, in check too well. And so now, as opposed to the ovaries releasing a much much higher level of estrogens in a relatively modest amount of testosterone, it’s somewhat flipped, where now there’s way too much testosterone coming out and far too little of the estrogens. Indeed, too few estrogens to give this big estrogen spike and to which is necessary for ovulation.

And so, the ovaries go through the process of maturing follicles, but never actually being able to ovulate one of them, and having one become the dominant follicle and actually ovulate. So, all of those which is necessary for all of the other maturing follicles to get degraded and to go away.

And so, it happens in the absence of that actual act of ovulation because of the failure of the estrogen spike because of the high insulin. All of those follicles just stick around, swelling the ovary becoming cysts. And then, as she starts to come to another cycle, once again, we go through that process ,and more follicles mature but never actually ovulate. And then we end up with a polycystic ovary condition. 

Bret: 
Yeah, you can see your passion of taking this from a cellular level of how the cells behave and applying it to human health. And it’s a such an important connection. It’s not always so easy to understand or so obvious, but it’s clear that insulin resistance is going to affect multiple different organ systems, and you just gave a very good example.

So now, let’s translate that to the brain where until recently, maybe people haven’t been talking about insulin resistant quite as much because it’s harder to measure in the brain than just in in the blood? But yet, we know insulin resistance is correlated with cognitive of decline. We know it’s correlated with symptoms of mental illness of various different types.

So, how do you connect the dots of looking at being able to study the cells in our body and connecting that to symptoms that we also experience from a neurologic standpoint? 

Ben: 
Yeah, so briefly on the history of how I even came to start studying some of the central nervous system or brain specific effects of insulin resistance, which we have now published a few papers on. So, I can speak to it with some degree of authority, but I will never forget the first time I ever found a paper, and it said something like is Alzheimer’s disease type III diabetes. 

And I was so struck by that, as a diabetes scientist, that I read the paper. And to be frank, I don’t love that term, just as a point of really being clear. To me, I worry that it makes someone think that it really is a novel type of diabetes suddenly. But in reality, a more accurate way of describing it would be that some of the cells of the brain have become insulin resistant. 

Or to put it more simply, an insulin resistance of the brain. And the brain is, there’s an interesting kind of biochemical, bioenergetics aspect to this, which is that the brain is among this kind of wholly metabolic trinity. It is among the top three metabolic rate organs in the entire body. There are these three tissues that are called high metabolic rate organs, and that is, in order, kidney which is ridiculously metabolically active.

I’ve done some of these experiments in my own lab. And it’s just almost ,you’re giggling at how high its metabolic rate is because it’s just so insane. And then, far below that but still far above anything else, is the heart and then the brain. So, the brain at any moment, is at any moment, even when we’re asleep, it is a high metabolic rate organ and is demanding a lot of energy.

Now, the brain also, unlike the kidneys. The kidneys have the capacity to store some energy within itself. Even the heart has a limited capacity to store a little bit of glycogen and a little bit of fat ,albeit a modest amount. The brain does not have that. The brain has this absolute constant demand for energy pulling it in from the blood. And so, if there is some compromised energy coming from the blood to the brain, the brain senses it immediately.

It’s very sensitive to that reduced energy. And as energy availability starts to drop, the brain is left with two terrible options, which is I can continue to try to function at this higher rate and then die, or I will reduce my function and and then I can meet the energy that I’m being provided, although I have to reduce my function to do so. And that’s where, it’s that latter option that the brain chooses, which then becomes manifest with plenty of neurological disorders.

So, we and others have now found that there are distinct cells, and there are many cells within the hippocampus, the so-called memory learning center. That’s the site of the brain that gets so compromised with dementia that it becomes insulin resistant, that some of the glucose that needs to get in is dependent on insulin coming and knocking on the door, and opening the door and then the glucose is able to come in and fuel the brain. It’s not working as well.

Now the brain, as a brief tangent, has two energy sources. It can rely at any point on glucose or ketones, but we put the body in this terrible metabolic state. It’s a tragedy metabolically where the same body that is becoming insulin resistant, which is depriving the brain of its glucose energy, is the same body, because of the high insulin, that is not allowing the production of the brain’s only energy source, namely ketones

And so, you have an insulin resistant body, which is high insulin, which is preventing the production of ketones. And you have an insulin resistant brain, which is preventing the brain from accessing the glucose well, even though ironically the brain is, the body is swimming with glucose. Glucose levels could be substantially higher than they normally are, and the brain still can’t use them because of the compromised insulin action.

And to varying degrees, this metabolic phenomenon, which is commonly referred to as brain glucose hypometabolism, appears to be a fundamental triggering event in not only Alzheimer’s disease but a host of other neurological pathologies, including Parkinson’s disease and most especially migraines. In fact, as far as I know, some of the earliest research on the use of ketogenic diets came as a therapy in the early 1920s for Alzheimer’s disease.

These are actually published little reports that physicians put together documenting the improvement in migraine headaches. Also epilepsy, that was one of the other early origins of the use in the study of the ketogenic diet. Every one of these problems, again, manifests with a demonstrably reduced brain glucose use, of course, as demonstrated in very intense research laboratories, not in a clinical setting, unfortunately.

And then, maybe my final thought on this is as much as people may think then it’s only relevant in the clinic. In fact, one of the more interesting prospective studies done looking at people and following them over time and then documenting the onset of Alzheimer’s disease, was published in Finland many years ago. And they found, I think it was eight different metrics that tended to predict the onset of Alzheimer’s disease.

Three of them were age, education, and APOE phenotype, APOE4 phenotype or genotype rather. And then the other five, every one of the other five was metabolic, having to do with some measurement of glucose or some measurement of insulin and insulin resistance and even APOE4. The traditional paradigm, of course, has been that is purely because APOE4 genotype results in plaque accumulation, and plaques then disrupt neurological function.

And that appears not to be true at all that. There are medications that reduce plaque load within the brain and it does not improve cognition. What it might be is that the APOE4, actual lipoprotein, appears to interact with and disrupt the insulin receptor. And so, this genetic predisposition, which absolutely exists with an APOE4 genotype, it may simply be once again taking advantage of this metabolic pathway.

And to me, there’s some good news there because if it is through metabolic disruption, then that does empower a person to do all they can to improve their metabolic health. 

Bret: 
Yeah, such a great point. That last point is crucial. Like you can’t change your APOE genes. You can’t change from being an APOE4 to an APOE3, which is very disempowering, unempowering. That oh, I’m just APOE4, I’m going to get Alzheimer’s, I’m going to get dementia. No, because of the mechanism involving metabolic function, metabolic health, you can control that.

And I think that’s so important. And same thing for if metabolic dysfunction leads to bipolar disorder. Like we’ve interviewed Hannah Warren, who is now part of Metabolic Mind, and she calls it neurometabolic dysfunction because that’s gives her the power to say, I can treat this with improving metabolic health.

So, when it comes to the plagues of prosperity, when it comes to metabolic dysfunction, what are the key interventions that research has shown that can improve this? 

Ben: 
Yeah, I have a very high level of rigor when I speak about the solutions to this problem. And to be specific, how can we reverse or prevent insulin resistance, and thereby, prevent or correct this metabolic decay that starts to happen across the tissues of the body, including the brain? And my high bar is set by only acknowledging a contributing factor if it has been validated as an independent cause of insulin resistance.

In all three commonly used biomedical research models, namely isolated cells grown in culture laboratory, rodents and humans. So, to show that there’s direct effect in all three of those models and with that level rigor, that filter applied to all of the possible contributing causes to insulin resistance. There are three that are left standing, each capable of causing insulin resistance on their own in all used biomedical models.

In no particular order, I’ll end with the most what I consider to be the most important. So, I guess there is a particular order, stress. Stress will cause insulin resistance. Now, by stress, I’m using that term as an endocrinologist would or a professor who teaches advanced endocrinology. And that really could be defined most aptly as being an elevation in the two prototypical stress hormones, cortisol and epinephrine.

Now, it’s important to note, people hear those hormones and think anyone who’s somewhat informed would say they’re both coming from the adrenal glands. So, it’s no surprise that they have similar effects. But in reality, that’s not fair because the adrenal gland has two separate parts to it, and they’re unlike they’re not like each other. And so, these two hormones come from two totally different cell types.

They’re created in two totally different ways, transported through the blood in totally different ways, act on cells throughout the body in totally different ways. They have nothing in common except they both want to increase glucose, and they do so very well and very rapidly. That then these two hormones, who want to increase glucose, puts them both at odds with a hormone whose job it is, in part, to lower glucose, namely insulin.

And so it’s no surprise that if cortisol and epinephrine are elevated, the body becomes insulin resistant, and it does so very quickly. This happens all the time. And even something as modest as a poor night of sleep, which increases cortisol the next day, will contribute to insulin resistance. Too much caffeine consumption, which increases epinephrine, can then contribute to insulin resistance.

So, stress is a primary cause. The other cause is inflammation. Anytime inflammatory cytokines are elevated in the body, tissues of the body will start to become insulin resistant. And this is relevant not only in the cases of overt infections, like someone who has a cold or a flu, they will notice if they’re wearing a continuous glucose monitor that things are higher and much noisier as the body becomes insulin resistant.

The same goes in people with autoimmune diseases. As the autoimmunity ebbs and flows, so too does the insulin resistance. It goes along with it. Indeed, it’s following it. And now, the third final, and what I would argue is the most important variable in causing insulin resistance, is Insulin itself. Too much insulin causes insulin resistance. Now a lot of people want to misinterpret that, and then assume that I’m vilifying a single insulin spike.

No, a single insulin spike is no problem. It’s just when the spikes keep happening all day because you continue to take starchy, sugary foods every two hours because we have such a snacky culture when it comes to eating. But this is the one that I believe, while it is a little more subtle, although we have shown that this happens. We’ve published reports from cells and rodents, and others have published reports in humans. It does happen fairly quickly, albeit a little slower, than the other two.

It is the one that I believe is a little more insidious and lingering just because we do it all the time. The way we eat, how frequently we eat, and what we eat means that our insulin is elevated every waking moment of the day ,and even well into the first several hours of our non-waking part of the day. And that it’s not only is it such a heavy contributor, but it’s also such an essential part of the solution. Because it’s maybe, anyone listening or worried about insulin resistance, it is very difficult for them to know what their stress is and how to fix it.

If, for example, their stress hormones are elevated because they sleep poorly, you can’t just tell them, alright, just sleep better, and that will solve the problem. It’s not that simple. Of course, similarly with inflammation, if they have higher inflammation, they might not know why the inflammation is elevated. However, we know why insulin gets elevated, and that’s because the incessant consumption of refined starches and sugars.

And thus, that part of the solution becomes simple, where you just simply control the starches and sugars that are coming in, or as I like to say, control carbs that will immediately start to lower insulin, which will immediately begin to improve insulin sensitivity. 

Bret: 
Yeah, I think it’s so interesting. You talk about stress inflammation and insulin, all three of things that we need, right? In the acute phase, in the acute sense, all of those are necessary for life, but it’s when it becomes chronic and it becomes over time persistent that it becomes the problem. And and I like how you said it’s really hard to understand, how do you reduce inflammation and stress? How do you measure it?

Those are much more complicated than insulin. Harder to reverse than the chronic insulin hyperinsulinemia. So, changing our diet is certainly one. You’ve already mentioned a ketogenic diet a couple times, but we also hear things about, you know, exercise and other types of interventions.

So, what does the research say, specifically for the type of diet, specifically for the type of exercise, which are the biggest bang for your buck in helping reverse that hyperinsulinemia? 

Ben: 
Yeah, so just to be very, very magnanimous and brutally honest, any dietary intervention that lowers insulin will improve insulin sensitivity. And this can include even a plant-based diet, especially if it is whole foods-based. And mind you, a very important caveat that the person is supplementing to make up for whatever they’re deficient in. I’m not an advocate of a plant-based diet, even less of an advocate, in fact openly opposed, to vegan diet.

But if, for whatever reason, a person chose to take that route, it will improve their insulin sensitivity, albeit maybe in the short term, if they’re able to sustain that. But again that’s a very tricky thing. I’m generally an advocate of a low-carb diet, not because and I hope people will just believe me and take me at my word, not because I want to be a kind of drumbeat marching member of a of a ketogenic diet fan club. It doesn’t even need to be low-carb to the point of ketogenic. It’s just, to me, the simplest approach is control carbs. Focus on whole fruits and vegetables, and eat them liberally. Prioritize protein, particularly from animal sources, because you know, you’re going to get everything you need.

And don’t fear fat. By that, don’t fear the fat that comes with that protein. And don’t even fear being a little liberal with the fat when it comes to olive oil or coconut oil or butter. That is, these are very nutritious things, but especially the fat that comes with protein in nature. Because in nature, all proteins come with fat. They’re designed to come together, and I believe that’s how we should eat them.

But even that those three simple things will go so far to lower a person’s insulin and improve insulin sensitivity. Now beyond diet, you’d mentioned exercise, and of course, that’s a great one. I am increasingly, the older I get, an advocate of resistance exercise over aerobic or endurance-based exercise. As wonderful as all of that is and despite everything I’m about to say, the best exercise for everyone listening is the one you will do.

Now having said that, if you are able to incorporate some degree of fatiguing your muscles very deliberately, that is going to go a long way because muscle mass is the great equalizer when it comes to blood glucose. If you’re indulging in carbs from time to time, the more muscle you have, the more rapidly you’re able to clear that glucose from the blood. And thus allow insulin to, well allowing insulin, to do its job.

And then go right back to normal, retreating into the background, which is where we want it kept the majority of the time. So, muscle mass ends up giving us a lot of metabolic wiggle room where we can play with our diet a little more than than otherwise. And this is just something both sexes, men and women, the more you can have a deliberate time of just fatiguing your muscle where it’s starting to get a little, starting to burn a bit, then you’ve stimulated a signal for a little more muscle growth happening before you do it again 

Bret: 
Yeah, and I think that’s such an important point, especially in a, I guess you could say, a society that where the common message is frequently that we have too much protein. And we can lower our protein intake, and just getting out and walking is plenty of exercise. The two combined are in medications that we give that help us lose a lot of weight But both fat and muscle combined, that kind of combination just seems to be setting this up for a sarcopenic world in the future where everybody is deficient of muscle mass.

Do you have similar concerns or am I overplaying this? 

Ben: 
Oh, for sure, with the medications, in particular, yes. I think any approach that is shrinking your fat mass, which will improve insulin sensitivity but comes with a shrinking of the lean mass, is maybe not worth it. Because the moment that intervention stops, let’s just really hit the nail on the head, like GLP-1 agonists, Wegovy and Ozempic. They result in a significant degree of weight loss based on pharmacology.

Although we both know that a really good low-carb diet can beat that all day long. But even still, it does result in meaningful weight loss because it slows the rate of which, that which food is moving through your guts, and it makes you feel fuller longer. That is the main mechanism of action for weight loss. You just eat less because you feel a little sick now, unfortunately, by having a weight loss strategy that is completely based on eating less.

You become a little deficient. And so that study published in a New England Journal of Medicine over a two year period of time, found that up to about 40%, and I this is what you were alluding to, 40% of the weight loss came from lean mass in these people. And so now, what happens if we extrapolate?

Let’s go a little further and imagine a day approaches in the lives of these individuals, and every individual who’s on these drugs, where either they get tired of feeling a little sick all the time, a little nauseous. They get tired of the nausea and, or they get tired of the 1500 or $2,000 a month that they have to pay, and so they get off the medication. But again, they’ve lost mass fat mass and lean mass.

One of those masses will come back very easily. One of them won’t, especially if we’re talking about a mid to late aged woman or man. Even especially a case of a woman, it’s going to be incredibly difficult to make up any ground in the lean mass department whereas the fat mass will come back greedily. And now, they’re left in a far worse metabolic body composition scenario than they were before they ever started.

They will be significantly fatter as a percent than they were before. Not only because the fat came back, but it didn’t come back with the commensurate lean mass that they used to enjoy. 

Bret: 
Yeah, that’s well said .And there are a number of studies pointing out the correlation between resistance training and cognitive benefits, mental health benefits. Do you think it comes down to metabolic benefits or do you think there’s even more involved there? 

Ben: 
Yeah, I’ll just for the sake of ease I guess, I would say, I would point the finger more at metabolic benefit, although there are myriad benefits, of course. But I’ll just stick with what I know and that is the absolute inarguable benefit improvement in metabolic health. 

Bret: 
Yeah, I like how you’ve walked us through from the cell to the organ to the person connecting metabolic health to so many different disease processes, including neurologic, and then, what we can do about it .The empowering part that we can do something about it. And I guess that’s what you’ve devoted your life and your research to. So, what’s next for you?

What other research projects are you working on or what other projects do you have going? 

Ben: 
Yeah, so it is a beautiful life being being a professor and a scientist, but it’s not always enough for a guy who’s a bit ambitious, like me. And so within the realm of just pure science, namely within my own laboratory, we have a few very interesting projects going on. And just very briefly because they’re so cool, one of them is studying the effects of ketones on mitigating the Inflammation of uric acid.

It’s a little known fact that in a ketogenic diet state, there’s this apparent paradox where their metabolic markers are all getting better, and they’re feeling amazing, including reduced levels of inflammatory proteins. But at the same time, their uric acid may go up a little bit. And those two things shouldn’t go together. That has been shown in multiple papers in what we found, we haven’t published it yet, is that the ketones are blocking the inflammation that would come from uric acid.

And so, the ketones are actually acting as a direct inhibitor, signaling throughout the body, to keep inflammation in check despite uric acid. Another study we have, and I’ll I’ll end with this one for this part of the question, is looking at the effects of diesel exhaust particles on changing the growing and shrinking of fat cells That when a body has inhaled diesel exhaust particles, they actually directly act on the fat cell to promote fat cell hypertrophy, which is something that I’ve spoken about before.

But it’s the unique growth of each individual fat cell that really initiates, or is the first tissue to really experience, insulin resistance. And so anyway, an interesting kind of non-nutrient aspect to our environment, and its contributions to metabolic health. And then as I mentioned, I, as a professor, I sometimes push against the limits of academiand. By that, I’m not a conventional academic, where I don’t like the idea of just publishing results in peer-reviewed papers that no one will ever read, and it will benefit no one’s life.

I really rail against the limits of academia, in that regard, where my thought is, as an academic, and to my good fortune, as a biomedical scientist, if I am studying something that actually matters in the life and living of the average individual, it behooves me to find an opportunity to share that. And so to that end, of course, working on another book and very heavily now contributing academic or educational content to my site, InsulinIQ.com.

And any I’ll direct anyone to InsulinIQ.com to look up what I’m doing currently and some upcoming efforts. 

Bret: 
Yeah again, so wonderful how you’re taking what you know from a research standpoint but saying that’s not enough. The end result is helping people live better lives and trying to find an avenue to implement that. So, thank you. I think that’s wonderful, and thank you for taking the time to join me today and help us understand all this so much better.

Ben: 
Oh, my pleasure. I look forward to meeting up at a meeting at some point in the future, Bret. Thanks again, of course. 

Bret: 
Thanks for listening to the Metabolic Mind Podcast. If you found this episode helpful, please leave a rating and comment as we’d love to hear from you. And please click the subscribe button so you won’t miss any of our future episodes.

And you can see full video episodes on our YouTube page at Metabolic Mind. Lastly, if you know someone who may benefit from this information, please share it as our goal is to spread this information to help as many people as possible. Thanks again for listening, and we’ll see you here next time at The Metabolic Mind Podcast.