Ep. 168 – What To Do About Insulin Resistance Disorders (and the Role that Digestion Plays) with Dr. Benjamin Bikman

I am delighted to have Dr. Benjamin Bikman back on the podcast today! He was with us once before in Episode 114, where he spoke about the role of insulin resistance, metabolic health, and the COVID-19 pandemic. Dr. Ben is the author of a book I frequently recommend, called Why We Get Sick. 

It can be quite challenging for many women to maintain a healthy weight and good metabolic health after about forty years of age. Just about all of our fat cells are made during childhood and puberty, and when we reach our sixties or seventies, the number of our fat cells starts to decline. Insulin plays a vital role in how fat cells can change and respond to sex hormones. In this episode, Dr. Ben talks about insulin, fat cells, and sex hormones in women. Stay tuned for more!

Benjamin Bikman earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. Currently, his professional focus as a scientist and associate professor (Brigham Young University) is to better understand the role of elevated insulin in regulating obesity and diabetes, including the relevance of ketones in mitochondrial function.

“Estrogens play a very interesting role in fat metabolism, particularly in a woman who has so much more estrogens than a man does.”

Dr. Benjamin Bikman

IN THIS EPISODE YOU WILL LEARN:

• Dr. Ben explains why insulin is such an important topic for women, especially as they get older.
• The role of insulin in terms of how fat cells can change and respond to sex hormones.
• How estrogens protect women against too much fat.
• Why you need to be mindful about certain plant-based foods and the plastics, detergents, and chemicals we use.
• Why animal protein is undeniably superior to plant protein.
• Why your diet does not require carbohydrates even though some cells need glucose.
• The effects of seed oils and carbohydrates on insulin resistance.
• How digestion relates to insulin resistance and insulin instability.
• Vitamin D deficiency will contribute to insulin resistance.
• Why you need to know what your fasting insulin number is.
  

Connect with Dr. Benjamin Bikman

On his Insulin IQ website

On the getHLTH website

On Instagram

Connect with Cynthia Thurlow

• Follow on Twitter, Instagram & LinkedIn
• Check out Cynthia’s website
• Check Out Dry Farm Wines: www.dryfarmwines.com/cynthiathurlow

About Everyday Wellness Podcast

Welcome to the Everyday Wellness podcast with Cynthia Thurlow! Cynthia is a mom of 2 boys, wife, nurse practitioner, and intermittent fasting and nutrition expert. She has over 20 years experience in emergency medicine and cardiology, but pivoted to focus on food as medicine. She loves to share science-backed practical information to improve your overall well being and is grateful to be interviewing leaders in the health and wellness field.  Her goal with Everyday Wellness is to help her listeners make simple changes to their everyday lives that will result in improved overall wellness and long term health.

Presenter: This is Everyday Wellness, a podcast dedicated to helping you achieve your health and wellness goals, and provide practical strategies that you can use in your real life. And now, here’s your host, Nurse Practitioner Cynthia Thurlow.

Cynthia: Well, today, I’m delighted to have Dr. Ben Bikman back. We originally recorded on episode 114 talking about the role of insulin resistance, metabolic health, and the current pandemic. He is the author of a book I recommend frequently called Why We Get Sick. Welcome, Dr. Bikman. It’s a pleasure to have you back again.

Benjamin: Oh, my pleasure. It’s all mine, the pleasure. I’m glad to be here. This is always a fun opportunity to chat about topics that people really feel strongly about. I’m glad to share any knowledge I can.

Cynthia: Yeah, absolutely. I know we were talking before we started recording, and so the bulk of the people that really listen to the podcast in a very dedicated manner are women north of 35, and the concept of insulin for many of them seems a little bit intangible. But let’s unpack why this is so important, especially as women are chronologically getting a little bit older, and how the role of insulin plays in terms of how our fat cells can change, how they respond to our sex hormones. Because I think this is really important for women to understand, because it’s not just in their head that suddenly things get a little more challenging at trying to maintain a healthy metabolic health as well as a healthy weight, and I don’t like people to focus on their weight, but we can definitely agree that maintaining a healthy weight is absolutely critical, especially, as we start creeping north of 40.

Benjamin: Yeah, so, that is an interesting time. Men and women as they age, there are changes in fat cell number. Now, there are so many ideas floating around in my head, and I’m going to try to put them all into a linear stream of thought. Both sexes, there’s a relevance with fat cells. That is fat cell number. One of the interesting things about the fat cells as we age is that we make almost all of our fat cells during childhood and puberty. Then, once we finish puberty, we’re done. That number of fat cells, in most people, there are some people who are an exception to this, that’s about 15% of people who are in the obese category. But most people reach a limit, and that’s their fat cell number, essentially, for adulthood.

Then around as we are getting past adulthood, which of course is beyond 40, so I’m just presenting a bigger spectrum of time at the moment. Then we get to our 60s or 70s, and then the number of fat cells we have starts to decline, well, that sounds like it’s a good thing and I promise I’ll bring this back to women specifically, but just to give the big picture. That sounds like that’s a good thing. But what’s happening is if a person is continuing to eat the same way they were before, that grew their fat cells to however big they got, big or small, too much, too full or not, whatever they were, if they had fat cells that were big, and now over full, and now they’re starting to lose their fat cell number, that doesn’t mean they’re losing fat mass. What that does mean is that, the fat that was being stored in five fat cells as you cut off two of them, because they die now and they aren’t replaced with another fat cell, which is what’s been happening the whole time before then. One dies every 10 years-ish and another one takes its place. Now you don’t have that turnover.

The fact that was being held in five fat cells, well, now that’s only being held in two or three fat cells. Meaning, those remaining fat cells have had to carry a larger fat burden. What you’re doing is putting the fat cell in the perfectly wrong situation, which is forcing fat cells to be overfull or what’s called hypertrophied or hypertrophic. A hypertrophic fat cell is a bad fat cell. That’s a fat cell that’s misbehaving, it’s becoming pro-inflammatory and insulin resistant, and then promoting that insulin resistance throughout the rest of the body. Unless we look at the decline in fat cell number as a good thing, it could be, I do think there’s an opportunity there. but it would involve the aging person to change their diet accordingly to make sure that there is lower energy and lower insulin that when that fat cell is turned over, well, there was nothing really left in it anyway or when it died. We’re not forcing a remaining fat cell to carry the burden of this dying fat cell that has dropped at its feet.

Now, to bring this back to a woman, say, in her 40s are getting towards menopause, estrogens are undeniably a protective effect when it comes to insulin sensitivity and overall healthy fat storage. Now, estrogens, that family of hormones that we call estrogens, there’s not one single hormone called estrogen, of course, they play a very interesting role in fat metabolism, particularly in a woman who has so much more estrogens than a man does. But estrogens are overall protective against too much fat. We know this from animal and human studies. If you remove the ovaries and remove those big strong estrogen signals, fat mass starts to go up quickly. So, there’s something protective against too much fat mass when it comes to the estrogens in general.

Then, separate from this is that estrogens actually promote a healthy form of fat storage. By promoting fat storage primarily on the butt and hips of the woman, which is the main site of fat storage for most women, that is actually a site of fat storage that promotes greater hyperplasia, where rather than having fat cells grow bigger and bigger and bigger, it rather says, “All right, you’re a little fat cell, there’s high insulin, we’re telling you to store more. Well, rather than get really big, let’s just make a new little fat cell right beside it.”

It might seem like a bit of a paradox, but estrogens essentially help a woman store fat in small, healthy fat cells. Even though there are more fat cells in general, it ends up being an overall healthier profile. That’s why women are almost always fatter than men, but healthier than men at the same time. Her body is literally supposed to have more fat than the man’s, and she needs more fat than the man’s to be healthy for normal fertility and other processes as well.

So, as a woman is now transitioning and leaving the high estrogen days behind her, there is a risk that comes with that, which is as the estrogens are coming down, it’s a bit of a double whammy, which is, you are losing the general fat protective effect that estrogens are playing, not allowing or discouraging the body from storing too much fat. And two, you’re losing that healthy way of storing fat. Now, in the absence of estrogens, if there’s still a signal to be storing fat, more of that relatively is going to be stored like her male counterpart, which is going to be more central fat storage and hypertrophic fat cells rather than subcutaneous fat storage or the fat stored right beneath the skin, and hyperplastic fat cells, which is small, but more multiple.

The woman transitioning, again to maybe put a fine point on at all, I think it is still an opportunity to get lean even, as crazy as that may sound. I don’t think it’s hopeless. I think it is an opportunity to leverage the changes that are happening and maybe even capitalize on those to be leaner than before. There might be a benefit to just the steadiness that comes from that transition period, where you don’t have these really dramatic changes in hormones. Maybe there’s an opportunity for her to get into habits that aren’t at the whims of these hormones and the wild changes that she’s had before then, if we can put any positive spin on this. I’m certainly trying to, because as much as– and I don’t mean to overstep my bounds here, as much as this transition period is so often reviled and hated, it is a natural thing. I can’t help but think this is how humans have been built. It happens. There’s a reason for it. It can’t all be bad, and maybe that’s just an overly naive thing, where I’m always determined to see the body as having been built as a rational series of events. I can’t help but look at this transition into menopause as something that is undeniably natural, and even something that’s supposed to happen. So, I cannot look at it as something that’s purely pathological, or purely harmful, or purely something to be reviled. There must be something about it that we can take advantage of.

Cynthia: Well, I love the positive message, because I think for a society that’s largely very ageist focused, there are a lot of women that feel a tremendous amount of shame, when they are making that transition, when they’re no longer fertile or unable to conceive and carry a child on their own, maybe without a lot of technology. Now, one point about estrogen that I’m just curious about. We know the predominant form of estrogen is estradiol prior to going through menopause, and then, estrone takes over. I know this is a weaker form of estrogen. Is that what is being generated viscerally, the hypertrophic, as you refer to, the less healthy type of fat? Is that the type of estrogen that you’re focusing on predominantly in the menopausal female? I’m just trying to put all the pieces together and [crosstalk]

Benjamin: Yeah, estradiol is the main estrogen that is helping the woman store fat at a limited amount and in a healthier way. It is the loss of estradiol that then accounts for the seemingly harmful changes in fat metabolism. As you note, other estrogens are just weaker, and they might– I have to speculate. They might have a similar effect, and maybe, it’s just that there’s not enough of that signal anymore, or it might be that because it is in fact a different hormone, it might not have the same effect at all. I don’t know.

Cynthia: It’s really interesting, because I know, as you mentioned, there’s this preoccupation, concern with all these bodily changes, and one of the roles of estrogen that I find fascinating, and it’s also really critically important for people to understand this that if we want to be metabolically healthy irrespective of our age, we really have to be mindful of the influence of our sex hormones in conjunction with our fat cells, in conjunction with insulin. You brought up a really good point that the body really does try to be very efficient, and try to ensure that things are working in the manner they’re supposed to, and what I find really interesting, and I never learned this in nursing or my nurse practitioner program. I learned this many years later, is that the first two weeks of our menstrual cycles, and this is when estrogen, estradiol predominates, and we are much more insulin sensitive versus the latter part of our menstrual cycle prior to menstruation when progesterone predominates, and we are tired and cranky, and we become more insulin resistant. So, is it any surprise we get these cravings for foods that may or may not be in our best interest to consume?

But I love just how the body is trying to intuitively gravitate towards exactly the way that it needs to work efficiently. I think unfortunately, what’s happened is that we have these gross abnormalities in our sex hormone balancing, whether it’s a byproduct of synthetic contraceptives, or PCOS, or infertility, or any number– I know in podcast I listened to yesterday, you were saying the term ‘estrogen dominance’ isn’t really a scientific term, and seeing a lot of the influence of toxins in our environment, endocrine disrupting chemicals, how a lot of people’s hormones, their sex hormones can really get offline.

Benjamin: Oh, yeah, that’s right. In fact, I love that you’re bringing that up. It’s something that I don’t talk about often, because it’s not my area of expertise. But as a father, I think of that more actually in the context of my children, my little girls and my little boy, especially, I am very mindful of the plastics that we have that they’re drinking water from. I’m very mindful of the detergents that we’re using, and perhaps the pesticides or other chemicals, many of which remarkably act as estrogens or they have these estrogen mimetic effects. That’s something I’m very mindful of. I don’t want my daughters having too much estrogens. I don’t want them to develop physically too early, not only because of the social ramifications, but also the genuine health concerns with increased risks and brought in breast and uterine cancers. My little boy, of course, I don’t want him to be developing in an environment of high estrogen activity. This is a result though of the world that we live in. There’s something I can’t really speak to, because I’m not a chemist. But the fact that these molecules are so widely used with such a broad application coming from things like pesticides, detergents, and plastics, those are all three very different things, and yet, there are molecules found in all of them that are estrogen mimetics or acting like estrogen to varying degrees.

That’s even more the case when we look at some of the foods we’re eating that are increasingly plant based. When you are refining a plant, especially a seed, in order to get its proteins, you end up getting a lot of other stuff. I’m very mindful of these other supplements or whatever foods that we have in the home to make sure that not only are we controlling the plastics in the detergents, for example, but also that my kids when I’m focusing on them getting protein, which is almost my simplest strategy for feeding my kids, it is based on real protein. I want it to be protein that’s coming from animal sources, because I know that they’re not going to get– Among the benefits of just getting real fats and real proteins which will work better, they’re not going to be contaminated with these things I don’t want these like, say, phytoestrogens which have a genuine biological effect.

Cynthia: It’s interesting that you bring this up because it was part of the trajectory of our conversation. I was hoping it would go in this direction. I truly believe that in many ways, there’s a plant base agenda that’s going on. I’m seeing peers on many social media platforms that are being attacked, because they are pro-animal based protein and yet, when you really look at a lot of the research and ironically enough, one of my nurse practitioner journals came recently and probably the soybean agenda that was being pushed through out there. “Oh, women in perimenopause and menopause need soy. Lots of soy milk, lots of edamame, use these soy-based products, soy-based protein,” and so, I’m very grateful that unbeknownst to you, that you touched on this topic, because on many levels, I think it all starts with food. I think on every level, the way to ensure that we can properly balance hormones, especially insulin, is based on the food choices that we’re making. For so many people, they’re really quite confused.

Even reflecting on your book, which is so beautifully written, and I’m always recommending it to people, because I think it’s such a tangible information, and makes things very clear, and concise, and cohesive. When you’re talking to people about food choices, satiety is something that we don’t talk about with our patients. We just tell them, “Go, watch the MyPlate” nonsense, which is so carbohydrate focused, and yet, that’s the antithesis of what you’re suggesting, what I suggest, and plays along with the plant-based agenda, the animal-based proteins versus plant-based proteins, there’s little to no comparison between either of them.

Benjamin: Oh, that’s right. That is absolute quantifiable objective data. By any conceivable metric, animal protein is superior to plant protein, full stop. The case that some would make the perimenopausal women need to be focusing on soy is absolutely mind blowing to me. Mind blowing. Not only are you going to be getting an inferior source of protein by again, every metric, and of all the times to start cutting out good protein, that would be the worst way to do it, where you are losing the bone-protective effects of the estrogens, you want to do everything you can to keep those bones as strong and dynamic as possible. That’s what the proteins provide. They turn what would be a hard but brittle structure, and turns into a hard and pliable structure, allowing the bone to bend and not break. It is the worst thing to do, to focus on the vastly inferior source of protein that would come from soy.

But also, there’s an honest to goodness clinical case study that I’d seen. I can’t cite it off the top of my head, but I know it where there was this was a case report of a woman who would experience frequent uterine polyps and bleeding, and they scrutinized her diet and found that it was just soy everything. It was soy milk, it was tofu, it was soy protein, powder, whatever. They had her cut all of that out and it stopped. The uterine bleeding stopped, the polyp stopped growing. That’s pretty damning evidence against this just ridiculous notion that a woman ought to be focusing on soy, that’s unethical based on the data that suggests it’s unhealthy. It’s unethical based on the absolute lack of data, clinical data suggesting that it’s healthy at all. We have evidence suggesting it’s not, we have a dearth of evidence suggesting that it is. Yeah, that combined with the fact that it is by every metric, a worse protein than literally any animal protein, not to mention the beneficial fats that come with that protein rather than the harmful fats that come with the soy. Well, then, to me, the court is out on the decision that a verdict is in animal protein all day.

Cynthia: Well, it’s interesting. I think a lot of women are afraid of protein. They’re afraid of eating enough protein. When I started doing just food diaries with middle-aged women, I’m oftentimes shocked that they are eating really tiny, itty-bitty portions of protein for too many carbohydrates, and quinoa’s a great example. I think Dr. Gabrielle Lyon said, six ounces of steak equate to six cups of quinoa, which if you just take the calorie piece out the amount of carbohydrates and we know that we become physiologically more insulin resistant as we age. The worst thing you can be doing is eating copious amounts of carbohydrates which is not to suggest that there are good quality choices of carbohydrates, but certainly in middle age, and I think that’s also very likely applies to men as well. We’re looking at the average American 88% of individuals are metabolically unhealthy. Most if not all of us need to be eating less carbohydrates, non-starchy vegetables, certainly low glycemic berries, if you’re doing those kinds of things and less focus on breads, and pastas, and these very highly hyper palatable, highly addictive processed carbohydrates.

Benjamin: That’s right, and they always come with fat. That’s where we are bucking nature and certainly an ancestral way of eating, the diet we have nowadays is high carb, high fat. Those two don’t come together. It is carbohydrates on their own, which is every fruit, or vegetable, or grain that’s almost purely just starch or sugar. Then, you have in contrast, fat and protein, which essentially always come together. Now, we have some exceptions where we have gotten oil from, say, some plants or some fruit. Fruit oils are fine. That’s coconut, avocado, olive, those are fats that we’ve been eating since the beginning of time. But the other than those exceptions, fat always comes with protein. That’s how we should get them. Part of the frustration for me is that when people are told to base a diet primarily on carbohydrates, I have two significant sources of resentment against that advice. One is that you are now focusing on the macronutrient that spikes insulin the most. I have a problem with that. I’m an insulin guy. So, of course I do. Two, you are now focusing on the one macronutrient that is not essential to humans. Now, neither you nor I are saying, well, then let’s not eat any. We’re not saying that. We’re more nuanced than that. Yes, you can eat them, you can enjoy them, but eat them in its natural state as possible.

But at the very least, we should say, what is essential in the human diet? There are essential fats, there are essential amino acids. Thankfully, animal proteins have all of those. Let’s focus the diet on those two. The fact that they also have little to no effect on insulin, well, that’s just icing on the cake. But let’s not base the diet on the one macronutrient that is actually not essential to humans. That’s not debatable. Even the most dogmatic dietitian has to admit that carbohydrates are not essential to humans. Now, again, none of us are saying let’s not eat them at all, but let’s certainly appreciate that is the extra stuff. That is the stuff that can be sprinkled around the edge of the plate, whereas the bulk of the plate should be made up of the things we actually have a biological need for, protein and fat.

Cynthia: Well, I think sometimes people forget if they– maybe it’s been 20 plus years since they were in a biology class, but gluconeogenesis is a real thing. Our bodies can produce carbohydrates if they need them, and it’s beautiful that our bodies can do this. If you’re getting adequate protein, then your body can make adequate carbohydrates systemically. I think on many levels, I feel like this concept really triggers people because really dogmatically, they love their carbs. In fact, sometimes, my teenagers– and I would say, healthy, lean teenage athletes are the exception. [crosstalk] will eat whatever they want. But when they hear me talking and I remind them, I’m like, just think about how metabolically unhealthy the average person is, and it’s even more reason to focus on satiety, even more reason to focus on things that don’t provoke an insulin response.

I was going through someone’s food diary the other day, and I was gently pointing out some things that I think we could definitely work on. She had no idea that fat has the most negligible impact on insulin followed by protein and then carbs, and I explained to her– and this kind of explains on many levels, why we put meals together in a certain way. I said, I’m not anti carb, certainly for full disclosure, I tend to be low carb all the time, and I’m happy there, and that works well for me. But I think it’s this total rethinking, turning things on its head, reminding people that if we get back to a more ancestral health perspective as it pertains to nutrition, we will be much more healthy for sure.

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Benjamin: Yep. Part of this in what you said here, there is something that is so often misunderstood and is then weaponized, again, because of it being misunderstood, and that is the difference between glucose in the blood and carbohydrates in the diet. There are some cells of the body that have a genuine and total reliance on glucose. The red blood cells can only metabolize glucose. That is literally the only fuel for a red blood cell. There are other cells that appear to have some need some cells of the kidney, and perhaps, in portions of the brain, where it does appear that glucose is playing some role there. Essential or not, we don’t know. But let’s just regardless, the brain is happily or gladly using the glucose.

But that is confused with then suggesting that carbohydrates are now absolute and required in the diet. No, just because some cells need glucose like red blood cells, the most obvious, does not mean the diet requires carbohydrates, because to your point, because there is the need, the liver makes all we need. It literally makes– every gram of glucose we need, the liver makes and the body adapts, and where it knows, the brain knows, ah, we’re not eating as much glucose now, I’m just going to start using less glucose, then, so that maybe other cells like the red blood cells can get all they need, and I will In contrast shift over to using fat products like ketones. Now, the brain is getting 75% of its energy from ketones. The body adapts to the lower glucose state, but also the low glucose demands that the body has at any moment are met by the body itself, which is why we can say so authoritatively, there’s no such thing as an essential carbohydrate. But that nuance is lost on people who have a little bit of education, and yet they end up confusing the issue tragically. So, they know a little bit and it ends up working against them, where they know the red blood cells need glucose, and they think that means the diet requires carbohydrates. When in reality, it doesn’t.

Cynthia: I think on many levels and certainly I reflect back on my childhood, and my mom was crunchy before her time. I didn’t realize we were eating organ meats, and fresh baked bread, and lots of vegetables with every meal, how unusual that was. It certainly instilled really good habits but I think somewhere along the way, we really lost sight. I said, we as a country, as a nation, Big Ag convinced us that we didn’t know how to cook for ourselves, and we needed to really rely on these processed foods. In many ways, I think the processed food industry really has contributed to this escalating rate of obesity, and diabetes, and insulin resistance, and all of these problems that we’re mitigating and trying to navigate.

I’m curious what your feelings are, and I would imagine they’re very aligned, a lot of the questions that came in were about digestion and about micronutrients. But when we’re talking about these hyperpalatable, very highly processed foods, do you feel that seed oils are any better or worse than high-fructose corn syrup, or are they about the same in terms of damage to the mitochondria, damage creating inflammation, and inflammaging, and also facilitating this insulin resistance state that we’re dealing with?

Benjamin: Yeah, what a great question. Carbs versus seed oils. That’s one of the modern debates. Now, the reason I have a healthy respect for dietary carbohydrates is because of what they do to insulin. We know in every biomedical model tested, cells, rodents, and humans, high insulin causes insulin resistance. That is why I point the finger at carbohydrates. Because truly in light of insulin, there’s a direct effect. Now, some people will say, “Well, what about these traditional cultures where they’re eating tuberous vegetables?” That is not the same. Because even in those cultures like the [unintelligible [00:27:32] in the Pacific Island, they’re fasting insulin levels are exquisitely low. I’m not just blanket saying all carbs are bad. No, it’s what you and I have said, where there’s a nuance where processed carbohydrate is going to have a significantly higher effect on your insulin than an unprocessed carbohydrate. Eating a baked potato is a very different thing than eating potato chips. That matters, because when you are spiking your insulin too often, you’re going to cause insulin resistance. So, there’s a known effect.

Now, seed oils are absolutely relevant to health, and we’re eating thousands of times more of them than we ever have before. At a superficial level, the body knows what to do with glucose better than it knows what to do– like a high load of glucose, the body knows what to do with. A high load of seed oils, I think is probably in and of itself more pathogenic, that’s going to do more harm. That’s because the primary fat from seed oils is so readily oxidized. It is turned into what’s called the lipid peroxide, and that is this unholy result, the bastard child of this unholy union of oxidative stress and this readily oxidized fat. The problem with the lipid peroxide is that, it can now induce oxidative damage anywhere it wants, in DNA, in proteins, in the mitochondria, in the nucleus. It can go anywhere and induce oxidative damage. So, they’re highly pathogenic.

The degree to which these seed oils are directly contributing to insulin resistance, well, that’s just a little less clear. People will cite studies in rodents and humans, when they’re infusing fat and that causes insulin resistance. Any fat will do that to some degree. If you just start infusing a lot of fat directly into the blood which is not the same as eating the fat, you start infusing fat directly into the blood but the body needs to burn that fat. Naturally, it will turn off glucose burning by inducing some insulin resistance to account for this load of fat that has just been thrown into the body. In that direct model, sure, seed oils are going to provide a direct effect but every fat would.

The evidence that eating seed oil is directly going to cause insulin resistance, that is less clear. I can say with certainty when you put seed oils on cells, it doesn’t make them insulin resistant. There’s not a direct effect. However, there are other effects that the seed oils are inducing that are all harmful and pathogenic. But within the realm of insulin resistance, I suspect there is a connection, and it’s more of an indirect connection, and that is high consumption of seed oils results in high accumulation of these fats in fat cells. The seed oil metabolites in fat cells will cause a fat cell to grow through hypertrophy rather than hyperplasia. Of course, as we discussed at the outset, that is the more harmful insulin resistance way for fat cells to grow. So, there is that indirect effect. The evidence that there’s a direct effect is weaker. It might be there, but I’ve not seen it, and if I may be so bold, I’ve seen a lot. So, I don’t think it’s there.

Cynthia: [laughs] Well, I think it just goes against the general consensus that it’s not important to read food labels. I encourage anyone that’s listening that, if you spend a little bit of time in a grocery store, and you’re looking at something in a box, or a bag, or a can, more often than not, you’re going to find a seed oil. In fact, my kids know. I have teenagers, and I’m very realistic with them. Try to find a chip, again, I have teenagers, that doesn’t have seed oils in it. We have maybe four brands, and I love that there are brands of some of these options for people that live in a realistic environment but they come in very small bags, and they’re much more expensive. So, I remind my kids, please don’t go overboard, because I’m not going to buy the same quantity that you get in the seed oil laden options that are out there. So, just know that when it’s done, it’s done.

Benjamin: Yep, that’s right. There are chips. My kids like one that’s an avocado oil, but just like you said, they’re small and they’re expensive, and the kids know that’s a finite resource, dad’s a professor, which means we can only afford so many, so much of it. Yeah, there’s a lesson there. But also, one other note on seed oil, or more specifically to the fat that’s in seed oil, is polyunsaturated omega-6 fat called linoleic acid. It is likely one of the essential fatty acids for humans, and it is everywhere in nature. Every animal food will have some linoleic acid in it. There’s an important distinction where in and of itself, linoleic acid, the culprit in these seed oils is not always a villain, where it does appear to be a hero at modest amount. Of course, the poison is in the dose. We’re eating thousands of times more than we ever did before. We’re also eating it in the absence of natural antioxidants that should come with it, because when you’re eating an animal fat with some a little bit of linoleic acid, you’re also getting some trace amounts of natural antioxidants like, say, vitamin E. To some degree, that’s going to be in this animal fat as well. I don’t think that’s an accident. T

The fact that you’re getting this linoleic acid, which might be essential for humans with an antioxidant that might help it stay in its original form, I think there’s something to be said for that. What is interesting about linoleic acid is that it is used by the brain to create ketones. The brain can make its own ketones from linoleic acid, but only if it’s in its original state. If we’ve taken that linoleic acid and turned it into a lipid peroxide, it’s done, it’s committed. It’s harmful now. Nothing else, full stop. If we can keep it in its original state just as polyunsaturated fat, well, the body can do something with that. The cell can do something with that whether it is using it for fuel by burning it, or whether it is turning it into arachidonic acid, which is not the villain everyone thinks it is. Every arachidonic acid is relevant to inflammation. Because linoleic acid is a precursor to arachidonic acid, people will say that it’s inherently proinflammatory. That’s just not true. We need arachidonic acid. There is no recovery, there’s no immune response if it’s not for arachidonic acid. But at the end of it all, to use linoleic acid well, must stay in its original form, not become lipid peroxide. I think when we get it from animal sources, any like in beef, and eggs, and dairy, wherever it’s coming from, it’s always coming with some miniscule amounts of antioxidants, and I don’t think that’s an accident.

Cynthia: I think it’s a beautiful balance. For anyone that’s listening and thinking, I don’t know what we’re talking about. Broad-based omega-3s tend to be anti-inflammatory, omega-6s tend to be proinflammatory, but much to your point, we need some degree of inflammation acutely. That’s absolutely critically important. I’m not a scientist, but I remind people that if you overall look at the typical standard American diet, it is more proinflammatory, less anti-inflammatory, and those seed oils are what helped drive those imbalances. I was taught many years ago that it should be a one-to-one balance and that most Americans, it’s 22:1, which explains a lot of the health things that we’re touching on.

Now, I want to pivot a little bit and talk about digestion as it pertains to insulin resistance, insulin instability, because oftentimes people don’t put some of these problems together and correlate them with an imbalance in insulin. The one that stands out the most to me is gastroparesis. I cannot tell you how many diabetic patients and cardiology I took care of that had this delayed gastric emptying, and I was always taught with a byproduct of they’ve had insulin problems for far too long. But we know that it also ties in to things like gastroesophageal reflux disease, it ties into gallstones. Can we touch on that a little bit, because I’m getting quite a few questions from people asking where their interrelationship is between these disorders and insulin resistance?

Benjamin: Yeah. This is a bidirectional phenomenon, where you can have gastrointestinal problems, which always in some form, almost always will result in some form of inflammation. In subsequently causing insulin resistance itself, so, you can have a gut problem causing insulin resistance. In contrast, or let me say it a little more broadly. A gut problem causing a metabolic problem, and then it can go the other direction, you can have a metabolic problem causing a gut problem. The prior direction that I mentioned, gut to metabolic, that’s obvious, and it’s usually through inflammation, where when the gut is compromised, one, it’s invoking a direct immune response at the gut, because that is the single site of more immune cells than anywhere else in the whole body. This site of interaction between what we’ve ingested, and it now coming into the body. No surprise that we have a huge wall almost of immune cells to make sure that whatever’s coming in is supposed to be coming in. So, a gut problem often will result in an inflammation problem. Then, the more that problem will continue, of course, the more we lose the integrity of the gut, and molecules that are supposed to stay in the gut, now start moving into the bloodstream causing now systemic inflammation, all of which is contributing to insulin resistance. Inflammation is a primary cause of insulin resistance.

Now, the direct molecular mediators that result or mediate insulin resistance now causing a gut problem is simply unclear. We do know that people with more insulin resistance have a much, much greater likelihood of developing or already having some of the problems and you just mentioned them, gastroparesis, and GERD, and irritable bowel but the mechanisms aren’t clear. Some of what might explain it, and I’m speculating, could be a lack of energy to some of these cells, where if the cells have become insulin resistant, they might be compromised in their ability to pull in glucose to some degree, meaning, that they can’t do what they need to do including, say, a smooth muscle around the intestines to be contracting and moving the food along through peristalsis. Those are muscles that are helping that happen, and it might be that those muscles are insulin resistant, and now they’re just more lethargic due to a lack of energy. It might also be a lack of overall protein synthesis within those cells, or the maintenance of those proteins, because insulin is anabolic. It wants to tell cells to grow things and keep those things. Now, that has to be checked, of course. You need to anabolic and it needs to be checked with catabolic. But as the cell is becoming insulin resistant, you might be losing some of the anabolic effect of that insulin, and so the cells themselves are compromised in that they aren’t making their proteins, or they can’t keep their proteins. Proteins are really what lets a cell do whatever it wants to do in some way, shape, or form. Whether it is proteins on the surface of the cell, or proteins inside the cell, or proteins within the organelles of the cell, it’s the proteins that allow the cell to do whatever the cell is trying to do, and insulin likes making proteins.

Cynthia: Now, one of the other questions that I got, it was interesting, I tend to ask questions all over social media, and sometimes, it’ll be Twitter that’s very focused. Everyone on Twitter wanted to talk about insulin resistance, so that makes complete sense. A lot of people on Instagram were asking questions about vitamin D, how that interrelationship with insulin sensitivity or lack thereof, because most Americans are low in vitamin D, talking about essential fatty acids, as well as a few other things. But I’d love to dive into the existing research talking about the interplay between vitamin D as a hormone and then also insulin.

Benjamin: Yeah, I hate to disappoint the audience. I don’t know the specific mechanisms with regard to vitamin D enhancing insulin sensitivity. But it is there. It’s real. We know that people that are vitamin D deficient. You do nothing but give them vitamin D, high-quality usable vitamin D that increases their plasma vitamin D, and that alone will improve their insulin sensitivity. We know there’s something there, but I don’t know that we know the mechanism. I don’t. I don’t know the mechanism whereby sufficient vitamin D is promoting insulin resistance. I wish I did. But we know that it’s there, that there’s something about it. That if someone is vitamin D deficient, there’s no question that’s going to be contributing to a greater propensity for insulin resistance.

Thankfully, it’s a pretty simple solution where you know that if someone does have confirmed low vitamin D, that when you have that clarity, it gives you a simple plan of attack. There’s a simplicity to that, which is, “Okay, I just need to enhance my vitamin D,” if the person’s trying to take one step at a time. You have a role there that I don’t have, I don’t act as a clinician in any way, shape, or form. I have no direct interaction with a patient or a client like you do. I’m only the guy who sits back and thinks of ideas. My great hope is that some of these ideas become useful to someone who’s on the front lines, and that represents this perfect version of how this is supposed to work. People come up with answers to questions, and there are people who apply those answers in interacting with the client or a patient. Anyway, my point being, when someone is told they have low vitamin D, I think they ought to do a fist pump, thinking, “All right, I can do something about that,” and it doesn’t have to be overly uncomfortable or overly expensive.

Cynthia: Absolutely. I do love that there is a true– and this is true, like the beauty of academics is that this is really how it’s meant to work. There’s a scientist looking at problems in different ways, and then sharing that information in a way that’s accessible, because one of the things that I value and appreciate about you and your platform is that you make information– you make insulin interesting for people to know more about, even the lay public, I’m serious. But also, clinicians are saying, I think there’s something to this. We’re looking at the wrong metric. We’re very focused on fasting glucose and hemoglobin A1c, and yet, we really need to be looking deeper. I think we were speaking before we started recording, and I was saying, I had this really lovely patient and she was working concurrently with someone locally, and I kept saying to her you need to know your fasting insulin number, because her fasting blood sugar didn’t look all that bad. She had a CGM, her hemoglobin A1c didn’t look all that bad, and I suspected she was leptin resistant just based on what she was sharing with me. I would be surprised that she’s also not insulin resistant, and her fasting insulin was 20. I said you’re never going to lose weight. [laughs]

Benjamin: You know what, Cynthia? Adding insult to injury intellectually is that to the average clinician, they could very well look at that number and say, “I know that’s a good number.”

Cynthia: [laughs]

Benjamin: Not only is conventional medicine overlooking insulin entirely, even the little bit of scrutiny that they are giving insulin is so wildly off base that you can find– First of all, there’s no consensus for what good insulin levels are like we have with glucose. We have such clear consensus cutoffs for glucose. This is good, this is bad, and this is terrible. That doesn’t exist with insulin. It’s a series of different entities, different groups who have their own metrics of insulin, and they’re all way too high. Because they will look at the average American, and they will say, what is the average American and you don’t appear to have obvious disease. Your insulin is 15. So, 15 must be good. You don’t appear to have obvious disease. And yet, behind the scenes, they have hypertension to some degree, they have some hyperlipidemia, whatever, but it doesn’t reach the point of being overtly clinically relevant perhaps. So, even when they do measure insulin very often, a patient would have 20 micrograms per mil, and the average clinician would say, “I know that’s below 30. That’s fine.” I’m thinking that’s four times higher [crosstalk] not quite. That’s a lot higher than what it should be, double what at least what I would consider to be a good number.

That really is my central thesis, that at the end of my career, professionally speaking, if I can look back and say people look at health differently, and they include insulin, and appreciate insulin in a way they didn’t before, average clinical medicine, then I will retire with a great sense of satisfaction. But I am increasingly cynical, because conventional medicine doesn’t want to. I don’t know. Maybe, how can I put that diplomatically, give them the benefit of the doubt. Glucose is a druggable target just like LDL. You can look at glucose and there’s a whole cupboard of drugs that will lower glucose. Some of them, many of them act by increasing insulin. So, that’s an inconvenient truth. They don’t want to acknowledge that by lowering the glucose, because they’re increasing the insulin that they’re making the patient fatter and sicker. They don’t want to acknowledge that glucose is a druggable target, and so, it is much more clinically sexy. They want to look at glucose because insulin isn’t a druggable target. So, that’s an inconvenient clinical marker that can only really be moved by changing diet, and there’s no money to be made by telling a patient to change diet.

Cynthia: Yeah, well, working in cardiology as an NP for 16 years, I got to a point where I was truly at a breaking point. I said I can’t keep writing for statins, I can’t keep doing this when there’s an elephant in the room, every time I see a patient. Much to your point about insulin, it’s interesting. I had mine drawn like I do it once or twice a year, and my midwife didn’t know what to do with my numbers. She said, I’ve never seen an insulin of 2.

Benjamin: [laughs]

Cynthia: But she said, “I’m going to assume that you know what that means, and you’re okay with that.” I said, “Sure.” [crosstalk] also, in the setting of the age that I am and probably that my estradiol is not as high as it was 15 or 20 years ago, but I agree with you that the hard work is the lifestyle changes. Whether it’s cognitive dissonance, or apathy, or burnout, and I think there’s probably a combination of all of the above for many clinicians that are practicing right now. I think anyone that’s listening, you need to know what your fasting insulin is. You need to know that number, because that is a metric that you can track, you can improve, and much to your point that you made earlier, you’ve got to change what you’re doing. You have to change what you’re putting in your mouth, you need to get better quality sleep, you need to manage your stress. Those are all critically important. Especially for many of us that have children, it’s like, “I want to be healthy so that I can play with my grandchildren one day.”

Benjamin: Yep, that is one of my prime motivations. When the value of looking at insulin is now, you’re looking at a much more sensitive predictor, by the time the glucose is changing, your insulin has already changed 10 or 20 years before, so you can detect the problems much, much sooner. Then by addressing the insulin, you’re actually addressing the root problem. Because when you’re trying to fix glucose, you’re just addressing one of the manifestations of the problem. It’s like you’re trying to fix the hypertension or the cognitive decline, all of those are manifestations of one single problem, which is the elevated insulin. So, you’re getting so much more bang for your buck and getting a much more sensitive diagnostic marker.

But I liked that you mentioned the clinicians in a more favorable light. I don’t ever intend to just throw clinicians under the bus. That’s not fair to expect someone to know what they haven’t been taught. I don’t even mean to say that in a derogatory way as if I’m so clever, because I know this. No, I know one thing, and that is insulin. I know it really, really well, because I’m an academic. I can make a career out of knowing one thing. A clinician has to know a lot of things. They have a huge breadth of knowledge, and while they don’t go as deep as I am in one area, well, they can’t afford to do that, because that’s not as much as I love insulin. We can’t say that that’s the explanation for every clinical visit. It’s just, “Oh, check your insulin. Next patient, check your insulin.”

Cynthia: [laughs]

Benjamin: No, and I’m not suggesting that at all. But to the nurse or the doctor, he or she only knows what he or she has been taught or taught themselves. A physician doesn’t get paid to ask scientific questions. A physician gets paid to see patients. At the end of a long day where the physician just has to get the patients in and out, it’s just the way the structure is built. That’s the incentive or that’s the profit system. I get paid to do nothing but be curious. When we end our discussion, I can spend the rest of the day asking myself questions like, “Do we know exactly how vitamin D influences insulin resistance?” I need to look into that a little more and I get paid to do that. I don’t get paid very well, it’s not lucrative being curious. But it is still cool, and it’s not something that ought to feed my ego. Just because I know more about one topic than someone else, it’s not a source of ego for me. Truly, not at all. But it is something where I have an utter conviction that this does matter.

If the clinician, like everyone else, only knows what they’ve been taught, well, then let me teach you. Let me give you this little bit of education, and I know that there are others with me like you and others that are aligned in this effort. But that requires a little bit of humility and unfortunately, that is something that does tend to not exist in abundance the more educated someone gets, and that might even be myself. But the more degrees or the more terminal the degree after someone’s name, the less inclined we are to admit when we don’t know something.

Cynthia: Well, I think being a lifelong learner is something we should all strive for irrespective of what initials we have after our name or what our education is. I’m so very grateful that our paths crossed because you’ve definitely influenced, and on so many levels, influenced the way that I practice, influenced the things I talk about, influenced things that I discussed with individuals and talk about on social media. So, what’s next for you? What projects are you working on? I’m sure you’re probably getting out and doing more virtual plus virtual, probably more in person speaking opportunities. What’s new for you?

Benjamin: Yeah, so there are some opportunities at conferences at the end of the year. I don’t even remember what they are. But I’ll start doing those a little more, which I enjoy, of course. But in the lab, we have a couple projects that are cool. One is continuing to look at the effects of ketones on the bioenergetics of the hippocampus. The hippocampus is the part of the brain that’s involved in memory and learning. That’s what’s particularly compromised in Alzheimer’s disease. We have a rodent study, where we are really pushing up the ketones and detecting some of the changes in how the mitochondria are behaving in the hippocampus. The early results are pretty cool, and we’ll see when it’s all said and done, how the data all shake out.

We also have a study looking at these things called SARMs, S-A-R-M. SARMs, that stands for selective androgen receptor modulator. These are proteins that have been used to basically hijack one aspect of anabolic steroids. So, when someone’s taking testosterone or anabolic steroids, of course, they get big and jacked. But there are other consequences to that potentially, because testosterone does more than just tell muscle and bones to grow, and those are consequences that usually a person doesn’t want. However, there are situations where you want muscles and bones to grow like, say, in cachexia or the wasting away that happens with cancer. That’s the one context these have been used in.

We’re just looking at the degree to which these things that act anabolic steroids, but only act in muscle. We’re trying to see what they do to the mitochondria in the muscle just to get a better idea of the relevance for these molecules, maybe in cancer or maybe even in just general performance. These are regulated substances. I think that’s a little unfortunate, because there’s little question that they promote muscle growth quite well. I want to know a little more about that. So, that’s interestingly something that has nothing to do with insulin whatsoever. Maybe, we’ll find a connection to insulin, but at the moment, it’s just looking at the degree to which these selective androgen receptor modulators influence muscle growth and influence the way the mitochondria are behaving.

Cynthia: Well, that sounds fascinating. How can listeners connect with you? I know you’ve got an amazing– Your insulin IQ was something that I tried to catch on Facebook. You seem to be everywhere. Everywhere I’m looking, I see something that you are [crosstalk]. No, it’s great content, and you make it accessible, and I think that’s really important. It is easy to talk on a level that you’re just speaking with other scientists. It’s quite more challenging to take complicated concepts and make them concise and clear for the lay public or even for clinicians, because I’m not a researcher. I trained in a big research hospital, sat through many doctoral dissertations that my friends were providing. But for those of us that are not scientists, I greatly appreciate and value that you take the information and make it presentable.

Benjamin: I appreciate that. Thank you. In fact, I actually enjoy it. I genuinely enjoy that interaction of taking wonderfully relevant scientific ideas and making sure people appreciate them. That was the whole reason I got involved in social media in the first place. I’m mostly active on Instagram. People can find me there @BenBikmanPhD. I don’t do as much on Twitter anymore, which is funny, because that’s where I really started. Twitter is just not a place I enjoy anymore. A nice– [crosstalk] Yeah, it’s just such a hostile environment now, I just don’t care for it. I usually just use Twitter for getting updates on sports. [laughs] I hate to say it. I’m mostly active on Instagram, where a time or two a week, I try to put out a little video of whatever is on my mind about human health and human metabolism. Again, @BenBikmanPhD.

Then, I have two entrepreneurial efforts. One is Insulin IQ like you mentioned, which is just my effort with some others to create an online coaching platform that really works to get people through low carb diets. Then, the other is a website called Get HLTH and health is spelled H-L-T-H. No vowels in health part of it, gethlth.com. That’s a site where people can learn more about a low carb meal replacement shake that I designed. Actually, with a couple of my brothers, so, it’s a little family business. Anyone can go there, learn more about the shake, and I have blog posts that I put there every week as well. So, those are the entrepreneurial efforts, my social media efforts. At the end of all of it or what they all have in common is, I truly just want to convey information and some solutions to problems. So, try to make it as easy as possible.

Cynthia: Well, I’m so grateful for your contributions and to let you know that my 13-year-old really likes your vanilla.

Benjamin: Oh, good.

Cynthia: That’s his favorite. Because he’s a swimmer, he comes home and just eats a voluminous amount of food. That is oftentimes part of his post-recovery meal, and we will make sure that put all the links to all that as well as a discount that your team has graciously given us. [crosstalk] So, thank you again for your time, Ben, and we’ll connect again soon.

Benjamin: Yeah, my pleasure. This was great. Thanks so much.

Presenter: Thanks for listening to Everyday Wellness. If you love this episode, please leave us a rating, and review, subscribe, and remember, tell a friend. If you want to connect with us online, visit the link in the show notes.