Preview Mode Links will not work in preview mode

The Health Evolution Collective Podcast


Aug 22, 2020

TRANSCRIPT BELOW

What a treat getting to chat to this man! In this podcast you will learn where things are going wrong with our health today, and what we can do about it.

When we can understand the lever that is insulin - and thus insulin resistance - we gain back a lot of control over our own health.

In terms of the lipid values we talked about: In the US, values are expressed as mg/dl: Ben was talking that the ratio of triglycerides to HDL should be less than 1.5. In Australia, values are expressed as mmol/L, the ratio of trigs to HDL should be less than 0.87.

I encourage you to buy Ben's book: Why We Get Sick. It is an an excellent read, and while he is a Professor, he puts things in really easy to understand terms. A true gentleman and a lovely man in every way.

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.

You can find Ben on all channels of social media, and here on his website: BIKMANLAB.BYU.EDU.

********

http://www.traceymcbeath.com.au

tracey@traceymcbeath.com.au

Instagram: @tracey_mcbeath_healthcoach

Facebook: Tracey McBeath Health Coach

To purchase the Summit Replay: http://bit.ly/longweekendreplay

If you are a health practitioner and are interested in learning how to bring low carb in to your practice and reverse insulin resistance in your patients, the Nutrition Network has a number of programs to help. For GP's; Dietitians; Nurses and Health Coaches. The Nutrition Network is run by the Noakes Foundation. To learn more, click here: http://bit.ly/nutritionnetwork

 

Dr Ben Bikman (00:00):

It's suffice it to say, virtually every chronic disease has some connection to insulin resistance where the insulin resistance is either explicitly causing the problem, or it's exacerbating it, or accelerating the problem.

Tracey (00:13):

Hello everyone, and welcome to the health evolution podcast. This is episode 66 and you are so in for a treat today. What an amazing chat I had with the incredible Dr. Ben Bickman, who has so much knowledge. Not only that, he puts this knowledge into such easy to understand terms. So this whole podcast, is talking about why we get sick. It's the title of the new book he has recently produced, and I highly recommend that you buy this book. It is amazing, and there's so much information in here. So that's really what we're going to be talking about. And of course, looking at the fundamental cause of many modern diseases today, which is the fact that our insulin isn't working the way it should. And that's due to lifestyle, genetics, a whole range of conditions that we also talk about. So these are things like type two diabetes, some cancers, heart disease; a lot of stuff that in today's modern world, we attribute to other causes and we just treat the symptoms.

Tracey (01:19):

But when you look at the reasons and the causes of these diseases - insulin resistance being the number one, and you know that it's actually possible to reverse and turn that around with lifestyle changes, then this podcast holds so much hope. So enjoy it. And I'd like to say a huge thank you to my friend, Carmel, who was kind enough to reach out and offer to do the transcribing for these podcasts. So I will release the podcasts as I get them done. And then when Carmel has the time to do the transcript, she will do that. And I will add it in as soon as it's done. So thank you, Carmel. I love the community I'm involved in. Thank you to you for listening to the podcast. Please, you can do me a favor by rating, by making a nice comment and by sharing this podcast so we can help as many people as possible see the potential that is a health evolution .

Tracey McBeath (02:37):

Today on the health evolution collective I'm here with Dr. Ben, big Ben, what an honor to have you here on my show. Thank you so much.

Ben (02:45):

Oh, Tracey. It is my pleasure. Thanks for the thanks for the invitation.

Tracey :50):

Oh, absolutely. So I have been following you for quite some time now. I absolutely love the work you do, and the way you present it to people. It just is so easy to understand, and you give people so much; so much information to help them with their health. Before we get into your talking about your awesome book, 'Why We Get Sick', can you just share a little bit about, I guess, you know, you're a scientist and professor, but what's led you to writing this book, 'Why We Get Sick'.

Ben (03:20):

Yeah, again, thanks for the invitation and for the introduction. My focus as a scientist is in general terms, metabolic health, but it was a bit of an unexpected route. Although it didn't take me long to get on it, but my initial graduate work was focused on muscle cells. And I was curious about the process whereby a muscle cell, well, muscles would get bigger and better. But by the end of my masters degree, I was actually far more interested in fat cells. Around that time, a few years prior to me doing a masters degree, I had stumbled across this study that explored the endocrine features of fat cells. Basically it was this to me, a discovery that fat cells actually release hormones, release proteins, and that some of these proteins are pro-inflammatory proteins. And that at the time , was thought to be really the single variable in how someone could be obese, and that would start spilling into type two diabetes.

Ben  (04:23):

It was this obesity induced insulin resistance, which started as a research interest in muscle cells that quickly shifted to a research focus on fat cells. And now I'd say that it's really the tissue or the cells that I focus on most as a cell biologist, namely the fat cells. My focus now is, what are the variables that are stimulating growth of fate cells, the shrinking of fat cells, and fat cells behaving entirely differently; you know the metabolic rate difference. That means I focus a lot on the hormone, insulin, because you really can't understand a fat cell without looking at it, at least partially through the lens of insulin.

Tracey (05:11):

Now we are going to really understand what insulin is and the term insulin resistance. This is talked about a lot, but I think a lot of people don't really understand this. But before we do, can I ask you, people also talk about metabolic health and I've been guilty of that; you know, I had someone say to me the other day, what do you mean by metabolic health? What does that actually mean? Can you explain that a little bit?

Ben  (05:33):

Right. I suppose metabolic health probably has a different definition according to every kind of biomedical scientist or clinician. To me, I suppose the simplest definition of metabolic health would be that the person is insulin sensitive. But if that's still a little too vague, then I would say metabolic health would be someone having an OK grade, if you will, on the five variables that are conventionally used to indicate the metabolic syndrome. And so in other words, the metabolic health would be someone who has a normal waist circumference (so if they measured their fatness around their waist,) and then second, they have a normal blood glucose, and normal blood pressure. Then the last two are basically just normal lipid levels - normal triglycerides and HDL cholesterol. Those five variables constitute the constellation of what's called the metabolic syndrome. And so I suppose if we use that as a foundation, we could say in turn, well metabolic health then is being OK in all of those categories. But the truth of the matter is back to my original answer. All of those things are very much related to; insulin resistance when they go poorly, or if they're working well, then it's an insulin sensitive person.

Tracey  (06:54):

Makes a lot of sense. So obviously when we're talking about metabolic health, i.e. how our body can make energy, and how it functions, then when we can have those conditions (our body is not functioning optimally); we're tired, we don't have a lot of energy because our body is basically struggling to keep us well .

Ben  (07:10):

That's right. But something you said also prompted another thought, one other perhaps definition of metabolic health would be based on this idea of fuel or energy that you mentioned. So for example, well specifically that would be someone who has metabolic flexibility. At its simplest, it's just this idea that the human metabolism or our energy needs, can shift between the two primary metabolic fuels; that when we've eaten a meal, we go to a glucose burning or sugar burning, you know, blood sugar, that being the primary fuel that the body is using. And then several hours after eating, in other words, getting into this at least mild state of fasting, then we shift to predominantly obtaining most of our energy from fat. So we go to fat burning if you will. So this ability to shift from glucose burning to fat burning very readily when we eat and when we aren't eating, that is a good, also a good definition of metabolic health. But again, that idea is metabolic flexibility. But once again, even that can be seen through the lens of insulin in so far as insulin dictates what fuel we're using.

Tracey (08:19):

Okay. So let's learn about insulin. So I think firstly, what is its role? I know in the book you go into a lot of detail and I definitely encourage people listening to get the book and really understand it. But just in terms of a brief summary on this amazing hormone.

Ben (08:38):

Yes, it is amazing. And I think it really is unappreciated given how relevant it is in so much health and disease.

Ben  (08:46):

The most obvious effect or role of insulin is to control blood glucose. And that's how most people understand it. And that's okay. That's fine, because it is a very powerful influence. It is really the single hormone that will lower blood glucose. Whereas, there are multiple other hormones that will increase blood glucose. So it does its job well. Now it's helped with other processes in the body that can also act to lower blood glucose, but that is the most sort of poster child example of what insulin does, it lowers blood glucose. But the truth is far more complicated and that's because insulin affects every cell in the body. Literally every cell in our bodies has insulin receptors. So these little sites where the hormone insulin can come in and dock and bind and then tell the cell to do something.

Ben  (09:39):

And because every cell in the body has these insulin receptors and the various cells in the body play different roles, they do different things. It's not surprising that insulin will do different things at different cells. But the theme of it, the general theme across all of the cells of the body is that insulin tells the cells what to do with energy. It can not only stimulate the uptake of energy in most cells, but it will also then tell that cell what to do with it. And once again, the theme of that is, storage. Insulin wants to store energy and even to the point that it will lower metabolic rate in the body to help the body store more energy. So insulin abhors wasting it abhors breaking things down. It just wants to build things up, including fat in our fat cells and have it get locked away untouched by the body.

Tracey (10:34):

So without insulin, then obviously we wouldn't be here. If we think about our evolution in times of when food we had to hunt for it, today we don't have to do anything for it, apart from a walk to the supermarket. Without insulin, we wouldn't have got through winter.

Ben (10:50):

Absolutely. We would have no kind of metabolic insurance, if you will. We would have no energy storage, if it weren't for insulin. It is impossible, to my knowledge. For any organism, from fruit flies to humans, and every other less complicated organisms and humans, and more complicated organisms than fruit flies; insulin must be present and indeed elevated in order for that organism to store any energy. I don't believe it is possible in any other, without insulin. You take away the insulin and immediately this is an organism that loses its ability to store energy in any way, including energy in the liver. And very obviously, loses the ability to store any energy in fat cells.

Tracey (11:40):

Where has it gone wrong. So you talk in the book, well Jason Fung talks about how, you know, how this has changed so much over probably only really a few generations. I mean, it used to be, you know, we got sick, from dysentery and diseases and things like that. So how has it changed, and why has it changed and what does it have to do with insulin?

Ben  (12:02):

Right. We see obesity strictly through this calorie centric paradigm or perspective. So we look at the fat cell regulation only in the context of, is energy being used or stored, as if the fat cell is just the simple kind of bank account idea. It's just these deposits and withdrawals that are just happening passively. Almost as if the energy we eat it, just comes into the fat cell and comes out when we need it. But that is just not true. We are far more complicated organisms. In order to understand human obesity, I strongly believe we need to consider, yes energy, calories, but also hormones. If we take hormones out of this equation we are doomed, because then we just fall into this cycle of failure of trying to starve ourselves to weight loss. And to your point a moment ago, in this environment in today's world, hunger will always win.

Ben (13:05):

I stole this analogy from Gary Taubes, a very wonderful author. I'd recommend anyone ,after they read my book, go read some of Gary's books. They're wonderful, but he once shared this and then I stole it and I share it with my students. When I discuss obesity in my patho-physiology class, I present this caloric paradigm and then we start poking holes in it. I show them some of the data that challenges that it is just purely a caloric imbalance. I present this analogy, which is, that I'm having the best chefs in the world come to my home. Everyone's invited. I want you to come as hungry as possible. What would you do to make sure you came to this glorious buffet as hungry as possible? And invariably my hundred and 30 clever young undergraduates come to these two ideas.

Ben  (13:57):

And that is that they would exercise more in the time preceding the dinner and they would eat less. Exercise, more, eat less; these are the two pillars of the current dietary advice that we give people when we need them to lose weight, but hunger always wins. In this environment of readily accessible food, hunger will win. Now, I'm not saying there's no role for discipline and denial of indulgence. I do think that's very important, but I think we can help the person through that, by not forcing hunger on them all the time. And when someone realizes that, they can start leveraging, changing their insulin levels in order to favour this process. They don't have to be hungry; they can be eating in such a way that keeps their insulin down. You are then allowing the fat cells to share their energy, their fat ,with the body to be used and you also shift into that highest rate of fat burning and your metabolic rate, actual accounting for calories, which a caloric purist wants to do. The metabolic rate goes up even to the point where it can raise by almost 300 calories per day, if someone's eating meals that are keeping insulin low. So addressing the endocrine aspect of obesity, namely insulin, I think that the person really has a very effective tool that they now can use that they wouldn't have had otherwise, if they're were just focusing purely on calorie number.

Tracey (15:26):

Well, you've just really given us all a great reason to drop the belief that we have to be hungry in order to lose weight, because I see it every day. It's one of the biggest challenges with most of my clients, you know, getting them to see that we actually can lose weight. And in fact, we do it so much easier when we are not hungry. And it does come from manipulating insulin if you like, understanding it, working with it, working with those hormones in our body. It's a huge thing because I know certainly until I was 40, that's how I thought. And I was a personal trainer then, and I was continuing to spread that myth that it is about calories in calories out. And if you're not feeling hungry, you're not going to be losing weight. What a revelation to see, we don't have to do that.

Ben  (16:13):

The nuances with insulin and obesity, I certainly touch on that in my book, but there are some other wonderful books, including Jason Fung and Gary Tobbs that I would recommend anyone read to just get more of a well rounded idea of obesity.Because while I certainly touch on that, and I'm a fat cell scientist, I look at it more in the context of overall disease in the book.

Tracey (16:34):

Absolutely. So then what happens when things go wrong with insulin? And one of the scariest things I read, was that most people are actually walking around, not even realizing that insulin isn't working, that they have insulin resistance.

Ben (16:50):

It is, I consider it the most common or widespread disorder in the world. And so we are not only, not diagnosing it correctly, but we're also not appreciating its role in other diseases, which means we're missing the potential to treat a patient much, much better. And so basically with insulin resistance, the simplest definition, and you kind of mentioned this, it's just when insulin isn't working the right way at various cells in the body. Now at some cells , insulin's working perfectly fine, but at other cells it is not. And that imbalance actually becomes a problem. And we appreciate the fact that in a body that is insulin resistant, insulin levels themselves are much, much higher than before. So those two features come together; insulin isn't working the right way throughout the body, and insulin levels themselves or itself is much higher. So some cells that are continuing to respond to insulin normally now are hyperactive with their insulin.

Ben (17:54):

Insulin is now telling the cell to do too much, and the cell is sensitive to that signal, so it keeps doing too much. Then there other cells that aren't really getting the signal very well at all. So those two variables are what comes into play, making insulin resistance, the problem that it is. And in this, we could almost, as you know, from going through the book, it is shocking how many diseases, chronic diseases that we think would have no metabolic origins actually have at their core, an unavoidable metabolic origin. For example, the hyperinsulinemia that comes with the high insulin levels that someone has an insulin resistance. If we look at what that does to the ovaries in a woman, it's profound. The most common form of infertility in women, is a disease called polycystic ovarian syndrome.

Ben  (18:45):

The woman is going through the menstrual cycle. The ovaries are developing a lot of little eggs every month, but in order for all the rest of the eggs to go away, one of them must ovulate. And with that one egg ovulating from one of the ovaries, then all the other kind of budding little eggs will go away. But in the absence of one ovulating, all of those little eggs stick around and they become these big cysts in the ovaries. That problem happens because the woman doesn't get this big estrogen spike, which she needs immediately proceeding ovulation, this big estrogen spike, and one other hormone. Well, many hormones come into play, but estrogen spike is a big one. Too much insulin blocks the ovaries from making that big estrogen spike. Insulin inhibits the process whereby, in fact this is fascinating, but all estrogen hormones were once testosterone, the ovaries convert the testosterone into the estrogens.

Ben (19:43):

And this happens in men and women. Of course, in women, it happens more in women, thus having higher estrogen levels than men. But that one enzyme that mediates that conversion from testosterone to estrogens is inhibited by insulin. And so the woman who has insulin resistance and high insulin levels at her ovaries, the insulin is directly preventing that big estrogen surge, preventing ovulation. And as a background problem, when she has too much testosterone she'll start to have other problems like more coarse body hair, for example, or acne like you might have in an adolescent boy, who's going through a big testosterone surge. So that's a problem with the ovaries. When we look at the brain, some of the brain's energy comes from glucose from the blood, and insulin mediates some of that movement of the glucose into the brain.

Ben (20:36):

And so when the brain becomes insulin resistant, it can't get enough of its energy from glucose anymore. And so there's this kind of gap of energy. You know, the brain's energetic need is up here. Glucose used to give all of it to the brain, but now the brains become insulin resistant. And now we have this gap where the glucose can't meet the need, and the person starts to develop brain disorders, including Alzheimer's disease and including migraines, frankly, even migraines are looked at as a bit of an energetic deficit in the brain. So I could keep going. We can talk about muscles, bones, joints, liver, kidneys, eyes; it's suffice it to say virtually every chronic disease has some connection to insulin resistance where the insulin resistance is either explicitly causing the problem or it's exacerbating it or accelerating the problem.

Tracey (21:26):

So what I find interesting with what you're saying there, that there isn't a neat and homogenous condition. You know, it's not that you're either insulin resistant or you're not, it is a spectrum. And as you said, clearly it affects the body in different parts and in different ways. I just wanted to ask, is that kind of potluck. So if I was insulin resistant in the brain versus somebody else in their ovaries, is that a genetic thing? Is it just pot-luck? How does that work?

Ben (21:54):

Yeah. That's a great question. There could certainly be some instances of that happening, but that would be very uncommon. The common process would be that the fat cells become insulin resistant first. So there is no total consensus on this. So I'd want anyone to sort of take this with a grain of salt where I'm speculating a bit, but at the risk of sounding smug, it's informed speculation. So I think the fat cells become insulin resistant first, that's the first domino to fall, but then it starts bumping into the other dominoes or basically spreading that insulin resistance around throughout the body. And then what would cause someone to then have say, the ovaries get affected before the liver would, for example, if we take two organs that are just right around the same area; I don't know.

Ben (22:46):

I'm not sure what would predispose one, what the next issue would be versus the other. But in general, I think it would be safe to assume that the fat cells are the first to become insulin resistant. And as they become insulin resistant, they start leaking fat throughout the body and they start leaking those pro-inflammatory proteins that I mentioned earlier, these what's called cytokines. And those two things are really the key variables, the key parts of the equation that equals insulin resistance; the leaking of fat, the free fatty acids from fat cells and the fat cells leaking these pro-inflammatory proteins. As these start to spread through the body, they cause other tissues to become insulin resistant.

Tracey (23:27):

So that leaking of fat is that triglyceride marker, is it?

Ben (23:31):

So actually these fats would be the free fatty acids. So when the the fat cells are breaking down their fats, they are leaked as free fatty acids. The triglycerides are predominantly coming from the fat we make in the liver, which is again, another insulin signal telling the liver to make triglycerides.

Tracey (23:52):

Okay. All right. So what I'm hearing from you here is that insulin resistance, isn't just a risk factor for type two diabetes. We haven't actually really even touched on that yet. You've talked about all of these other conditions that insulin resistance is the precursor for be it, most people will tend to think that it's type two diabetes that is the biggest risk factor, or the only thing we're likely to get if we're insulin resistance, but that's clearly not the case.

Ben (24:22):

No, that's right. Yeah. In fact, it's far from a guarantee that the person would progress to full on type two diabetes. What is far more likely is that they would have hypertension, so high blood pressure, fatty liver disease. Then a woman would have polycystic ovarian syndrome; a man would have erectile dysfunction that's also a common early symptom or sign of insulin resistance. Yes. So waiting and that's part of the problem. And I do emphasize the word waiting. When we look at insulin resistance strictly through the lens of type two diabetes, it is unfair to the hormone insulin, which I believe is the more relevant one. And we shift our focus to glucose. But the tragedy of that perspective, if we look at all metabolic health, just through the lens of glucose, as if it's like a progression just towards type two diabetes; then we're only looking at the glucose and we fail to acknowledge the reality that behind the scenes underlying that normal glucose is this ever increasing insulin level where the body has to work harder and harder.

Ben  (25:28):

The insulin has to work harder and harder in order to keep that glucose in check. That is the insulin resistance. In other words, if we looked at the insulin, we would have detected the problem potentially decades, 10 or 20 years before the glucose would have changed, but we don't look at insulin. It has not made its way into just the common clinical diagnostic. When someone comes in for a conventional or just routine lab visit, we always measure glucose. We always measure the lipids. And I think those are fine. They certainly have value, but if we really want to detect insulin resistance, we've got to bring in insulin. We have to allow it into the discussion

Tracey (26:10):

We do. But as you say, it's not a standard test. In fact, just yesterday, a client told me that a doctor refused to check it, because I give a recommended list of what are their blood tests to go and ask for from your doctor, and one of them is fasting insulin. No, doctor wouldn't do it. When you understand what you're saying, that this is going to tell us what's going on with our metabolic health, 10 to 20 years prior to being diagnosed with type two diabetes. We know PCO for females that usually teenagers are getting that. And then of course, breast cancer is another one I know you've spoken about and being mostly women, listening to these podcasts, that's something I'd love to talk about as well but why is this happening?

Ben (26:52):

I know isn't it. Well, I often say that it was forgivable. It was forgivable that the focus was exclusively on glucose because of two reasons. One, traditionally the most obvious sign of diabetes was the excessive urine production, what we call polyuria. The person was just urinating gallons and gallons of urine every day. And that was because of the high glucose. And we knew that even early physicians hundred thousands of years ago, because the urine was enriched with the glucose. They'd see animals, dogs would want to come and lick up that glucose and the flies with just swarm to it, to eat all those sugars from the urine. And so the most obvious symptom, polyuria, was directly a result of the high glucose levels. And then the second reason why it was forgivable is that scientifically we were able to measure glucose from the blood far, far earlier than we could ever measure insulin.

Ben (27:51):

So we had the technology to measure this molecule when we did not have the technology to measure insulin. And even nowadays, as you just mentioned, it's getting the insulin measure is not a simple test. It is a full on blood test at the lab. It often incurs a cost that depending on the healthcare model or in the U S the insurance that a person has, it might not get covered. And so the physician may be reluctant. Even if the physician appreciates the value of insulin, they may be reluctant simply because they know the insurance won't pay for this. I can't bill it and the patient doesn't want to pay for it. Then I have to get in a fight with the patient. So it's unfortunate, but given how it is getting easier and easier to measure insulin, these costs are coming down. It's getting less forgivable to not measure insulin.

Ben (28:43):

Now I will say there is a poor man's method where if someone has gone into their physician and gotten, or the clinic and gotten a blood test, if they can measure their triglyceride, they will almost always get a triglyceride number and an HDL cholesterol number. And they can take at least in the U S in the milligrams per deciliter. I don't know how it would equate with Millie Mueller in Australia. But if it's looked at with milligrams per deciliter, it's 1.5. If the triglyceride divided by HDL cholesterol is less than 1.5, it is a strong indicator that the person is insulin sensitive. So even if they don't get their insulin measured, if they meet that or below that 1.5 ratio of triglycerides to HDL cholesterol, then they're very likely.

Tracey (29:30):

Fantastic. I will put that down below in the show notes for people and I'll work it out. I've got a couple of clients in the U S, so yes, it can get a bit tricky.

Ben (29:42):

I'm from Canada originally, so I should be able to actually do this fluently, but I can't. I'm too American now.

Tracey (29:47):

Well, of course. So just going on then, from what you were saying, you can get a blood test and looking at your triglycerides and your HDL is one great one. And of course we've got the HBA1C which is another good marker. But what would be some of the signs we might be looking for in our body to give us an indicator that maybe we are insulin resistant?

Ben (30:08):

Yeah, so I believe the most obvious often is hypertension. If a person has high blood pressure and, they are even a little overweight like they have a bit of a bigger waist circumference, very likely they need look no further. They're very likely insulin resistant. There are some other signs that we see in some people, which is changes in the skin, Where if the person has a little more fat on them, they'll have a little bit of a ring around the back of their neck. And that is the most obvious spot that can also happen on the armpits, but they will start to have two skin changes. And this is typically more advanced insulin resistance, but they will have these little skin bumps called skin tags. And they do kind of bump up like a little stalk almost, like a little column of skin. And then they will have a dark and thickened more rough skin. And that's a condition called [inaudible] anthesis nigricans. But basically it's that the skin gets kind of darker and rough. Now, of course, on a pale fellow like myself, that becomes quite obvious. On the darker, the complexion, the darkening of the skin will become harder to see, but the touch, the feel, the very coarse rough skin, that will, of course still be very obvious to the touch even to the site.

Tracey (31:31):

So there's some definitely clear markers, but again, we have to be aware of it. And also knowing that how much of what we carry on and think is normal, we put down to a normal part of aging. I've actually been told myself. I went to a local GP, I needed to just get some bloods done. And I asked for, I think it was just the HBA1C. He was like, what do you want that for; you're thin, you don't need to worry about anything like that. So this is the stuff I think people are up against when they do go to their doctor and ask for these types of things. But there's so much that we can do ourselves to see where we're at in terms of our metabolic health and not put it down to aging. Because so much of what we think is normal, is not normal and it can be reversed.

Ben (32:17):

Oh yes, yes. I absolutely agree. We should fight the good fight. We should not just look at our worsening metabolic health and just shrug our shoulders. There's too much to live for. There's too much to enjoy. Much of my motivation nowadays is I look at my little kids and first of all, I tremendously miss them not being babies anymore, but I'm already looking forward to them having babies. And they're still all young, but I'm thinking I want to be a really fit grandpa. But even if someone doesn't have that sort of familial motivation, if you will, it's just self-interest to want to just live healthy and then die. We don't want that prolonged morbidity of not being able to get up, not being able to do things we enjoy. And then having a miserable last 20 years of life just filled with pain and disease. No, we should fight it and then be healthy, fit up until the end and then have this, what we call a compressed morbidity. We get sick and die, you know, in months.

Tracey (33:19):

Yeah. That's what I want too, and I don't think people realize that this is what happens. You know, we're so clever in medicine at prolonging life. It's the quality of life that is just crap and extended and the impact that that has on the family. I think, you know, we have to look at all of that, them having to care for you, all the stuff they've got to do to look after you. You know, I think if we can take all that into consideration, we're going to be a little more motivated to go the hard yards, to do lifestyle change or change what we eat or do whatever it is that we need to do to help reverse this stuff. Even if it's hard, because it is hard, as we know, you. There's so many factors that come into it, but it's worth it. I'm with you, I just want to go. I don't want to have to go through 20 years of slow progressive, horrible stuff.

Ben (34:12):

No, but I like what you said. I totally agree. I love what you said though, where modern medicine technology basically allows us to live with disease. And that's a sad reality where now more than ever, it's an interesting kind of dichotomy. For example, if we look at heart disease, which I believe I'm sure in Australia is the same in the US, that is the leading cause of death. What's so interesting though, is that the number of people dying from heart disease actually has trended down a little bit, but the number of people with heart disease has spiked dramatically. And so we have more people than ever getting it, which is totally a result of our lifestyle, but because of modern technology, the person can live with it. And I think we almost disincentivize them from, like you said, doing the hard work to turn that around. We are increasingly a global culture that is really just interested in taking a pill, but no pill can cure a chronic disease. It can only treat symptoms. It can never fix it. And that is even more the case with insulin resistance and all the chronic diseases that stem from it. These are not diseases that are caused by the absence of a drug. These are diseases that are caused by poor lifestyle and thus lifestyle is either the culprit or the cure. We've just got to do the hard work to change it.

Tracey (35:40):

So I definitely want to talk about the lifestyle next, before we get into that, which is to the more, you know, what we can do about it. Can you just share a little bit for my listeners around the link between insulin resistance and something like breast cancer.

Ben (35:53):

Yeah. Right, right. And you mentioned that earlier. I should have mentioned it then. The risk of breast cancer, I don't believe the insulin resistance is causing the cancer, but there's no doubt that insulin resistance and bad glucose management is exacerbating. And by that, I mean, there was a study done in women where they compared a biopsy of normal breast tissue with a breast tumor. They found in the breast tumor, it had seven times more insulin receptors than the normal breast tissue did. That was part of the mutation that part of it that's in cancer. It is just a series of mutations that allow the cancer cell an advantage over the normal cells. It can grow better and faster. Insulin tells cells to grow. And so by having seven times more insulin receptors in the normal breast tissue, this tumor, we can conclude, seven times more responsive to insulin's growth signals.

Ben (36:52):

Now that alone is bad, but when we combine it with the high glucose that people have often, or at least constantly eating foods that turn into glucose in the blood, glucose is the fuel for cancer cells in tumors. If you look at human tumors, they use glucose as a fuel. In fact, their glucose use is roughly 200 times greater than normal cells. So these things have an incredible need for energy. And so in the case of insulin resistance, it's a perfect storm. We are giving them a lot of insulin, stimulating that growth to which they're more sensitive, very likely anyway, with more insulin receptors. And then we are fueling that growth by giving them all the glucose they want, because that is the only fuel like a bacteria. It is the only fuel a cancer cell can use. It exclusively relies on glucose as its fuel. So in the case of insulin resistance in breast cancer, we are giving the cancer, the tumor cell, all it needs.

Tracey (37:52):

Wow, and we've got a long way to go I think, for specialists to give that advice to women. I don't think it's common knowledge.

Ben (37:59):

Oh no, no, certainly not here. And I'm sure it's the same in Australia. The American cancer society, as much as ever is still promoting a low fat, high carbohydrate diet, rich with complex carbohydrates and whole grains. The reality is all that stuff turns into glucose. You can put a pretty little package on it and say that it's a whole grain. The intestines don't care, it digests it into the same glucose molecules that we get from any other source of starches and sugars , and the cancer cell doesn't care where the glucose came from.

Tracey (38:29):

So that's a nice way to move into what we can do about it then. So in terms of lifestyle change, food is obviously a pretty big one that we can ultimately at the end of every day or during every day, we choose what we put in our mouth. Now we may be driven by metabolic imbalances and, you know, addictions or sugar urges spiking through us, but there's certainly a lot we can see around that. So let's talk about your take on what we should be eating, I suppose, to give ourselves the best chance of having metabolic health?

Ben (39:00):

In fact, I, I like what you mentioned a moment ago, sort of alluding to this habit, or even dare I say addictions. And so the advice, I won't even call it advice. My sentiments on the best dietary changes in order to improve insulin resistance are simple, as I'll explain in a moment. But I wouldn't want any of your listeners to think I'm being condescending or smug when I say that, because while the ideas are simple, I fully understand implementing them is not so easy. And that's because we start dealing with addictions and namely, when someone is sitting around on a Saturday night, enjoying a movie at home, no one is sitting there thinking, Oh, I sure could use a plate of scrambled eggs. No, no one says that. What a wonderful world that would be. We are, or at least for me, I am craving something salty and crunchy or sweet and gooey.

Ben (39:55):

And each of those is going to be essentially built on some sugar and starch of some kind, you know, with some yummy fat thrown in there. And that combination is a wicked delicious one. So I appreciate anyone listening. I know these are not easy, even as long as I've been doing it, the little kind of addictions or the cravings that I just mentioned, I still feel that regularly. And it's just, there is that matter of willpower or even dare I say a support network, you know, letting your loved ones know what you're trying to do and genuinely soliciting their help, but that's outside my territory. Let me just stick with what I think are the scientifically sound principles. So first one is, to me, it is first for a reason because it is the most important and possibly the hardest. And that is control carbohydrates.

Ben (40:46):

Essentially someone just needs to be smart about their starches and their sugars. With regards to sugars, it's acknowledging the sugar when you're getting it, but people don't know. They might think they're cutting out sugar, but sugar is in virtually every condiment. I think over 70% of all packaged foods, there is sugar in there in some substantial amount. So we need to control the amount of sugar we're eating and, and then just be smarter about the starches we're eating. And basically the simplest idea there is to, focus on whole fruits and vegetables. And there's maybe a little more nuance there depending on how healthy the person is. But basically that's going to be a safe bet; focus on fruits and vegetables, dump everything else. Then the second idea is to prioritize protein, to make sure you eat enough protein that you feel satisfied and that you're meeting your body's genuine needs for protein.

Ben (41:44):

I don't want it this to sound controversial or smug or offensive; that can't come from plant proteins. Plant proteins are inferior in every way. I hate if that's an offensive idea to some, but it is quantifiably true . Plant proteins, neither have the right mix of amino acids, nor do they have the full availability even. So there are molecules in these plant proteins that directly inhibit our intestines ability to digest the protein. Anyone who's curious about this, look up molecules called tannins or trypsin inhibitors or fighting acids. These are found in all of the plant proteins and it is explicitly inhibiting our ability to break down those proteins from the plants. So it's a double whammy. We don't get the amino acid mix we want in the first place. And even second, we can't even get the ones we think we're getting because we can't digest the plant very well.

Ben (42:38):

So focus on the animal proteins, and the best way - egg white, and meat. Interestingly, the best proteins, and those that are the best proteins for humans, especially eggs, I should say, or dairy and eggs. Interestingly, those three best sources, dairy, eggs, and meat all come with fat. Fat - and so that's the third pillar. Don't fear fat, eat fat, enjoy fat, focus on natural or ancestral fats, namely fats from animals and fruits. The fruit fats are pretty much coconuts, olives, and avocados. And those are fats (the oils ) that you get just from pressing the flesh of the fruit; nothing to do with the seeds or pits. Nope. It's the flesh of the fruit that our early ancestors for thousands of years, all they needed to do was just step on them. And they would have started getting the oil from these, the flesh of these fruits.

Ben (43:33):

So they are ancestral. We are well suited to eat them. My point about fats and proteins coming together is relevant because there are studies to show that when you combine fat and protein together, you help the protein work better. So this one study in particular found that muscle growth was the highest when fat and protein were mixed and that was higher than protein alone. So there's something kind of doubly anabolic about that mix and fat helps the guts digest protein. I have had so many people tell me their stomach gets very upset when they eat just pure whey, like a, just a pure whey protein shake. Then I say to them, mix it with fat ,mix one to one fat to protein by mass, not by calorie, but by mass. So if you're getting 20 grams of whey, get 20 grams of fat with that whey.

Ben (44:26):

And when you eat fat , you have the release of bile acids from the gallbladder and bile facilitates those protein digestive enzymes. So you actually help the guts digest the protein better. So now you're getting more of the amino acids that you want. So those are the three pillars sort of refresh them or reiterate them; control carbohydrates, prioritize protein and don't fear fat. And then the fourth principle is don't be afraid to skip meals, basically intermittent fasting, or time restricted eating can be extremely effective.Then someone just needs to be smart, be deliberate about it. And I say that, because too often I see people who, almost look at intermittent fasting as a glorious form of bingeing and purging. And I don't mean actually like bulimia, but they will wait all day and then eat a big dinner. And they got so hungry.

Ben (45:16):

They overeat, they indulge in junk food because they let themselves just get too hungry. They didn't plan well. And then they feel such remorse. They feel so full and they sleep so poorly that they wake up the next day saying I'm going to fast all day. And then they do the same thing. They get to dinner. They they've gotten too hungry. They overeat. And I say this because I have seen that tendency in myself, where I end up using intermittent fasting as a crutch to indulge and behave in bad eating habits.But again, it can be extremely effective. I'm an enormous advocate of it, but a person needs to be smart about it. It's not just something I do. I don't believe there's a lot of value in just shrugging your shoulders and say, I'm going to fast and not have a plan for how you end the fast. In fact, I dare say how you end the fast is the most important part of the fast

Tracey (46:09):

There's so much in there, how fascinating. I would have asked you about the plant versus animal protein anyway, because I mean, I'm a huge advocate of animal proteins. I've looked into it so much. I've had so many amazing people on this show. You just peel it back. We're not talking about ideology here. We're talking about physiology and what our body is optimum on. And when we understand it from that perspective, it's all so much easier. Of course, it's all those other layers as we know around it. But at least for us to make decisions around what to fuel our body, it's much easier to do when we understand what is going to be optimum and what we're going to get the most out of when we do eat.

Ben (46:53):

Yes and true. In fact, I look at plant protein as a bit of a racket, and I say this with some informed experience. When a couple of my older brothers and I wanted to make a low carb meal replacement shake, we talked about (my brothers not being scientists), said we should look at P protein. That's because it's, it's just such a commonly used protein. And I would want a listener to know, they should be very cynical when they look at the branding on a meal replacement shake or a protein shake because P protein or any of the plant proteins are a fraction of the cost of animal proteins. They are so cheap, but you can see the incentive from a manufacturer or the company. They can, one, buy a protein that is very, very cheap, and then two, they can kind of virtue signal.

Ben (47:43):

They can brag about how they have plant proteins. These are not animal proteins. These are plant based proteins. Nowadays, people are so seduced by that idea, where, kind of pop culture is just waging war on our omnivorous nature as humans, our absolute undeniable evolutionary reliance on animal products. Now it's like, we're ashamed of that. We're doing everything we can to walk away from our absolute natural biology. And so they want to brag about how it's, plant-based. That's nothing to brag about. It is not healthy for the individual. It is not healthy for the planet, (that's a bit beside the point), but it also just creates a wonderful profit motive or incentive for the company. They can make a lot more money off of you , by selling junk.

Tracey (48:34):

Yes. People like Diana Rogers from Sustainable Dish, that fantastic book she released. I mean, there's so many great people doing great things to show sustainable farming is actually going to help the planet. So again, what we're up against is dogma and misinformation. And, you know, I think we have to just be cynical; exactly what you said. We've got to come across everything with a cynical perspective. But it can be very, very hard, can't it for the lay person to know what to believe and to know what's true. People are saying black and white. No, there'll be someone that will say plant, but no you're wrong. Plant based is optimal.

Ben (49:11):

I know. And I absolutely appreciate that. I have nothing but genuine compassion for people that are struggling with this. And indeed, even for people that they may know, the fact that humans are omnivores and yet they still have a conflict in them, this ethical dilemma of eating an animal. There's something sad about that, but it doesn't change the reality of our world, and this is cliche to say, but something must die for something to live. Even the plant that person is eating, that plant grew from the nutrients that came from dead things. And that dead thing once lived because of the nutrients that came from a plant. It is an undeniable reality of our world. And so for those of us that embrace this omnivorous nature of humans, of our species, I do think at the risk of sounding silly religious or philosophical; I do think there's something to be said for appreciating the life that is lost for ours to go on.

Ben (50:13):

I think there's something beautiful in that reality of acknowledging this was a death and it was necessary because I need to live. My family needs to live. We shouldn't be ashamed of that. We also, I think should acknowledge it. I do think there's something beautiful, acknowledging that I. I want my children to know that an animal dies. When we buy our meat from a local, (it's a professor actually in a different department here in my campus at my university, we buy all of our beef from him), I want them to know that this was a real animal and it died for us and that's okay. It's okay that that happened. But we can also feel a little sad, but grateful.

Tracey (50:56):

I absolutely love that. I think, that's fantastic. And it just puts another perspective on it. I think it's very easy to lose sight of that evolutionary omnivorous nature that we've come from, is to say, that we never have to hunt for food, we never have to be in a position where we're starving now. We have that luxury, most of us in the Western world. Of course not all the world has that luxury, but in the Western world, we can just go to the supermarket. There's no understanding of the processes behind that anymore. And I think that is important, that gratitude, and to understand where it's coming from in all this conversation. There's not enough of that around. So thank you for saying that.

Ben (51:36):

Yeah. Yeah. Sure, sure. That's it's the dad in me. I have to say it's part of my dad routine.

Tracey (51:41):

How many children have you got?

Ben (51:43):

I have three, three little babies, a13, 10, and seven. It's everything. I would just say as much as we're spending all our time right now, talking on science and that's appropriate. It's why I'm interesting. All of this, this career, it all serves one end, which is to provide for my wife and my children. So I am number one, husband, father far, far, number two is scientist professor.

Tracey (52:06):

Oh, I love it. Well, husband, father, I probably should let you get back to your family. Thank you so much for sharing. It's been such a pleasure. I have loved every second. I could ask you a million other questions, but I will let you go. And of course, please everybody buy Dr. Ben's book, because there is so much in there that can really empower you to make the choices that you need to make for your health. There is just is. Please buy it and thank you for coming on.

Ben (52:38):

Oh my pleasure. Thanks again for the invitation. I had a really, really great time.