The Art of Manliness - Why We Get Sick

00:00:00.000 I'm Rhett McKay here, and welcome to another edition of the Art of Manliness podcast.

00:00:11.140 Cancer, Alzheimer's, heart disease, diabetes, infertility.

00:00:15.360 While these prevalent and dreaded diseases are caused by multiple factors, my guest says

00:00:19.080 they also all share a common thread, a ubiquitous and too little understood condition called

00:00:23.960 insulin resistance.

00:00:25.140 His name is Dr. Benjamin Bickman.

00:00:26.600 He's a professor of biology and physiology, an expert in obesity and metabolic disorders,

00:00:30.780 and the author of Why We Get Sick, The Hidden Epidemic at the Root of Most Chronic Disease

00:00:34.820 and How to Fight It.

00:00:36.060 Ben begins our conversation by explaining insulin's role in the body, how it goes awry when it

00:00:40.180 comes to type 1 and type 2 diabetes, and how giving type 2 diabetics insulin to treat their

00:00:44.440 disease actually makes them, in Ben's words, fatter and sicker and kills them faster.

00:00:48.720 We then turn to the fact that even if you don't have diabetes, you very likely still have insulin

00:00:52.700 resistance.

00:00:53.160 Now, something to help keep in mind during this conversation is that insulin resistance

00:00:56.620 is bad and insulin sensitivity is good.

00:00:59.260 We also talk about the condition's three primary causes.

00:01:02.180 Ben then unpacks how insulin resistance correlates with cancer, obesity, cardiovascular disease,

00:01:06.700 reproductive health problems, including the fact that erectile dysfunction isn't a function

00:01:10.420 of low testosterone, but insulin resistance.

00:01:12.880 We then talk about the role of insulin resistance in someone's susceptibility to COVID-19.

00:01:17.040 We enter a conversation with the four pillars of reversing insulin resistance, including

00:01:20.480 the role of diet and physical activity, and how these lifestyle changes can work to help

00:01:23.960 relatively healthy people get healthier, all the way up to allowing type 2 diabetics to 0.55

00:01:27.800 get off their medication.

00:01:28.960 I can't tell you how motivating this conversation was for me to start walking more during the

00:01:32.560 day, especially after dinner.

00:01:34.600 I bet it'll have the same effect on you.

00:01:36.360 After the show's over, check out our show notes at awim.is slash sick.

00:01:40.420 Ben joins me now via clearcast.io.

00:01:42.480 All right, here we go.

00:01:56.160 Benjamin Bickman, welcome to the show.

00:01:57.980 Thanks so much, Brett.

00:01:58.700 I'm delighted to be able to chat with you about all things metabolism.

00:02:01.660 Well, so yeah, you are a professor, a scientist of diabetes and obesity, and you wrote a book

00:02:07.880 called Why We Get Sick, which you discuss a disease that's connected to both diabetes and

00:02:13.460 obesity, and we'll see here in a bit a lot of other diseases as well.

00:02:17.720 The problem with this disease, it's extremely prevalent, but doesn't get much attention,

00:02:21.280 and it's called insulin resistance.

00:02:23.440 So I think to understand what insulin resistance is, you got to understand what insulin is.

00:02:27.880 So I'll start off there.

00:02:28.820 What is insulin?

00:02:29.720 What does it do in our body?

00:02:30.720 Where does our body make it?

00:02:32.720 Yeah, it's a great place to start.

00:02:34.280 Yeah, insulin is a hormone that is flowing through the blood all the time.

00:02:38.500 It's made from these little cells in the pancreas, and unless a person is a type 1 diabetic,

00:02:44.780 then they have beta cells in their pancreas that are producing insulin all the time.

00:02:49.620 And I do mean all the time, whether you're eating or whether you're fasting, there's some

00:02:53.480 amount of insulin always coming out.

00:02:55.560 Of course, it's higher when you're eating and much lower when you're fasting, but insulin's

00:03:00.580 effect is quite robust.

00:03:02.280 It literally will affect every single cell in the body.

00:03:06.860 Every cell in the body has these things called insulin receptors, which are kind of like doors

00:03:11.980 on the cell that only insulin can knock on.

00:03:15.660 And because every cell has insulin receptors and every cell has a different function in the

00:03:20.680 body, it's no surprise then that insulin does a lot of different things at different cells.

00:03:26.120 But if we were to create a theme of insulin's effects throughout the body, I think it would

00:03:33.380 be best described as insulin tells a cell what to do with energy.

00:03:38.740 And then relevant to that is its effects or is its most famous effect, namely what it does with

00:03:44.560 glucose levels in the blood, where when blood sugar levels or glucose levels are going up,

00:03:49.620 insulin will come in and save the day because if glucose levels stay elevated for too long,

00:03:54.960 that's lethal.

00:03:56.320 And so insulin saves the body by essentially knocking on the doors of certain cells that

00:04:01.940 will then open to allow the glucose to come rushing in.

00:04:05.340 Now, not all cells need insulin to tell them to take in glucose, but some of the big ones

00:04:10.500 do like muscle cells and fat cells.

00:04:12.500 And so that's insulin's most famous effect.

00:04:15.320 And unfortunately, that's partly why insulin resistance itself has become such a problem,

00:04:20.020 though I won't get ahead of myself.

00:04:21.600 All right.

00:04:21.760 So insulin is a hormone that knocks on doors of cells and say, hey, let this energy in.

00:04:27.420 So you mentioned people with type 1 diabetes.

00:04:29.900 Their pancreas doesn't produce insulin, and so they have to take artificial insulin.

00:04:34.220 So what would happen?

00:04:35.220 Maybe this will help us understand the importance of insulin.

00:04:37.980 What happens when your body doesn't make insulin?

00:04:42.500 Yeah, yeah.

00:04:43.420 So that is very lethal, which is why a diagnosis of type 1 diabetes 100 years ago, well, a little

00:04:49.760 more than 100 years ago before insulin was used or discovered as a therapy, it was lethal

00:04:54.980 within weeks to months.

00:04:57.000 Very usually, it'd be very rare to live a couple years with it.

00:05:01.000 And that's just because the body essentially doesn't know what to do with energy.

00:05:05.360 And this is very powerfully affected where you can have a person with type 1 diabetes,

00:05:12.500 and in the absence of insulin, because they're not making any, they will have a voracious

00:05:17.120 appetite.

00:05:18.300 They are eating thousands and thousands of calories, 4,000 or 5,000 or 6,000 calories a

00:05:22.720 day, and yet their body doesn't know what to do with the energy, and so the person is wasting

00:05:27.960 away.

00:05:28.540 They look like they are an emaciated prisoner of war.

00:05:32.240 And yet, again, they're eating several times what their actual caloric needs are.

00:05:36.640 They should have ample fat.

00:05:38.120 They should have robust muscles and bones because there's all that energy.

00:05:42.180 But in the absence of insulin, the cells don't know what to do with it.

00:05:45.760 What are the, okay, if it's, they're eating all that 5,000 calories, 6,000, but they're

00:05:49.560 not storing it or it's not going to the cells, where does it go?

00:05:52.340 Yeah, yeah, yeah.

00:05:53.080 So this is, we're really diving in.

00:05:54.860 This is actually now touching on a bigger debate and a bigger topic, which is what is

00:05:59.420 the root of obesity?

00:06:00.500 I mean, we're kind of alluding to this, although maybe not explicitly, where there's this idea that

00:06:05.620 obesity is purely a metric or purely determined by caloric balance.

00:06:11.460 And based on caloric balance, these people should be gaining weight or at least maintaining

00:06:16.780 body weight.

00:06:18.000 But it introduces the complexity of obesity and weight management, which is that, yes, energy

00:06:23.140 matters, calories matter, but so too do hormones and specifically insulin.

00:06:27.920 So to reconcile this kind of the thermodynamics of the untreated type 1 diabetic, or in other

00:06:34.640 words, the body with no insulin, we have to appreciate that there are inherent wasting

00:06:38.840 mechanisms that start to take care of this.

00:06:41.220 And I just can think of three, and hopefully I can elaborate these as I come through them.

00:06:46.200 One is that metabolic rate itself is going to be much higher than it should be.

00:06:50.740 And this is very well documented, and we've known this for well over 100 years now.

00:06:55.880 Some of the most legendary physiologists in the early 1900s, and they really were legends

00:07:01.500 in their field, they identified that the metabolic rate in diabetes was about 20 to 30% higher

00:07:08.140 than it should be.

00:07:09.840 And so this touches on even studies that my own lab has contributed to in recent years,

00:07:15.100 finding that insulin has a depressing effect on metabolic rate.

00:07:18.760 It will literally slow the action or the rate at which cells are doing their work, which

00:07:24.920 is in some metabolic rate as we define it.

00:07:28.500 So they have a much higher metabolic rate than they should, so they're burning several

00:07:32.220 hundred more calories than they should.

00:07:33.960 They also have a wasting mechanism built in with regards to the excess glucose, that when

00:07:40.140 glucose levels are chronically elevated, and this touches on what I said a moment ago with

00:07:45.160 regards to chronically high glucose being lethal, you overwhelm the kidney's ability to keep

00:07:51.700 all of that glucose in the blood.

00:07:53.680 And now you start spilling glucose into the urine, and that starts pulling water with it,

00:07:58.680 which is why the untreated type of diabetic has such a high urine production.

00:08:02.560 But it's that loss.

00:08:03.580 I mean, the person's losing a few hundred calories or so of glucose in the urine.

00:08:07.800 And then the last part is what's happening with fat metabolism and the production of ketones.

00:08:14.320 When insulin is absent or low, the body is in an exaggerated state of fat burning.

00:08:20.660 And that sounds kind of like pop culture language in a way, and I don't mean for it to, fat burning

00:08:27.620 versus sugar burning.

00:08:29.060 But glucose or sugar and fat are the two primary fuels for the body, and insulin is what dictates

00:08:34.860 which fuel is primarily being used by the body.

00:08:37.760 If insulin is elevated, the body is primarily using glucose, or as I like to say, sugar burning.

00:08:43.500 If insulin is low, the body is primarily burning fat, or fat burning, of course.

00:08:48.240 When the body is in that fat burning state for a prolonged period, but roughly what could

00:08:54.280 happen within the span of a day, it's burning so much fat, it's burning more than it needs.

00:08:59.060 And this excess, if you will, is what is converted into ketones.

00:09:03.440 So ketones are essentially the byproducts of fat burning, but they do have a caloric value

00:09:08.920 roughly comparable to that of glucose.

00:09:11.440 And in ketosis, or in this state, it's gone beyond just mild ketosis.

00:09:15.300 This is ketoacidosis, where there's 10 times more ketones being produced than the average

00:09:21.100 person could ever get to, because the average person will always have some insulin.

00:09:25.380 But be that as it may, the untreated type 1 diabetic has an incredibly elevated rate of ketone

00:09:31.260 production or ketogenesis.

00:09:33.000 And when it gets to a point, now they are, once again, wasting this energy.

00:09:37.460 Again, ketones have a caloric value that we would say, well, do you have to store the calories

00:09:42.360 or you have to burn them?

00:09:43.640 Well, in this case, you're just dumping them from the body like the person is with their 0.70

00:09:47.120 glucose.

00:09:47.740 And the person is excreting ketones in the urine at a very high rate and excreting ketones

00:09:53.060 in their breath.

00:09:53.740 And again, that means every time the person's exhaling, they are literally exhaling molecules

00:09:59.460 that had a caloric value.

00:10:01.500 And so there are these built-in mechanisms to sum it all up.

00:10:04.360 It's the changes in metabolic rate, the changes in ketone production and ketone wasting, and

00:10:08.780 the changes in glucose wasting through the kidneys.

00:10:11.580 All of these allow us to appreciate the absolute necessity of insulin in storing energy.

00:10:19.400 And I don't just mean fat cells.

00:10:20.920 You could say that we're storing energy by helping muscle cells form protein and bones

00:10:27.060 form protein and helping the liver know what to do with energy, creating lipids to be stored,

00:10:33.660 for example.

00:10:34.240 The liver can't do that if insulin's not there to tell it to.

00:10:37.380 So this is, as I mentioned, of course, touching on the bigger topic of obesity and weight

00:10:42.260 management.

00:10:43.100 But if we just bring it back to the diabetic, it certainly, once again, is proof positive

00:10:48.200 that while calories certainly matter when it comes to having a body that can store energy

00:10:53.420 and be healthy, it needs a signal to tell it what to do with the energy.

00:10:58.440 Okay.

00:10:58.760 So type 1 diabetics, if your body doesn't have insulin, your body basically isn't going to

00:11:02.840 use that energy you give it through food.

00:11:05.020 It's just going to expel it because it doesn't know what to do with it because there's no

00:11:08.420 insulin to knock on the doors of cells.

00:11:10.300 So let's talk about insulin resistance.

00:11:12.400 So these are people who their body is making insulin, but for whatever reason, the insulin

00:11:17.960 is no longer, like the knocks aren't working as effectively.

00:11:22.940 So explain in simple terms, like what happens?

00:11:25.740 Like how does insulin resistance happen?

00:11:28.460 Yeah.

00:11:28.820 Yeah.

00:11:29.360 Yeah.

00:11:29.580 Awesome.

00:11:30.180 Wonderful.

00:11:30.840 Yes.

00:11:31.080 It's an interesting kind of paradox because if we were just comparing now the untreated type

00:11:36.420 one diabetic where there's no insulin, it would be tempting to conclude, well, if insulin

00:11:41.160 isn't working right, which it isn't in insulin resistance, then they should have the exact

00:11:46.400 same symptoms or same consequences, right?

00:11:49.200 It should be the same, that no insulin should be comparable to insulin not working.

00:11:53.480 But in fact, it doesn't play out that way at all because insulin resistance is just

00:11:57.800 a little more complicated than that.

00:11:59.900 So insulin resistance to define it is, I think the best analogy is like a coin that I'm holding

00:12:05.320 in my hand between my thumb and my index finger, a coin.

00:12:08.760 And I call this coin insulin resistance, the coin itself.

00:12:13.020 Now, this coin has two sides and there are two aspects to insulin resistance.

00:12:17.320 One is, as the name suggests, insulin isn't working the same way that it used to.

00:12:23.740 Now, the complexity there or the nuance is that that is not to say that every cell is failing

00:12:31.200 to respond to insulin.

00:12:32.460 If that were the case, then insulin resistance really would just be another, would be identical

00:12:37.840 to the untreated type 1 diabetic.

00:12:40.300 That is not the case.

00:12:41.900 And so by insulin resistance at the level of the cells, we have to more accurately say,

00:12:47.120 insulin isn't working the same way at some cells.

00:12:51.800 And that's important because while some cells are insulin resistant, like some fat cell effects

00:12:57.240 or some muscle cell effects, it's not even global within the cell itself.

00:13:01.520 It's some of insulin's effects may be compromised in some cells.

00:13:05.540 But in those very same cells, some of what insulin is telling the cell to do can continue

00:13:09.660 to operate just fine.

00:13:11.500 And in fact, the liver represents a tremendous example of that.

00:13:14.920 The liver, insulin will normally tell the liver to inhibit ketogenesis. 0.70

00:13:19.620 In other words, block the production of ketones.

00:13:21.440 Well, insulin can tell the liver to do that always, whether the liver is insulin sensitive

00:13:26.780 or insulin resistant, insulin always is able to inhibit ketogenesis.

00:13:31.380 In contrast, on the insulin sensitive liver, insulin would tell the liver to store glucose 0.92

00:13:37.100 as a molecule called glycogen.

00:13:39.380 It basically is telling the liver, hey, we got a lot of glucose in the blood.

00:13:42.480 I need you to pull it in and store it for later use.

00:13:45.200 But when the liver is insulin resistant, that doesn't happen anymore.

00:13:48.760 And now, in contrast to the liver storing glucose as glycogen, it's breaking down the

00:13:54.380 glycogen, releasing that stored glucose into the bloodstream, increasing the glucose even

00:13:59.660 more, which makes insulin have to work harder.

00:14:02.360 And now we're just self-perpetuating the problem or becomes a vicious cycle.

00:14:07.120 So that was the one side of the coin, that some cells are failing to respond to insulin

00:14:11.360 like they should.

00:14:12.520 The other side of the coin, and this is very important, is that blood insulin levels are

00:14:17.320 elevated.

00:14:17.760 This is a condition that we call hyperinsulinemia.

00:14:21.340 But this matters, especially because of the cells that still respond to insulin.

00:14:27.040 Because remember, only some of the cells have become insulin resistant.

00:14:30.800 Many of them still have a normal sensitivity to insulin.

00:14:34.140 They've never become insulin resistant.

00:14:36.100 Now they're simply suffering because there's too much insulin telling them to do too much.

00:14:40.680 And the best example of that, among many, is what happens in the ovaries of women.

00:14:45.840 Insulin will normally inhibit the production of estrogens from testosterone.

00:14:52.280 So it's a little known fact that all estrogens in men and women come from androgens, you know,

00:14:57.760 and testosterone being the prototypical androgen.

00:15:00.980 So there's this conversion from androgens to estrogens.

00:15:03.560 That's how it always happens.

00:15:04.620 In the ovaries, it happens more than it does in the testes. 1.00

00:15:07.260 But insulin inhibits that process.

00:15:10.460 And so now the ovary, who has perfect insulin sensitivity, is flooded with the insulin that

00:15:16.480 is rising in this condition called insulin resistance.

00:15:20.700 And so there's too much insulin inhibiting the production of estrogens too much.

00:15:24.560 And thus, her ovaries are releasing too few estrogens to maintain a normal ovulatory cycle. 1.00

00:15:30.940 And unfortunately, too many androgens for her body, giving her, say, the acne or the excess body 0.73

00:15:37.120 growth that comes along with polycystic ovary syndrome or PCOS.

00:15:41.640 Okay.

00:15:42.240 So just to summarize there, what's going on?

00:15:43.980 So insulin resistance, some cells, it's whenever there's too much insulin, some cells become

00:15:48.660 basically desensitized to it.

00:15:50.360 Not all cells, some cells.

00:15:51.620 And then as a consequence, the body makes more insulin to compensate for that.

00:15:56.980 And that can become another problem, like you said, on the other side of the coin, because

00:15:59.740 some cells that have no problem with insulin insensitivity get flooded with insulin, and

00:16:05.440 that can cause cascading problems.

00:16:08.760 Did I get that right?

00:16:09.520 Perfect.

00:16:09.980 Okay.

00:16:10.660 So I think when people have heard, talked about insulin, they typically see it connected with

00:16:17.080 blood glucose.

00:16:18.000 And that maybe they are a type 2 diabetic, or they're told by the doctor, you have pre-diabetes

00:16:24.260 because your blood glucose level is too high.

00:16:28.400 You make the case in your book that blood glucose is a useful marker, but you make the

00:16:34.640 case that it's probably more useful to focus on insulin levels as opposed to blood glucose

00:16:40.440 levels.

00:16:40.780 Why is that?

00:16:42.600 Yeah.

00:16:43.020 Yeah.

00:16:43.420 I'm so glad you're allowing me to elaborate on this because it's something, it's sort of

00:16:47.660 one of my missions and my professional mission in life.

00:16:50.720 My main mission, of course, is to be a good husband and father.

00:16:52.780 My professional mission is to spread the word of insulin.

00:16:56.120 So yeah, glucose has become the focus in any conversation of metabolic health.

00:17:00.500 And any invoking, any invocation of insulin almost always still will do so with a primary

00:17:08.680 focus on glucose.

00:17:10.440 And I think that is what has led us down the problematic path that we find ourselves on.

00:17:16.940 So as you and I both said now, one of insulin's, well, insulin's most famous effect is what it

00:17:23.020 does to blood glucose.

00:17:23.960 But that paradigm, that glucocentric paradigm is what has, again, put us on this problematic

00:17:31.580 path.

00:17:32.760 And it's best viewed temporally.

00:17:35.380 So if we look at an individual who's living their lives and living his or her life through

00:17:39.660 over the years, let's say this fellow is progressing towards type 2 diabetes.

00:17:45.020 And the fact is most of us are.

00:17:47.100 And over these years, he's becoming more and more insulin resistant.

00:17:51.320 And so if we had these two variables that we were tracking, we have glucose that we can

00:17:56.880 track and we have insulin that we can track.

00:17:58.920 What's been happening over these years, and this is a process that can go on for decades,

00:18:03.360 the insulin is climbing.

00:18:05.180 It's getting ever higher, higher and higher and higher, but it's working well enough to

00:18:09.980 keep the glucose in check.

00:18:12.760 And so every year, the patient's coming in for a visit and they're gaining weight.

00:18:16.780 They may have hypertension, high blood pressure.

00:18:19.380 They may have infertility.

00:18:21.680 And because the glucose is staying normal, the physician is simply prescribing an antihypertensive

00:18:27.820 medication or here's a fertility medication, not knowing, because our paradigm doesn't allow 1.00

00:18:34.240 a focus on insulin, that insulin has been waging this silent war behind the scenes for 10 or

00:18:38.780 20 years.

00:18:39.900 And then it's only when the body becomes so resistant to its own insulin, even though it's

00:18:44.020 swimming in a sea of it, that now the glucose starts to climb.

00:18:47.560 Insulin simply can't keep the glucose in check anymore, reflective of this growing insulin

00:18:53.260 resistance.

00:18:54.340 And now the glucose starts to climb.

00:18:56.360 And then 10 or 20 years later, we finally detect the problem.

00:19:01.440 And again, you can see the tragedy here.

00:19:03.780 We've detected the problem much, much later than we should have if we had been looking

00:19:07.860 at it through an insulin-centric paradigm.

00:19:09.960 And so, in other words, insulin is a much more sensitive marker, a much earlier indicator of

00:19:16.320 metabolic disarray.

00:19:17.600 But the tragedy in that paradigm persists when it comes to treatment because now the patient

00:19:22.820 who has this mounting blood glucose level, very often they are given insulin as a therapy.

00:19:29.640 And already I'm sure the listeners can see the problem with this.

00:19:32.480 I just described this person's situation, which is that they're swimming in a sea of insulin,

00:19:36.820 and now the glucose starts to climb.

00:19:38.880 This is not a disease of insufficient insulin.

00:19:41.980 It's a disease of too much insulin, and we've become too resistant to it.

00:19:45.800 But the traditional paradigm is that it's a glucose disease.

00:19:49.460 So they will, the average clinician, look at the rising glucose and say, well, you know

00:19:54.280 what, here's insulin.

00:19:55.240 Just take some insulin, and this will push the glucose down.

00:19:58.040 And it will.

00:19:59.060 It does.

00:19:59.740 By putting the type 2 diabetic or the person who's moving towards type 2 diabetes on insulin

00:20:04.380 as a therapy, it will help lower their glucose.

00:20:07.620 But the tragedy is not a single clinical outcome improves once we put a type 2 diabetic on insulin.

00:20:13.500 And in fact, the more aggressively we give them insulin to lower their glucose, they become

00:20:17.680 three times more likely to die from heart disease and twice as likely to develop Alzheimer's

00:20:22.620 disease, twice as likely to die from cancer.

00:20:25.480 And they gain a significant amount of weight.

00:20:27.180 They gain about 20 pounds in six months.

00:20:29.260 So when we do this, when we ignore the insulin, and we give them even more of what they already 0.96

00:20:35.560 have too much of, then we make them fatter and sicker, and we kill them faster. 0.74

00:20:40.260 Because this is not, it's not a glucose disease.

00:20:42.320 It's an insulin disease.

00:20:43.720 Okay.

00:20:43.880 And so just to clarify, there's a distinction there.

00:20:45.340 Type 1 diabetes, the problem is not enough insulin.

00:20:47.500 There are no insulin.

00:20:48.200 So you have to give insulin.

00:20:49.860 Yes.

00:20:50.120 Type 2 diabetes, the problem is too much insulin.

00:20:53.860 That's exactly right.

00:20:54.940 Yeah, Brett.

00:20:55.380 So allow me just to elaborate just for one second.

00:20:57.660 This is, I think it's tragic that we've ever put those two diseases together, that we call

00:21:02.680 them diabetes, both of them, type 1 and type 2, I think is a tragedy because it suggests

00:21:08.480 that they're similar diseases when in fact they're opposites.

00:21:13.060 As you just said, type 1 diabetes is a disease of deficient insulin.

00:21:18.020 Type 2 diabetes is a disease of too much.

00:21:20.240 And so giving, I mean, I haven't elaborated the paradigm this way, but we've already elaborated

00:21:27.920 on the fact that insulin resistance is a state of too much insulin.

00:21:31.060 But the fact is, too much insulin is a driver of insulin resistance.

00:21:35.060 Not that we've really dived into the causes of insulin resistance yet, but elevated insulin

00:21:39.600 is what I consider a primary cause of insulin resistance.

00:21:43.280 And so by giving the type 2 diabetic insulin, we're making the problem worse.

00:21:47.780 And pardon the kind of harsh analogy, but that's like treating an alcoholic with another

00:21:53.300 glass of wine or treating someone with hyperthyroidism by giving them more thyroid hormone.

00:21:59.860 Okay, let's talk about what's going on.

00:22:01.960 What causes insulin resistance?

00:22:03.420 And in the book, you say that the number of people in our population, particularly in

00:22:07.960 Western industrialized countries, and it's expanding beyond the West.

00:22:11.160 You're seeing it increase all over the world.

00:22:14.140 The number of people with insulin resistance is on the rise.

00:22:17.160 Do we have a figure like how many people have or perhaps have insulin resistance?

00:22:20.560 Because as you said, it's usually you don't know till it's too late, till the blood glucose

00:22:24.420 is measured because most people aren't measuring their insulin levels.

00:22:27.660 So do we have an estimate about how many people have insulin resistance or what percentage

00:22:30.800 of the population?

00:22:32.620 Yeah, yeah.

00:22:33.240 So we do have an estimate.

00:22:34.980 In the United States, this shouldn't be a surprise.

00:22:38.180 We actually have a pretty good idea.

00:22:39.720 Now, I understand a lot of people like to criticize the United States.

00:22:42.720 It seems, and I'm born and raised in Canada, and I've lived in multiple countries and traveled

00:22:47.780 to dozens and dozens of them.

00:22:49.840 No one likes to insult the United States like Americans do, unfortunately.

00:22:55.220 So we tend to be our own most harsh critics.

00:22:58.580 But the problem is bad here, in part because we've documented it so well.

00:23:03.080 But evidence suggests that in other countries, it's worse in some of them.

00:23:06.620 So some of our best numbers, and I believe this is an accurate assessment, a paper published

00:23:12.700 a couple years ago from University of North Carolina, Chapel Hill, they suggested that

00:23:17.640 88% of U.S. adults are considered metabolically unfit.

00:23:22.000 Not surprisingly, in their manuscript, they considered that a, quote, alarmingly low level

00:23:26.620 of fit individuals.

00:23:28.760 And I agree, that is alarmingly low.

00:23:30.840 So they based that assessment on whether or not the people had some markers of the metabolic

00:23:35.040 syndrome.

00:23:36.420 I'm sure everyone's heard of this.

00:23:37.720 This is the constellation of problems that encompasses waist circumference, high blood

00:23:42.820 pressure, high glucose, and dyslipidemia.

00:23:45.960 Like, in other words, low HDL or high triglycerides.

00:23:49.080 Mind you, no mention of LDL, importantly.

00:23:51.140 But they found only 12% of U.S. adults were good in all five of those metrics.

00:23:56.740 That's a problem.

00:23:58.060 And I think it's relevant to this conversation simply because while they were doing this with

00:24:03.820 the stated objective of determining the metabolic syndrome prevalence, the metabolic syndrome

00:24:08.660 used to be called the insulin resistance syndrome.

00:24:12.180 And so to me, and to others who are scrutinizing this, these are markers of insulin resistance.

00:24:17.600 So potentially, almost 9 in 10 adults in the United States have some degree of insulin

00:24:22.300 resistance.

00:24:23.160 Now, as I alluded to, this is not a local problem.

00:24:25.780 And I appreciate you mentioning that, too.

00:24:27.680 The problem actually might be worse in Mexico.

00:24:30.840 It could be worse in several countries in the Middle East.

00:24:33.280 In fact, the most diabetic countries, type 2 diabetes on the planet, I think 8 of the top

00:24:39.520 10 are in the Middle East.

00:24:40.920 It's a tremendous problem.

00:24:42.900 And then I think the 10th was a country in Southeast Asia, a country that I love.

00:24:47.400 And I've studied, done research there in a country called Singapore.

00:24:51.040 But even throughout some countries in Southeast Asia, we have a problem.

00:24:54.680 So the United States, yes, it's an enormous issue here.

00:24:57.880 But we don't, we're not in the number one spot of this dreaded list.

00:25:01.820 And again, we've not talked on the consequences.

00:25:04.360 But it's part of the problem is we simply don't detect it soon enough.

00:25:08.440 We don't talk about insulin enough.

00:25:09.860 We just talk about the glucose.

00:25:11.760 And as we said, that's the glucose is just a marker of insulin.

00:25:15.040 That's right.

00:25:15.400 Okay, well, so, okay, it's been increasing among, it's across the population, like 9 in

00:25:20.340 10 adults, like 90% of the adult population probably has insulin resistance.

00:25:25.020 I imagine, was this a problem 20, 30, 40, 50 years ago, or has it been getting worse?

00:25:29.940 And if so, like, do we know why it's getting worse?

00:25:33.280 Yeah, yeah.

00:25:33.820 So there's no question this is getting worse.

00:25:35.960 All of these diseases we have nowadays are disorders that our ancestors couldn't have even

00:25:40.540 dreamed of, and partly because they were more worried about infections than we are, you

00:25:45.280 know, that really is the single most telling difference is the presence of antibiotics that

00:25:50.660 we have now and the breadth of them and the efficacy of them is a testament to science.

00:25:56.200 But yeah, these diseases that we all think are distinct, things like cancers and Alzheimer's

00:26:00.420 disease, heart disease, fatty liver disease, infertility, they all share a common core of insulin

00:26:06.140 resistance.

00:26:06.560 Now, I'm not silly enough to claim that insulin resistance is the only input or the only cause

00:26:11.900 of these diseases.

00:26:12.800 No, they're all multifactorial.

00:26:14.920 But the fact is, insulin resistance is a common and prominent thread woven through all of them.

00:26:22.160 And the general premise of my book is that our ongoing reluctance to acknowledge the relevance

00:26:28.000 of insulin is partly what's putting us in this position, and it is wholly a function

00:26:32.400 of the environment we live in, and almost totally a function of the food we eat.

00:26:37.780 Okay, so yeah, I want to dig deeper into like some of the problems that are related to insulin

00:26:40.980 resistance.

00:26:41.520 So, okay, the environment, so what is it about our food today that basically causes the body

00:26:46.100 to have to create too much insulin, which will cause insulin resistance?

00:26:49.640 Yeah, so I consider there to be three primary causes of insulin resistance.

00:26:54.700 Two of them have nothing to do with food, and I'll start with them just because they're so simple,

00:26:59.180 but they are real.

00:27:00.800 And I consider these to be primary causes because you can cause insulin resistance with all three

00:27:06.780 of these that I'll elaborate on in a moment in every biomedical model that scientists will

00:27:11.440 use to study insulin resistance.

00:27:13.300 And that includes isolated cells, like cells that are grown in little petri dishes in a lab,

00:27:18.460 or it includes laboratory rodents like mice and rats that we will sometimes use in our studies,

00:27:23.200 and then humans, you know, the pinnacle of all life on the planet.

00:27:26.860 And even in humans, you can cause insulin resistance with these three stimuli, each on their own,

00:27:31.580 so they are independent.

00:27:32.880 One of them is stress.

00:27:34.600 And so the prototypical stress hormones, cortisol and epinephrine, will cause insulin resistance

00:27:39.800 in all three biomedical models.

00:27:42.020 And this is relevant to humans, of course.

00:27:43.960 It's mostly relevant to our sleep habits because bad sleep leads to elevated stress hormones,

00:27:50.200 and that will, in fact, cause insulin resistance even after one bad night of sleep.

00:27:54.660 Now, thankfully, one good night of sleep can correct it, but it just touches on the relevance

00:27:59.220 of the stress hormones.

00:28:00.600 So stress is a primary cause.

00:28:02.360 Another one is inflammation.

00:28:04.260 Now, inflammation is a term that it's almost cliche.

00:28:07.260 It's thrown around so often these days, and I'm using it quite carefully.

00:28:10.780 So the activation of these, what we could call inflammatory pathways within cells, or the

00:28:17.520 biochemical process of activating these immune-related pathways will cause insulin resistance in cells

00:28:24.100 and rodents and humans.

00:28:25.980 And so it's a primary cause.

00:28:27.200 And this is most obvious in conditions of autoimmune diseases, where if someone has an autoimmune

00:28:32.600 disease and the autoimmune disease is very active or aggressive for a period of time because

00:28:37.260 it tends to ebb and flow, then the insulin resistance will be quite pronounced.

00:28:41.380 Then as the autoimmune disease subsides for a time, so too does the insulin resistance and

00:28:45.780 they're insulin-sensitive again.

00:28:47.660 Now, I don't elaborate on those too much because it's hard to control them.

00:28:51.460 If, you know, you're talking to someone and you say, well, lower your stress and lower your

00:28:54.720 inflammation, they say, well, thanks.

00:28:56.900 You know, that's easier said than done.

00:28:58.660 The thing that is very potent now is the elephant in the room, and that's the food we eat.

00:29:03.860 Um, essentially, the problem is we have created a diet and a way of eating that is spiking our

00:29:11.000 insulin all day.

00:29:13.120 So the average individual wakes up in the morning and overnight insulin has been coming down and

00:29:18.960 helping the body be a little more insulin sensitive and, and frankly, get into a higher

00:29:23.820 state of fat burning, which is why some people may be in a very mild state of ketosis upon

00:29:28.800 waking.

00:29:29.180 And tragically, what do we do?

00:29:31.460 Well, breakfast has become basically a dessert and we eat a starchy, sugary breakfast.

00:29:37.400 It's some starchy, sugary cereal or a starchy bagel or starchy toast or sugary orange juice

00:29:43.260 or something or a sugar loaded coffee.

00:29:45.800 We then spike our insulin rapidly.

00:29:48.120 And we know that an insulin spiking breakfast, and by that, I mean, there are, there's clinical

00:29:53.400 studies to prove this in humans.

00:29:54.860 By spiking insulin for breakfast, we have quicker return to hunger.

00:29:59.980 So we get hungrier sooner.

00:30:01.960 And so then two or three hours later, what do they do?

00:30:04.640 They spike their insulin again.

00:30:06.280 Right as insulin was cresting and about to come down, we spike it again with a starchy 1.00

00:30:10.980 mid-morning snack.

00:30:12.140 And right when insulin's about to come down, we bump it up again with our lunch and we do

00:30:16.280 it again in the afternoon, again for dinner and again throughout the evening with our snacking.

00:30:20.100 So the average person is living every moment of their waking life in a state of elevated

00:30:25.160 insulin and frankly, into maybe half of their sleeping time too, because insulin will take

00:30:31.160 a few hours to come back down.

00:30:33.340 And that chronically elevated insulin is a primary driver of insulin resistance.

00:30:39.940 And of course, that I think really does point the finger at our excessive consumption of refined

00:30:45.220 carbohydrates.

00:30:46.520 We're going to take a quick break for a word from our sponsors.

00:30:48.720 And now back to the show.

00:30:53.180 Okay.

00:30:53.760 So yeah, we're just, the world is increasingly eating more, just pounding away processed carbs,

00:30:59.240 sugar.

00:30:59.860 And we'll talk a little more later on at the end about what we can do to become more insulin

00:31:04.400 sensitive.

00:31:05.240 But besides food, the other thing you talk about is we become more sedentary.

00:31:10.840 What role does movement play or the lack of movement play in insulin resistance?

00:31:15.980 Yeah.

00:31:16.200 One of the nice things about the way the muscles are built is that the moment the muscle starts

00:31:21.680 well, moving, contracting and relaxing, it becomes able to pull in glucose without the

00:31:29.480 need of insulin.

00:31:30.460 In other words, it opens those glucose doors, even though insulin isn't there knocking on

00:31:35.260 them.

00:31:35.900 And so it's an insulin independent mechanism of glucose uptake.

00:31:39.840 And this is very relevant.

00:31:41.300 You can take a person who eats a starchy, sugary snack or meal, and if they just get up and

00:31:47.060 go on even a modest walk of 10 to 20 minutes, their glucose levels will not get as high as

00:31:53.620 they would have.

00:31:54.640 It'll only go up to about half as high as it would have.

00:31:57.320 And it comes down much, much faster.

00:31:59.480 The same goes with insulin.

00:32:01.140 Because yeah, you're flushing your body, your blood with all that glucose you just ate.

00:32:06.120 But the moment you start moving those muscles, well, by mass, muscle represents the primary

00:32:12.340 tissue in the body.

00:32:13.760 And it is overwhelmingly the main consumer of glucose.

00:32:17.680 Roughly 80% of the glucose that gets cleared from our blood goes into the muscle.

00:32:22.680 And so if we just get up and start moving our muscles around, we start just pulling in

00:32:27.280 the muscles, begin greedily consuming all of that glucose.

00:32:30.140 And so insulin, right when the beta cells of the pancreas were about to load the system

00:32:34.700 with all that insulin, they sense that the glucose is dropping rapidly on its own.

00:32:40.360 And so what would have been an enormous insulin release becomes a very modest insulin release

00:32:44.520 because the muscles have essentially saved the day.

00:32:47.360 So that's at least some part of the power of exercise used in that acute moment after eating

00:32:53.000 a starchy or sugary meal.

00:32:54.940 But the implications are broader, where if someone is exercising frequently, especially

00:32:59.580 if it's a higher intensity exercise, then they have the potential to gain or at least

00:33:04.620 retain muscle mass.

00:33:06.380 And as I mentioned, muscle is the main consumer of glucose.

00:33:10.340 So if you have more muscle, you simply have more little mouths that are going to eat up

00:33:15.640 all that glucose from the blood.

00:33:17.380 And this certainly plays out.

00:33:19.360 People with higher muscle mass can clear glucose much, much faster from the blood than people

00:33:24.820 with less muscle mass, even if they weigh the same.

00:33:28.040 Okay.

00:33:28.200 So I think we have a good idea of what insulin resistance is, what causes it.

00:33:32.180 And as we said before, when people think about insulin resistance, they typically connect it

00:33:35.640 to metabolic conditions like pre-diabetes or type 2 diabetes.

00:33:39.980 But in your book, Why We Get Sick, you talk about, well, no, insulin or too much insulin not

00:33:45.420 only contributes to diabetes, but it's contributing to other sicknesses as well.

00:33:50.320 And you've kind of mentioned them throughout our conversation.

00:33:52.140 The first one is heart and cardiovascular disease.

00:33:55.360 What role does insulin resistance play in those?

00:33:58.740 Yeah.

00:33:59.060 In fact, that's an enormously intimate association.

00:34:02.880 The heart disease is a very broad term that applies to a lot of specific cardiovascular issues.

00:34:10.080 The most common is hypertension or elevated blood pressure.

00:34:14.140 And so maybe I'll just focus on that one for the sake of time.

00:34:16.940 But with insulin resistance, insulin has a direct effect on controlling blood pressure.

00:34:22.940 The most obvious one is that insulin, when it's elevated, will force the kidneys to hold

00:34:28.260 on to salt.

00:34:29.640 Normally, the kidneys, if salt goes up, if you and I were to eat a load of salt, our kidneys

00:34:34.100 would just excrete it all very easily without any complication.

00:34:37.940 And our blood pressure wouldn't really change a blip.

00:34:39.900 But when insulin is elevated, let's say you eat that salty food with an insulin spiking

00:34:46.260 starch or sugar, and let's face it, a lot of people do.

00:34:49.160 Salty and crunchy is one of the kind of vices of most people's eating.

00:34:53.320 Then now the kidneys can't excrete that salt. 0.94

00:34:56.900 And so they have to hold on to that salt.

00:34:58.600 And where salt goes, water follows.

00:35:01.380 And so as the blood is holding on to the salt, now it's holding on to all that water that

00:35:05.620 it wanted to excrete.

00:35:06.720 And more water means higher volume of blood.

00:35:10.120 And as physics demands, more volume means more pressure.

00:35:13.960 And so we have an increased blood pressure.

00:35:15.820 At the same time, as the blood vessels themselves are becoming insulin resistant, they can't dilate

00:35:21.980 as well as they used to.

00:35:23.560 And naturally, if a blood vessel can dilate, it's expanding.

00:35:27.800 And that would mean that the volume of the space there has gotten bigger, and so the pressure

00:35:32.960 will go down.

00:35:33.780 But it can't happen.

00:35:36.300 When the blood vessels themselves become insulin resistant, now they stay in a more constricted

00:35:41.000 or narrowed state.

00:35:42.660 And naturally, that keeps blood pressure, or it keeps it high, but it pushes it even higher.

00:35:48.340 And then maybe one last example, because there are even more than I could mention.

00:35:52.020 When insulin levels are chronically elevated, it activates something called the sympathetic

00:35:57.400 nervous system.

00:35:58.480 And I'm sure your audience has heard of this.

00:36:00.660 But this is the infamous fight-or-flight response.

00:36:04.280 And so when insulin's high, the heart rate starts beating harder or higher and harder, and the

00:36:11.140 blood vessels once again constrict.

00:36:13.700 That's part of the normal sympathetic response.

00:36:16.540 Like if we needed to run away from danger, for example, or react very quickly.

00:36:20.920 It's a pronounced benefit in that circumstance.

00:36:24.100 But in this case, of this kind of artificial sympathetic response because of the chronically

00:36:28.440 elevated insulin, it becomes purely pathological or pathogenic.

00:36:32.720 It starts to hurt the blood vessels in the cardiovascular system.

00:36:36.040 Okay.

00:36:37.020 So insulin, too much insulin, insulin resistance, it's not good for our heart or cardiovascular

00:36:41.080 system.

00:36:41.880 You also talk about the effect of insulin on our reproductive system.

00:36:46.580 And you mentioned a female reproductive issue, which is PCOS. 0.87

00:36:51.840 What about men?

00:36:52.580 Does too much insulin or insulin resistance affect male reproductive health?

00:36:57.240 Yes, it sure does.

00:36:58.580 I'm thrilled you mentioned that because I'm always reluctant to just mention PCOS and have

00:37:04.800 the gals just think I'm kind of coming after them. 1.00

00:37:06.720 No, it's certainly relevant to the guys as well.

00:37:08.900 So while PCOS is the most common form of infertility in females, the counterpart in males, the most

00:37:14.700 common infertility is erectile dysfunction.

00:37:17.380 And that is entirely a problem of blood vessels.

00:37:19.500 And in fact, I actually alluded to it or explained the problem just now, where when the blood vessels

00:37:23.860 become insulin resistant, they can't dilate or open as well as they used to.

00:37:28.360 And that, of course, is an essential physiological change in a fellow in order to have normal fertility.

00:37:33.480 And so if he suddenly has blood vessels that cannot dilate, well, then he has erectile dysfunction.

00:37:40.620 And it's entirely a consequence of the insulin resistance at the blood vessels.

00:37:44.920 A lot of people misunderstand erectile dysfunction, and they'll claim that it's a result of low

00:37:48.960 testosterone.

00:37:50.000 That is just not true.

00:37:52.260 More and more individuals study this.

00:37:54.240 In fact, there was a paper published just a couple years ago, and the title reveals everything

00:37:58.000 you need to know, and it was something like, is erectile dysfunction the earliest manifestation

00:38:04.480 of insulin resistance in men?

00:38:07.060 That was, you know, so the title of the manuscript was kind of posed as that question.

00:38:10.960 And the answer throughout the manuscript was, yes, it is.

00:38:14.760 And again, it's simply a matter of insulin resistance affecting the blood vessels.

00:38:20.260 And once affected, they can't dilate, and a lack of dilation means erectile dysfunction.

00:38:26.820 One thing, my sort of rudimentary understanding of endocrinology is that hormones affect hormones.

00:38:31.540 Do we know if insulin affects testosterone in any way?

00:38:35.320 Yeah, that's a great question.

00:38:36.940 It does through the reaction of converting androgens to estrogens. 0.52

00:38:41.700 And so you'd think, well, if the same thing's happening in a guy's testes, then he should

00:38:47.100 have more androgens being released, you know, because that's what's happening in the woman 1.00

00:38:51.020 with her ovaries. 0.98

00:38:52.300 Higher insulin is resulting in higher testosterone, but that does not happen in the testes.

00:38:57.300 There's not that same effect.

00:38:59.100 And unfortunately, there's not a direct effect of insulin on testosterone, but there's an indirect

00:39:03.820 effect through the fat cell.

00:39:05.700 As insulin is promoting the growth of the fat cell, which it does very readily, fat cells end

00:39:11.360 up acting kind of like ovaries.

00:39:13.880 And so the fat cells that are growing on the man actually will pull in testosterone and

00:39:19.280 pump out estrogens as a result.

00:39:21.420 It'll convert the androgens to estrogens, just like the woman's ovaries are doing. 1.00

00:39:26.260 Okay.

00:39:26.900 So we've talked about reproductive health.

00:39:29.140 The chapter that's kind of scary when I read it is insulin resistance role or potential role

00:39:34.440 in cancer are the particular cancers where there's a strong connection with insulin resistance.

00:39:39.260 Yes, yes, there sure is.

00:39:41.740 I share that kind of sobering sentiment that you do, that sobering view of cancer.

00:39:46.100 I have a very hearty respect for it and a fear of it because it seems like one of those

00:39:50.900 things that you can't do much about.

00:39:52.820 Well, in some instances, that's undoubtedly the case because cancer is such an unknown beast

00:39:58.580 of unknown origins.

00:40:00.900 But the most common cancers, breast and prostate cancers, have very strong evidence linking them

00:40:07.220 to insulin resistance.

00:40:08.600 For example, breast tumors will, one of the many mutations that they'll manifest with is 0.81

00:40:15.120 a mutation in the insulin receptor.

00:40:18.000 And breast tumors will have about seven times more insulin receptors than even neighboring breast

00:40:23.580 tissue that's not cancerous will have.

00:40:25.920 And at the kind of broader level, independent of any other variable like obesity, for example,

00:40:32.460 that is a risk factor for breast and prostate cancers, you can control for obesity and insulin

00:40:38.060 resistance still persists as a more relevant risk factor.

00:40:41.800 So the evidence is there's some direct evidence of insulin receptor mutations enhancing the effect of

00:40:48.880 insulin on the cancer cells.

00:40:50.260 And then there's that more indirect finding just these correlations.

00:40:53.380 But the relevance also has one other aspect to it, which is glucose.

00:40:57.540 Cancer cells eat glucose.

00:40:59.340 That is their primary fuel.

00:41:01.120 They eat about 200 times more glucose than the normal cell does.

00:41:05.020 And so the tragedy, of course, in the average individual who has rising insulin and rising glucose

00:41:09.500 is that you have all that insulin signaling the growth or stimulating the growth of the cancer cell.

00:41:15.480 And you have all that glucose fueling all of that explosive growth.

00:41:20.800 Okay, so here's the one.

00:41:21.460 You didn't talk about this in your book because the book came out before this hit.

00:41:25.600 But I imagine as a scientist who researches insulin resistance, the COVID pandemic provided an opportunity

00:41:32.820 to study the connection between insulin resistance and COVID.

00:41:36.000 Has there been any research done in that area?

00:41:39.280 Yes, there has been, but very, very little.

00:41:41.780 Now, there's no question that there's a metabolic aspect to COVID.

00:41:45.480 And at the risk of offending some, while many want to claim that this is a pandemic of the

00:41:51.020 unvaccinated, I just don't think that's fair. 1.00

00:41:54.400 I don't think that's accurate.

00:41:55.360 I think it is more accurate to say it's a pandemic of preexisting conditions because that just

00:42:00.300 continue, every single study continues to confirm that if a person has these relevant or underlying

00:42:07.120 metabolic preexisting conditions, they are much, much more susceptible to having a serious

00:42:11.980 infection and they carry a much higher load.

00:42:15.600 So there's higher potential for transmission.

00:42:17.740 And we know even further that the vaccines are less effective in these individuals.

00:42:23.400 And I hate for that to sound incriminating in any way.

00:42:26.060 And I really do.

00:42:27.000 I don't intend for it to sound like that.

00:42:28.560 But as a scientist, I do want to be precise.

00:42:31.740 And I don't think there's any value in ignoring data, even if it's a little inconvenient.

00:42:36.560 I think nobody benefits in that regard.

00:42:38.560 So the connection between insulin resistance and COVID-19, there is one study that I know

00:42:43.720 of that has looked at insulin levels versus glucose levels.

00:42:47.160 And the general finding was that they both appear to be predictive.

00:42:50.260 But I will maybe more focus on the glucose aspect and at the risk of diminishing insulin resistance,

00:42:57.800 the relevance of insulin resistance.

00:42:59.320 But when a cell has become infected with a virus, it tends to start using glucose at a

00:43:05.240 higher rate.

00:43:05.820 So once again, in this metabolically unhealthy individual, we have the potential where we're

00:43:10.660 fueling this growth.

00:43:12.700 And I'll be very brief on this because I feared that it would be getting off topic.

00:43:16.120 But fat cells are a very welcoming host for COVID-19.

00:43:20.600 A virus is very distinct from a bacterium where the bacteria is its own self-contained

00:43:25.080 cell.

00:43:25.800 A virus is simply a particle of peptides.

00:43:28.340 And it needs a cell to infect.

00:43:32.540 And then that cell begins producing more of the virus.

00:43:35.480 And in order to get in a cell, a virus needs a co-receptor.

00:43:38.800 It basically needs a doorway that allows it to come in.

00:43:42.780 And fat cells tend to have more of those doorways than almost any other cell.

00:43:46.120 And so naturally, if you have more fat cells, you have more potential homes for the virus

00:43:53.500 to come into.

00:43:54.440 And then it turns the home into a factory, producing ever more of itself.

00:43:58.780 Okay.

00:43:59.120 So let's talk about another problem or disease that we associate insulin or insulin resistance

00:44:05.480 with.

00:44:05.720 And that's obesity.

00:44:07.240 So just as insulin resistance has been increasing across populations, so has obesity.

00:44:11.740 So the question is, is it the insulin resistance that's causing obesity, or is it the obesity

00:44:17.960 increasing body weight causing insulin resistance?

00:44:21.880 Yeah.

00:44:22.400 Yeah.

00:44:22.780 So the answer to that two-sided question is yes, Brett.

00:44:26.600 I hate to take a...

00:44:28.680 But I'll elaborate very briefly.

00:44:30.580 So there's no question that when fat cells are growing, they start to promote insulin resistance.

00:44:38.040 There's no question that happens.

00:44:40.280 So fat tissue can grow through different ways.

00:44:42.760 But if it's growing through a process called hypertrophy, or each individual fat cell is

00:44:47.860 growing, rather than we are pulling in new fat cells and making new, have an increased

00:44:52.880 number of fat cells.

00:44:54.540 But if it's through hypertrophy, or each individual fat cell getting bigger and bigger, then they

00:44:59.360 start to become increasingly insulin resistant.

00:45:01.480 And they do that to try to control its own growth, because the fat cell is essentially signaling

00:45:06.240 to insulin, insulin, you want me to continue to grow, but I'm reaching a point of maximum

00:45:11.220 dimension, and I can't grow beyond this, so I need to become a little insulin resistant.

00:45:16.040 And that's why most people have a limit to how fat they can get. 1.00

00:45:20.060 You know, the individuals that are on these documentaries where they're super, super morbidly

00:45:24.560 obese, the average person can't get that fat.

00:45:27.500 Those are the few individuals who are getting fat through a process called hyperplasia, which

00:45:32.900 is when the fat cells themselves are pretty modestly sized, they just start making new

00:45:37.600 fat cells all the time.

00:45:39.580 So there's almost this limitless potential for fat growth.

00:45:42.240 And paradoxically, Brett, while these people become remarkably overweight and obese, they

00:45:47.560 actually maintain a pretty high level of insulin sensitivity.

00:45:50.840 And that's because the fat cells are always happily storing more energy, and they're never getting

00:45:56.200 too big, because anytime they start to get a little big, well, then they just have a new

00:45:59.660 fat cell get created.

00:46:01.300 So anyway, back to the discussion.

00:46:03.600 There's no question that fat tissue, if it's growing through hypertrophy, will contribute to

00:46:07.960 insulin resistance.

00:46:08.900 But there's also evidence to suggest the opposite, that as the body has higher and higher levels

00:46:14.060 of insulin, which is happening with insulin resistance, that that precedes weight gain.

00:46:20.320 And evidence from a guy named Jim Johnson, who's at the University of British Columbia, he finds

00:46:24.800 it that in these animal studies that he's done, that has to happen, that you can't promote the

00:46:30.260 fat growth without the elevated insulin.

00:46:32.760 I'm certainly suggesting the relevance of insulin at the fat cells.

00:46:36.640 So there's, I think the view that excess weight or the growing fat cells will cause insulin

00:46:42.080 resistance is absolute consensus.

00:46:44.200 Everyone would nod their heads to that.

00:46:46.940 There's less of a consensus that insulin resistance can proceed and even contribute to weight gain.

00:46:52.660 There's evidence to support it, and I just cited it, but it's a much less prominent view.

00:46:58.220 But I think it's a valuable one.

00:46:59.880 And I imagine that there's, it goes back and forth.

00:47:02.020 So as you, as insulin resistance causes an increase in fat cell size, that fat cell size

00:47:08.900 is going to cause more insulin resistance.

00:47:10.400 So it's sort of like this vicious cycle that's going on.

00:47:13.840 Yeah, that's right.

00:47:14.360 And my view is a, is a fat first perspective, which is the fat cell is generally the first

00:47:20.520 to become insulin resistant because through the process I just mentioned of hypertrophy.

00:47:24.500 And then that starts to spread the insulin resistance through other mechanisms, basically

00:47:29.060 through the rest of the body.

00:47:30.520 So, okay, let's talk about, we talked about all these problems that can be caused by insulin

00:47:34.240 resistance.

00:47:35.060 What do you, what do you do about it?

00:47:36.520 So like, the first question is like, how do you even know if you're insulin resistant?

00:47:39.380 Is there a test you can take to see if your insulin levels are elevated?

00:47:42.960 Because usually, you know, you, you go to the CVS and buy a blood glucose test, but I haven't

00:47:47.960 seen an insulin test there.

00:47:49.780 No, no, there isn't one.

00:47:50.940 And that's certainly an ongoing hurdle and, and why glucose continues to occupy the primary

00:47:56.740 position in this discussion, because it's just so much easier to measure.

00:48:00.560 But yeah, you can get insulin measured and that is kind of the least thing you can do or

00:48:05.580 you ought to do in order to determine your insulin resistance status.

00:48:09.000 So next time a person's going in for a blood test, just kind of beg, plead, cajole, pay

00:48:15.120 off your clinician to check the box and say, measure the insulin.

00:48:19.260 That's something that every lab can do nowadays, a clinical lab.

00:48:22.980 It's just whether or not the physician will do it.

00:48:26.920 And, and sometimes whether or not the insurance will pay for it, but more and more it will,

00:48:30.480 even if it won't, a person can get it done usually for like 20 bucks or something.

00:48:34.540 So yeah, get your insulin measured to know where your insulin levels are.

00:48:38.100 That's a great, great way to get a feel for where you're at.

00:48:42.260 Now, there are some surrogates here, like a poor man's method of measuring insulin resistant

00:48:47.020 status can be done just by looking at a ratio of your lipid levels in your blood.

00:48:52.620 And so if a person, every blood test thankfully will measure triglycerides and every blood test

00:48:57.480 will measure HDL cholesterol.

00:48:59.940 Well, those are the two ones you need.

00:49:01.360 So take the triglycerides number and divide it by HDL.

00:49:05.380 So triglycerides over HDL cholesterol.

00:49:08.000 If that answer is less than 1.5, then that's a very good sign that you are insulin sensitive.

00:49:14.520 If that answer is above 1.5 and getting higher into the twos or the threes, the higher it's

00:49:19.760 getting, the more insulin resistant you are.

00:49:22.460 So that's a very reliable indicator.

00:49:24.740 So if you can't get your insulin measured, then at least look at your lipids, which again,

00:49:28.420 are always measured, and that'll give you a pretty good idea of where you're at.

00:49:32.040 When you do measure insulin levels, what's the level where you're like, okay, insulin

00:49:35.400 resistance is probably happening right now?

00:49:37.060 Yeah, yeah.

00:49:37.680 Right, right.

00:49:38.360 Yeah, I should have said that.

00:49:39.160 It's around 10 microunits per mil.

00:49:41.340 So here in the US, those are the units that we'll use with insulin.

00:49:45.480 Microunits per mil.

00:49:46.320 In other countries, it may be picomoles.

00:49:48.360 We don't do that here.

00:49:49.580 So if a person's, if you're fasting, insulin is around 10 microunits per mil or less, that's

00:49:53.820 a great sign.

00:49:54.920 Okay.

00:49:55.320 Let's say someone has insulin resistance, and chances are, the person listening to this

00:49:59.120 right now probably does, because about 9 in 10 Americans have insulin resistance.

00:50:03.180 Is insulin resistance reversible?

00:50:05.140 And if so, what are some things you can do to reverse insulin resistance?

00:50:09.120 Yeah, yeah.

00:50:09.660 The good news is it is almost immediately reversible, and really within weeks.

00:50:14.700 You can take someone with profound insulin resistance.

00:50:18.040 They're really type 2 diabetic, deep into type 2 diabetes.

00:50:21.900 They're that insulin resistant, and within just weeks, they become so insulin sensitive

00:50:25.900 that they can get off all their medications, of course, under clinical supervision.

00:50:31.460 So in my view, there are four steps, or four pillars, rather, because it doesn't need to

00:50:35.980 be sequential, so I shouldn't say steps.

00:50:37.780 Four pillars that can be used to build the proper foundation of an insulin-sensitizing diet.

00:50:44.600 And the first one is control carbohydrates.

00:50:46.620 I'm not saying don't eat any, but those are the biggest offenders, so control them.

00:50:52.620 Don't eat your carbohydrates from a bag or a box with a barcode.

00:50:56.320 Focus on raw carbohydrates, or mildly cooked or processed.

00:51:01.700 Fruits and vegetables, those are the main ones to eat.

00:51:05.000 Be very careful with grains.

00:51:07.320 They always have much more starch, and will have a higher glucose and insulin effect.

00:51:11.060 And then, of course, the more processed it is, like even juicing the fruits and vegetables,

00:51:15.800 you want to avoid.

00:51:16.680 Eat your fruits and vegetables.

00:51:17.800 Don't drink them.

00:51:18.720 So that's what I mean by control carbohydrates.

00:51:21.000 And then next, prioritize protein.

00:51:22.920 Protein has a modest effect on insulin, but it's fine.

00:51:26.560 It's a very modest effect, and proteins are essential.

00:51:29.780 And most people aren't getting enough to sustain their lean mass, namely muscle and bone.

00:51:34.340 And so focus on protein, eat it frequently, and get it from animal sources.

00:51:39.460 It's a very uncomfortable thing for some these days, but there's no question, animal protein

00:51:45.820 is superior to any plant protein.

00:51:48.020 Every conceivable metric, and I know this is upsetting.

00:51:51.240 A lot of people truly are offended by me saying this, but I'm not going to deny human physiology

00:51:55.900 just to be politically correct.

00:51:58.820 Every animal protein is superior to any plant protein, full stop.

00:52:03.240 So make sure you're getting the animal protein.

00:52:06.440 Now, the third one is don't fear fat.

00:52:09.440 Fat has no effect on insulin, and we've been eating it for millennia.

00:52:13.420 Well, since the beginning of who we are, however humans came to be, we've been eating fat since

00:52:18.300 the beginning, and that includes animal fat most especially.

00:52:21.340 So focus on animal fats and fruit fats.

00:52:24.380 The fruit fats are coconuts, avocados, olives, and as much as you can studiously avoid the seed,

00:52:30.820 the refined seed oils, or what some people will call, through an act of clever marketing,

00:52:36.560 vegetable oil.

00:52:37.520 There's nothing vegetable about it.

00:52:39.340 These are seed oils refined from soybeans, cotton seed, or corn seeds, etc.

00:52:45.520 Avoid them like the plague.

00:52:47.160 And unfortunately, well, fortunately, if you're avoiding, if you're not getting your carbs from

00:52:51.960 a bag or a box or with a barcode, then you're doing a good job already, because it's those

00:52:56.800 processed carbs, and the main fat in them will be from these seed oils.

00:53:01.800 So as you're eating, be very liberal with fats from animals and fruits.

00:53:07.400 We're well adapted to those.

00:53:09.040 And then the last one, the fourth pillar, is take a break from eating all the time.

00:53:13.040 You don't need to eat three meals a day all the time.

00:53:16.460 You especially don't need to eat six meals a day all the time.

00:53:19.760 If you want to improve your insulin sensitivity, give your body a break from eating and engage

00:53:23.900 in some form of intermittent fasting.

00:53:26.260 There are so many ways to do this, but just give your body a break from eating all the time.

00:53:30.880 Occasionally, maybe even do a 24-hour food fast where you're just drinking water, no calories

00:53:36.280 during that time.

00:53:37.320 And then on occasion, skip a breakfast or eat a very, very modest dinner in order to

00:53:42.560 just help insulin get down a little faster or stay low longer.

00:53:46.620 Besides diet, what role does movement play in preventing insulin resistance?

00:53:50.080 Yeah, yeah, yeah.

00:53:51.640 Excellent question.

00:53:53.040 I'm often asked what's the best exercise, and my kind of witty response is the one you'll

00:53:58.120 do.

00:53:58.540 But I do mean it.

00:53:59.960 Any form of movement is going to be beneficial, so just get up and move.

00:54:03.540 If you can strategically do that, if you know you've only got 30 minutes a day to exercise,

00:54:08.900 well, you can do a hell of a lot in 30 minutes.

00:54:11.000 But maybe if you're older and less capable physically, then couple that with the meal

00:54:15.020 in which you eat the most starches, just like I explained earlier.

00:54:18.280 Do a brisk walk at the end of that.

00:54:20.280 But for those of us that are more capable physically, then the more aggressive we can be, the better.

00:54:24.980 Have a high-intensity workout as often as you can.

00:54:27.400 It doesn't need to be long.

00:54:28.440 Mine are only around 30 minutes.

00:54:30.280 I'm in my mid-40s, and it's been sufficient to keep my muscle.

00:54:33.020 I just do very, very brief rests, basically to failure every set.

00:54:37.200 But whatever you're doing, do what you can to move the muscles, and especially do what

00:54:40.480 you can to increase your muscle mass.

00:54:42.440 Yeah, and strength training.

00:54:43.500 You're getting free pumping of glucose into your body without insulin, which is—

00:54:48.460 That's right.

00:54:49.000 And by helping increase your muscle mass, you're walking around every moment of the day with

00:54:54.700 a better glucose sink, so to speak.

00:54:57.220 And there's some other weird things you can do.

00:54:58.760 I mean, I wouldn't bank on these little things to do to increase insulin sensitivity.

00:55:02.140 But they're interesting.

00:55:03.260 Like, we've talked about and written about cold showers on the website and the podcast

00:55:07.000 before.

00:55:07.480 And there's actually research that say that cold showers can help increase insulin sensitivity.

00:55:11.700 Yeah, yeah.

00:55:12.360 There's two distinct mechanisms.

00:55:14.160 One is just through shivering.

00:55:15.920 And when you're shivering, your muscles are spasming.

00:55:18.680 And that's a muscle contraction.

00:55:20.360 So they start pulling in the glucose just like they would if you were exercising.

00:55:23.120 And then the second thing during cold exposure is you're activating this unique type of fat

00:55:28.540 called brown fat.

00:55:30.040 And brown fat, oddly, has a very high metabolic rate.

00:55:34.400 It's not designed to store fat like your white fat cells are.

00:55:38.680 This is designed to burn energy, glucose and fat, to produce heat.

00:55:43.520 And so cold therapy will activate brown fat very aggressively.

00:55:46.780 And then you're just chewing through your glucose that much faster.

00:55:49.340 All right, so these are all simple lifestyle changes that people can make.

00:55:53.420 What if someone does all these things, the insulin is still staying high?

00:55:57.100 Is there a certain point where you feel like, well, there's other medications you take or

00:56:00.880 there are medical interventions you might have to do?

00:56:03.780 Yeah, so frankly, Brett, usually they won't.

00:56:07.280 But just for the sake of argument, let's say that maybe they would just to introduce the

00:56:12.140 drugs.

00:56:12.540 But again, they're not nearly as effective.

00:56:15.260 Even the most effective drugs, and that'll be the first one I mentioned in a moment, is

00:56:18.920 only half as effective as even modest lifestyle changes.

00:56:23.000 So if the lifestyle changes don't work, then you're hosed pretty much.

00:56:28.040 So usually it's people go to lifestyle changes once the drugs stop working.

00:56:31.460 That's usually the way it goes because drugs do have heavy diminishing returns.

00:56:35.580 But the most common that is prescribed because of its efficacy and the minimal side effects,

00:56:41.960 because every drug has a side effect, is one called metformin.

00:56:46.600 That's the most widely prescribed anti-diabetic drug in the world.

00:56:49.860 And for good reason.

00:56:50.840 It's very affordable because it's off patent now.

00:56:53.580 And it's very effective with generally minimal side effects.

00:56:57.720 So that's typically the first one.

00:56:59.080 And that's one that I give the highest grade to of all the available drugs.

00:57:02.500 But there are so many more that would take too much time for me to get into.

00:57:06.700 So I'll just end it there.

00:57:07.540 Usually metformin will be the first one.

00:57:09.700 And thankfully, it works pretty well with minimal side effects.

00:57:12.840 But the take-home point is that you're better off doing these lifestyle changes because one,

00:57:16.900 they're free and there's no side effects.

00:57:19.020 And they work.

00:57:19.780 And the only, yep, that's exactly right.

00:57:21.920 Yeah.

00:57:22.140 So you could imagine someone whose physician says, all right, you have type 2 diabetes or you're

00:57:27.120 really pre-diabetic.

00:57:28.140 You're on the doorstep of type 2 diabetes.

00:57:30.480 You have two options.

00:57:31.400 One is to go and do a lifestyle change.

00:57:34.740 And then you'll probably reverse the disease if you're smart about it.

00:57:38.860 Alternatively, you can leave my office with a prescription for, say, metformin.

00:57:43.000 If this is the only path you take, the drug path, you will never get off the drugs.

00:57:48.880 All that will happen, and this sounds like I'm being hyperbolic here, but this is exactly

00:57:53.540 how it goes, where the person will be given a prescription.

00:57:56.540 The only outcome is that they increase the dose of that drug.

00:58:01.700 And then as that becomes increasingly ineffective, then they have a different drug that they add

00:58:06.200 on to it and then a different one.

00:58:08.100 And that puts them on this path of never reversing the disease.

00:58:13.040 That is why conventional medicine will say type 2 diabetes is irreversible.

00:58:17.340 Because if you treat it in the conventional way with drugs, it is.

00:58:21.680 The drugs will never solve the problem.

00:58:23.840 If, however, you acknowledge that type 2 diabetes is a disease of the food we eat, essentially,

00:58:28.300 that the food is the culprit or the cure, then you can let it be the cure and start making

00:58:32.840 changes accordingly.

00:58:34.280 Well, Benjamin, this has been a great conversation.

00:58:35.880 Is there some place people can go to learn more about the book and your work?

00:58:38.740 Yeah, thanks so much, Brett.

00:58:39.860 The book is available anywhere books are sold.

00:58:41.640 Again, the title is Why We Get Sick.

00:58:44.080 And notice, I didn't say in the title Why Insulin Resistance Matters for the very reasons

00:58:49.940 we've spent an hour elaborating on.

00:58:51.480 It's because most people don't know the value of insulin.

00:58:53.960 And so they would never pull it off the shelf.

00:58:56.760 So yeah, anyway, go buy the book, Why We Get Sick.

00:58:59.740 And I'm moderately active on social media, mostly Instagram, where I usually put out a few

00:59:04.740 videos a week just about insight into human metabolism.

00:59:07.220 And then one shameless plug, I have a little business with a couple of my brothers, a

00:59:12.100 little family business where we make low-carb meal replacement shakes.

00:59:15.800 And people can learn more about that by going to the website gethealth.com.

00:59:20.400 And health is spelled H-L-T-H, gethlt.com.

00:59:25.740 Fantastic.

00:59:26.160 Well, Benjamin Bickman, thanks for your time.

00:59:27.440 It's been a pleasure.

00:59:28.500 My pleasure.

00:59:29.140 Thanks so much, Brett.

00:59:30.380 My guest here is Dr. Benjamin Bickman.

00:59:31.980 He's the author of the book, Why We Get Sick.

00:59:33.920 It's available on Amazon.com and bookstores everywhere.

00:59:35.980 You can find out more information about his research and work at his website,

00:59:39.420 bickmanlab.byu.edu.

00:59:42.060 And if you want to learn more about his supplement health code, you can go to gethealth, that's

00:59:45.740 health, which is H-L-T-H.

00:59:47.560 Check it out if you want to learn more information about that.

00:59:49.520 Also check out our show notes at aom.is slash sick, where you find links to resources, where

00:59:53.040 we delve deeper into this topic.

01:00:01.360 Well, that wraps up another edition of the AOM podcast.

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The Art of Manliness - October 11, 2021

Why We Get Sick

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