Why We Get Sick
Episode Stats
Summary
Benjamin Bickman is a professor of biology and physiology, an expert in obesity and metabolic disorders, and the author of Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease and How to Fight It. While these prevalent and dreaded diseases are caused by multiple factors, my guest says they also share a common thread: a ubiquitous and too little understood condition called insulin resistance.
Transcript
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
00:00:26.600
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
00:00:36.060
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
00:00:53.160
Now, something to help keep in mind during this conversation is that insulin resistance
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
00:01:12.880
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
00:01:28.960
I can't tell you how motivating this conversation was for me to start walking more during the
00:01:36.360
After the show's over, check out our show notes at awim.is slash sick.
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,
00:02:23.440
So I think to understand what insulin resistance is, you got to understand what insulin is.
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
00:02:55.560
Of course, it's higher when you're eating and much lower when you're fasting, but insulin's
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
00:03:15.660
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,
00:03:56.320
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
00:04:15.320
And unfortunately, that's partly why insulin resistance itself has become such a problem,
00:04:21.760
So insulin is a hormone that knocks on doors of cells and say, hey, let this energy in.
00:04:29.900
Their pancreas doesn't produce insulin, and so they have to take artificial insulin.
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?
00:04:43.420
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
00:04:57.000
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
00:05:18.300
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
00:05:28.540
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.
00:05:38.120
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?
00:05:54.860
This is actually now touching on a bigger debate and a bigger topic, which is what is
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
00:06:18.000
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
00:06:41.220
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
00:07:09.840
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
00:07:28.500
So they have a much higher metabolic rate than they should, so they're burning several
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
00:07:53.680
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.
00:08:03.580
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
00:08:29.060
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
00:09:11.440
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
00:09:33.000
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
00:09:43.640
Well, in this case, you're just dumping them from the body like the person is with their
00:09:47.740
And the person is excreting ketones in the urine at a very high rate and excreting ketones
00:09:53.740
And again, that means every time the person's exhaling, they are literally exhaling molecules
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.
00:10:20.920
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,
00:10:34.240
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
00:10:43.100
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.
00:10:58.760
So type 1 diabetics, if your body doesn't have insulin, your body basically isn't going to
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
00:11:12.400
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.
00:11:31.080
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
00:11:49.200
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
00:11:59.900
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
00:12:32.460
If that were the case, then insulin resistance really would just be another, would be identical
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
00:13:11.500
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.
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
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
00:14:02.360
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
00:14:12.520
The other side of the coin, and this is very important, is that blood insulin levels are
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.
00:14:36.100
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.
00:15:04.620
In the ovaries, it happens more than it does in the testes.
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.
00:15:30.940
And unfortunately, too many androgens for her body, giving her, say, the acne or the excess body
00:15:37.120
growth that comes along with polycystic ovary syndrome or PCOS.
00:15:43.980
So insulin resistance, some cells, it's whenever there's too much insulin, some cells become
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
00:16:10.660
So I think when people have heard, talked about insulin, they typically see it connected with
00:16:18.000
And that maybe they are a type 2 diabetic, or they're told by the doctor, you have pre-diabetes
00:16:28.400
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
00:16:43.420
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
00:17:10.440
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
00:17:23.960
But that paradigm, that glucocentric paradigm is what has, again, put us on this problematic
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.
00:17:47.100
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
00:17:58.920
What's been happening over these years, and this is a process that can go on for decades,
00:18:05.180
It's getting ever higher, higher and higher and higher, but it's working well enough to
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.
00:18:21.680
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
00:18:34.240
a focus on insulin, that insulin has been waging this silent war behind the scenes for 10 or
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
00:18:56.360
And then 10 or 20 years later, we finally detect the problem.
00:19:03.780
We've detected the problem much, much later than we should have if we had been looking
00:19:09.960
And so, in other words, insulin is a much more sensitive marker, a much earlier indicator of
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,
00:19:41.980
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
00:19:55.240
Just take some insulin, and this will push the glucose down.
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
00:20:29.260
So when we do this, when we ignore the insulin, and we give them even more of what they already
00:20:35.560
have too much of, then we make them fatter and sicker, and we kill them faster.
00:20:40.260
Because this is not, it's not a glucose disease.
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.
00:20:50.120
Type 2 diabetes, the problem is too much insulin.
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.
00:21:20.240
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.
00:22:03.420
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.
00:22:14.140
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
00:22:34.980
In the United States, this shouldn't be a surprise.
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
00:22:49.840
No one likes to insult the United States like Americans do, unfortunately.
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
00:23:30.840
So they based that assessment on whether or not the people had some markers of the metabolic
00:23:37.720
This is the constellation of problems that encompasses waist circumference, high blood
00:23:45.960
Like, in other words, low HDL or high triglycerides.
00:23:51.140
But they found only 12% of U.S. adults were good in all five of those metrics.
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
00:24:23.160
Now, as I alluded to, this is not a local problem.
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
00:24:42.900
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.
00:25:11.760
And as we said, that's the glucose is just a marker of insulin.
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?
00:25:35.960
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
00:26:06.560
Now, I'm not silly enough to claim that insulin resistance is the only input or the only cause
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
00:26:41.520
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,
00:27:00.800
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
00:27:13.300
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,
00:27:34.600
And so the prototypical stress hormones, cortisol and epinephrine, will cause insulin resistance
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
00:28:04.260
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
00:28:27.200
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
00:28:47.660
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
00:28:58.660
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
00:29:13.120
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
00:29:31.460
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
00:29:48.120
And we know that an insulin spiking breakfast, and by that, I mean, there are, there's clinical
00:29:54.860
By spiking insulin for breakfast, we have quicker return to hunger.
00:30:01.960
And so then two or three hours later, what do they do?
00:30:06.280
Right as insulin was cresting and about to come down, we spike it again with a starchy
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
00:30:33.340
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
00:30:46.520
We're going to take a quick break for a word from our sponsors.
00:30:53.760
So yeah, we're just, the world is increasingly eating more, just pounding away processed carbs,
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
00:31:05.240
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?
00:31:16.200
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
00:31:30.460
In other words, it opens those glucose doors, even though insulin isn't there knocking on
00:31:35.900
And so it's an insulin independent mechanism of glucose uptake.
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
00:31:54.640
It'll only go up to about half as high as it would have.
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
00:32:13.760
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
00:32:54.940
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
00:33:06.380
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
00:33:19.360
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.
00:33:28.200
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?
00:33:59.060
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
00:34:29.640
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.
00:35:01.380
And so as the blood is holding on to the salt, now it's holding on to all that water that
00:35:10.120
And as physics demands, more volume means more pressure.
00:35:15.820
At the same time, as the blood vessels themselves are becoming insulin resistant, they can't dilate
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
00:35:36.300
When the blood vessels themselves become insulin resistant, now they stay in a more constricted
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
00:36:00.660
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
00:36:13.700
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.
00:36:37.020
So insulin, too much insulin, insulin resistance, it's not good for our heart or cardiovascular
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.
00:36:52.580
Does too much insulin or insulin resistance affect male reproductive health?
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.
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
00:37:17.380
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
00:37:54.240
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
00:38:07.060
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?
00:38:36.940
It does through the reaction of converting androgens to estrogens.
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
00:38:52.300
Higher insulin is resulting in higher testosterone, but that does not happen in the testes.
00:38:59.100
And unfortunately, there's not a direct effect of insulin on testosterone, but there's an indirect
00:39:05.700
As insulin is promoting the growth of the fat cell, which it does very readily, fat cells end
00:39:13.880
And so the fat cells that are growing on the man actually will pull in testosterone and
00:39:21.420
It'll convert the androgens to estrogens, just like the woman's ovaries are doing.
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.
00:39:41.740
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
00:39:52.820
Well, in some instances, that's undoubtedly the case because cancer is such an unknown beast
00:40:00.900
But the most common cancers, breast and prostate cancers, have very strong evidence linking them
00:40:08.600
For example, breast tumors will, one of the many mutations that they'll manifest with is
00:40:18.000
And breast tumors will have about seven times more insulin receptors than even neighboring breast
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
00:40:50.260
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.
00:41:01.120
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.
00:41:21.460
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.
00:41:41.780
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
00:41:55.360
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
00:42:17.740
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.
00:42:31.740
And I don't think there's any value in ignoring data, even if it's a little inconvenient.
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,
00:42:59.320
But when a cell has become infected with a virus, it tends to start using glucose at a
00:43:05.820
So once again, in this metabolically unhealthy individual, we have the potential where we're
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
00:43:32.540
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
00:43:54.440
And then it turns the home into a factory, producing ever more of itself.
00:43:59.120
So let's talk about another problem or disease that we associate insulin or insulin resistance
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?
00:44:22.780
So the answer to that two-sided question is yes, Brett.
00:44:30.580
So there's no question that when fat cells are growing, they start to promote insulin resistance.
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
00:44:54.540
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.
00:45:20.060
You know, the individuals that are on these documentaries where they're super, super morbidly
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
00:45:39.580
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
00:46:03.600
There's no question that fat tissue, if it's growing through hypertrophy, will contribute to
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
00:46:32.760
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
00:46:46.940
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.
00:46:59.880
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
00:47:10.400
So it's sort of like this vicious cycle that's going on.
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
00:47:30.520
So, okay, let's talk about, we talked about all these problems that can be caused by insulin
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
00:47:50.940
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
00:49:01.360
So take the triglycerides number and divide it by HDL.
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
00:49:24.740
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
00:49:41.340
So here in the US, those are the units that we'll use with insulin.
00:49:49.580
So if a person's, if you're fasting, insulin is around 10 microunits per mil or less, that's
00:49:55.320
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.
00:50:05.140
And if so, what are some things you can do to reverse insulin resistance?
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
00:50:37.780
Four pillars that can be used to build the proper foundation of an insulin-sensitizing diet.
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.
00:51:07.320
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,
00:51:18.720
So that's what I mean by control carbohydrates.
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
00:51:48.020
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
00:51:58.820
Every animal protein is superior to any plant protein, full stop.
00:52:03.240
So make sure you're getting the animal protein.
00:52:09.440
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.
00:52:24.380
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,
00:52:39.340
These are seed oils refined from soybeans, cotton seed, or corn seeds, etc.
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.
00:53:09.040
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
00:53:26.260
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
00:53:37.320
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?
00:53:53.040
I'm often asked what's the best exercise, and my kind of witty response is the one you'll
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.
00:54:20.280
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.
00:54:30.280
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
00:54:43.500
You're getting free pumping of glucose into your body without insulin, which is—
00:54:49.000
And by helping increase your muscle mass, you're walking around every moment of the day with
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.
00:55:03.260
Like, we've talked about and written about cold showers on the website and the podcast
00:55:07.480
And there's actually research that say that cold showers can help increase insulin sensitivity.
00:55:15.920
And when you're shivering, your muscles are spasming.
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
00:55:30.040
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?
00:56:07.280
But just for the sake of argument, let's say that maybe they would just to introduce the
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.
00:56:50.840
It's very affordable because it's off patent now.
00:56:53.580
And it's very effective with generally minimal side effects.
00:56:59.080
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.
00:57:09.700
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,
00:57:22.140
So you could imagine someone whose physician says, all right, you have type 2 diabetes or you're
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
00:58:08.100
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.
00:58:23.840
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
00:58:34.280
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?
00:58:44.080
And notice, I didn't say in the title Why Insulin Resistance Matters for the very reasons
00:58:51.480
It's because most people don't know the value of insulin.
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.
00:59:33.920
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,
00:59:42.060
And if you want to learn more about his supplement health code, you can go to gethealth, that's
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
01:00:01.360
Well, that wraps up another edition of the AOM podcast.
01:00:03.820
Make sure to check out our Art of Manless website at artofmanless.com, where you find
01:00:07.000
our podcast archives, as well as thousands of articles written over the years about pretty
01:00:11.260
And if you'd like to enjoy ad-free episodes of the AOM podcast, you can do so on Stitcher
01:00:14.700
Head over to stitcherpremium.com, sign up, use code MANLESS at checkout for a free month
01:00:18.620
Once you're signed up, download the Stitcher app on Android or iOS, and you can start enjoying
01:00:23.720
And if you haven't done so already, I'd appreciate if you'd take one minute to give us a review on
01:00:29.840
Please consider sharing the show with a friend or family member who you'd think would get something
01:00:33.500
As always, thank you for the continued support.
01:00:35.060
Until next time, it's Brett McKay reminding you to only listen to the AOM podcast, but put