00:00:00
when we're looking at smoking versus vaping vaping is probably worse in terms of the damage to the airway and the
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insulin resistance that comes from it but this gets worse because we know that insulin resistance is the core for most
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chronic diseases that are killing us and there's a handful of other lifestyle habits that's contributing to it that's horrifying so tell me everything Dr
00:00:18
Benjamin bman is a leading metabolic scientist whose research focuses on the hidden epidemic of insulin resistance and its devastating consequences and by
00:00:25
regaining control of your insulin levels he says you can regain control of your life insulin is a hormone affects
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literally every single cell of the body but if those cells become insulin resistant you start to spread the disease for example they call
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Alzheimer's insulin resistance of the brain and even the most common forms of infertility erectile dysfunction and PCOS insulin resistance is a heavy
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contributor now 88% of adults in the US have some degree of insulin resistance and people hear this and think America
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is just fat and metabolically sick but we're not actually the worst country when it comes to this and part of it is because of how different ethnicities
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store fat I'll come back to that there's two roads to insulin resistance so there's the fast lane and I could make
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you insulin resistant in 6 hours with either of these common three things but if I removed them your resistance would
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go away just as quickly now the slow lane that's a problem and there's certain lifestyle habits and problems
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with our diets that are massively contributing to slow insulin resistance now thankfully this can be resolved through four pillars which are very
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simple we'll get into that but why don't we just sack all this off and just take as EMP well because people may not know about the negative side effects for
00:01:24
example 40% of the weight that people are losing on these drugs is coming from highly
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I have been forced into a bet with my team we're about to hit 10 million subscribers on YouTube which is our
00:01:37
biggest Milestone ever thanks to all of you and we want to have a massive party for the people that have worked on this show for years behind the scenes so they
00:01:45
said to me Steve for every new subscriber we get in the next 30 days can $1 be given to our celebration fund
00:01:52
for the entire team and I've agreed to the bet so if you want to say thank you to the team behind the scenes at di of
00:01:58
all you've got to do is hit the subscribe button so actually this is the first time I'm going to tell you not to subscribe because it might end up
00:02:05
costing me an [Applause]
00:02:13
[Music]
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awful Benjamin what is the mission that you're
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on my mission is to help people appreciate that much of chronic disease
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we look at them as these siloed individual distinct disorders with totally distinct Origins and yet much of
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them share a common core it's as if their branches growing from the same tree in the conventional clinical care
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will look at these branches and give someone a prescription for a medication which is only going to prune the branch
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back a little bit never actually solving the problem it can just grow right back
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and so we can look at most of these chronic diseases that are killing us globally and and then say
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okay there are in fact some simple lifestyle changes that can be implemented that will help reduce the
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risk of not only one or two but all of the top killers from things like Alzheimer's disease to uh heart disease
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to type two diabetes to uh liver failure fatty liver disease all of them share a
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common metabolic core that's my mission and what is that common metabolic core
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yeah it's a little known problem called insulin resistance in fact when I first
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started this topic I stumbled on one paper that documented how when fat
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tissue is growing it increases the risk of type two diabetes that was this concept in the early 2000s that was
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really getting a lot of attention diabesity this kind of dual epidemic of wherever we see obesity we see more type
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two diabetes in this manuscript outlined something that was to me a revelation at
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the time it was so fascinating where when fat tissue is growing it starts releasing pro-inflammatory
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proteins that inflammation caused a problem called insulin resistance and
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then that got me into this realm of understanding that other tissues of the
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body as they become insulin resistant then you start to spread the chronic disease and and
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essentially coming to the conclusion that something like hypertension high blood pressure which is the most common
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cardiovascular problem and the main contributor to heart disease well insulin resistance is the main cause of
00:04:39
hypertension um they call Alzheimer's disease type 3 diabetes or more accurately um insulin resistance of the
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brain even the most common forms of infertility in men it's erectile dysfunction well that's because of
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insulin resistance of the blood vessels in women the most common form of infertility is polycystic ovary syndrome
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or PCOS that's because of the insulin resistance affecting her ovaries and the ability to produce the proper sex
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hormones I guess the really important question here is what is insulin
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resistance and can you explain this to me like I'm a 10-year-old oh yeah for sure insulin resistance is it's kind of
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a it's a disorder that has two parts it's like a coin with two sides that as much as we think of we we think of one
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side just because we hear the word insulin resistance but there's another part to it that I need to that is very
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important so insulin first of all is a hormone that we make from the pancreas a
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long kind of gland tucked underneath the stomach and the pancreas is a very busy organ it makes a lot of different
00:05:41
hormones it makes hormones that come into the blood it also makes enzymes that go into the into the intestines to
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help digest food but among the hormones that are being released into the blood is insulin now in the person with type
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one diabetes their immune system has destroyed their beta cells so they don't
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make insulin anymore that's why for a person with type 1 diabetes insulin is a life-saving therapy you're giving them
00:06:06
what they're not making anymore but for everybody else we have beta cells and
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they're releasing insulin when they need to now usually the main
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stimulus the main reason the beta cell is releasing the insulin is because blood glucose levels go up so I eat
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sugar you eat sugar or not even something as obvious as sugar but bread or or crackers White chips oh yes yes so
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basically anything that falls into the family of a carbohydrate so if the Earth grows it that's a carbohydrate um if
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it's a plant it's a carbohydrate maybe that's a better way of describing it and so it's going to have starches and
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sugars which all is kind of falls into this family of carbohydrate depending on how much starch or sugars that it has
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then that will result in a bigger or smaller blood glucose or blood sugar response but then if blood sugar is too
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high for too long that becomes very harmful to the body so insulin comes in um and helps lower the blood glucose and
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then having done its job insulin comes back down so insulin comes out like a taxi and transports all the glucose in
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my blood to various places around the body to St perfect yeah tax that's right
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that you can sit look at it's a shuttle it's a taxi saying hey glucose come on in I'm dropping you off at the muscle so
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mostly just as an interesting tangent of insulin before I finish answering insulin resistance insulin will open the
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doors for blood sugar to come in and drive the taxi in mostly at the muscle
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and the fat muscle and fat tissue need insulin to come and bring the sugar in
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Via taxi however other tissues and and the brain a little bit as well other
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tissues will still respond to insulin but they don't need insulin to tell it
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what to do with the sugar it just takes it in but even on those like the liver for example if the liver sees sugar
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driving by in the taxi it just opens the doors and lets it in it doesn't need insulin to come and tell it to let the
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sugar in however even at the liver and O every other cell has a similar degree of
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this the liver doesn't know what to do with it so this is back to something I'd mentioned earlier where insulin's
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thematic effect at the entire body is to tell the body what to do with energy in
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all of its forms as as these kind of caloric Rich molecules what to do with lactate what to do with ketones what to
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do with fats or glucose what to do with Pro amino acids so insulin will tell the
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body what to do with all of those things but again its most famous effect is to
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control blood sugar and that's not wrong because its most powerful activator is
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blood sugar so with all of that in mind insulin resistance is two problems wrapped into one the one problem is the
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most obvious vious one which is that insulin isn't working as well as it used to so back to the analogy of the taxis
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dropping off sugar if the muscle tissue has become insulin resistant insulin is
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coming and trying to pull the sugar-loaded taxi into the muscle but the muscle's not listening so say that
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again so the yeah insulin's coming past with the glucose inside it well not
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technically yeah but just to sort of go with your metaphor but maybe to use another one insulin comes and knocks on
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the doors it's like the bouncer yeah at the door it's coming and knocking on the door of the muscle saying hey muscle
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I've got some sugar that wants to come in and normally the muscle will say oh yeah sure okay open it up the doors and
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let the sugar come in when the muscle is insulin resistant the bouncers is knocking maybe there's even I'm almost
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getting ahead of myself but one bouncer maybe two or three bouncers pounding on the doors of the muscle cell but the
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muscle cell is not listening it's become deaf that's the insulin resistance of
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what we call insulin resistance where some of insulin's effects like helping lower blood sugar it's not working very
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well anymore and the muscle is just an obvious example because there's so much of it you know it is the biggest tissue
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on the average individual someone who's very obese perhaps now has more fat tissue but even people who are
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overweight most of us is muscle so that's a good it's a good tissue to look at so part of insulin resistance is that
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of all the things insulin is trying to do including including lower blood sugar it doesn't do it quite as well as it
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used to some of the cells or tissues of the body have become deaf to insulin's
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demands now however at the same time that's happening insulin levels are
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higher and that is really important um and I'll I'll mention an example in just a moment that highlights the difference
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between the two but we have to consider anytime we talk about insulin resistance we think of two things happening um in
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concert one insulin isn't working quite as well as it used to in various places
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of the body at the same time insulin levels are higher and that kind of takes
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us back to the um the muscle cell where I'd mentioned getting a little ahead of myself that a bouncer is knocking on the
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door and Once Upon a Time the muscle cell would hear that one polite knock from that one bouncer or one molecule of
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insulin if you will and it would open the door and let the glucose or the blood sugar come in but now the muscle
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cell um the the the bouncer insulin's knocking on the door but the muscle doesn't listen it's resistant and so the
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body has adapted and it learns okay well if one bouncer wasn't enough let's send
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an angry mob of bouncers and then the glucose the muscle will start to open the door and and and indeed it can so
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those two problems go together on one hand insulin isn't working as well as it used to that's what gives it the name
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insulin resistance but there's another part that is equally present which is that blood insulin levels are higher now
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there's um earlier at the outset of the conversation I mentioned that even infertility has an origin sh has some
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degree of um development because of insulin resistance and it's a perfect
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example of both of these parts of insulin resistance where in some instances insulin isn't working very
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well always with insulin resistance blood insulin levels are higher so for example erect stle dysfunction is the
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most common form of male infertility in fact its connection to insulin
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resistance is so strong that just a few years ago I I was so struck by a title of a paper that had just been published
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which stated something like is erectile dysfunction the earliest manifestation
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of insulin resistance in otherwise young healthy men now what is the connection it's because in a normal erectile
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function in order for the man to have normal erectile function he has to experience a pretty dramatic increase in
00:13:03
the size of the blood vessels in his body the blood vessels expand that increases blood flow and then he has
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normal function part of that signal that tells the blood vessels that it's time to expand is actually insulin and so
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this is what I said earlier where insulin does so many things in the body and we only think of it as being relevant to glucose and that's not fair
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insulin does a lot of stuff again including telling blood vessels to expand
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now unfortunately in the case of this un this unfortunate man his blood vessels
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become insulin resistant so now it's insulin coming and knocking on the doors of the blood vessel saying hey it's time
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to expand and increase blood flow but the blood vessels don't respond they don't listen so they stay constricted
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blood flow stays insufficient and thus he has a rectile dysfunction no I don't
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want to be insulin resistant no no one does no one does so so tell me how it happens yeah right yeah so the origins
00:14:01
are so important because it helps us understand why we've gotten into this situation we are where it's the most common problem worldwide there are two
00:14:08
Pathways to insulin resistance so uh two two roads that get to the same destination again the destination being
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insulin resistance there's the fast lane which I call fast insulin resistance and
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it actually has three lanes which I'll describe in a moment then there's the slow insulin resistance which is a more
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it takes a little longer get there but at the same time it takes a little longer to get away from it so I'll start
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with fast insulin resistance because the slow one ends up getting a little excitingly complicated but in a cool way
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so with fast insulin resistance there are three things that I could take you to a clinical lab and I could make you
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insulin resistant in six hours with either of these three things but as quickly as it settles in if I remove
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those things your insulin resistance would go away so so these are fast causes and they're fast resolution they
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are stress is uh is a primary cause of fast insulin resistance SO2 is
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inflammation and then lastly and this is going to sound somewhat paradoxical too
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much insulin is also a cause and I'll end with that one because I think it's the most important then transition to
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slow insulin resistance so anytime the body is experiencing too much stress it will very quickly become insulin resist
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istent now as a professor who teaches Endocrinology no surprise I Define
00:15:35
stress in the context of hormones and there are two primary stress hormones cortisol and what we call in the US
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epinephrine or in the UK adrenaline those are the two stress hormones now those hormones are very distinct they
00:15:50
have almost nothing in common but like when you are feeling a little stressed it's both of those especially adrenaline
00:15:57
epinephrine that are making you feel a little jittery it's making your heartbeat a little faster you're a
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little more alert um that all starts to play into a stress response but what
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those two hormones have in common is that they both want blood glucose levels to climb it's kind of their way of
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saying hey we don't really know what's going on right now but we want to be ready to run away or to that's the fight
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ORF flight kind of aspect to stress and so they want to push blood glucose levels up and they do very well that of
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course puts them at odds with the hormone insulin cuz these two epinephrine or adrenaline and cortisol
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the two stress hormones they're pushing glucose up insulin wants to push it down
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so the more the body is has those stress hormones elevated because of say sleep
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deprivation that's a very effective way to increase cortisol or they are taking
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too much drinking too much caffeine that is a way to increase epinephrine quite strongly if both of those signals are
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too incess or you know they continue to be present and climb then insulin has to
00:17:03
work harder and harder and then we have insulin resistance so stress is a cause
00:17:09
of insulin resistance but then next is inflammation you you know you and I were
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commenting about earlier about how boy there's a cold going around people it's flu season even then if a person were
00:17:22
wearing a continuous glucose monitor on the back of their arm measuring their glucose levels they would see their
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glucose levels are much much higher like significantly higher during the time that they're struggling with this
00:17:34
infection that is a reflection of insulin resistance insulin's having a harder time keeping the blood glucose
00:17:41
levels in check anytime inflammation is up insulin resistance will be up as well even in
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things like autoimmune diseases there are reports in humans that document the degree to which someone has say active
00:17:55
rheumatoid arthritis their their joints are achy because of of an autoimmune
00:18:00
attacking of the joints they will note on some days like every autoimmune
00:18:06
disease there is an EB and a flow some days it's good some days it's bad and on
00:18:11
the bad days if you measure their insulin resistance it is absolutely locked with the degree to which their
00:18:18
immune system is turned on or off or higher or lower so inflammation is another cause and then the last one of
00:18:25
the Fast Lane of insulin resistance is too much insulin itself now the astute
00:18:31
listener will realize the kind of circular thing I've just presented by invoking high insulin as a cause of
00:18:37
insulin resistance because they will also think but wait a minute Ben you just said that high insulin is also a
00:18:43
consequence of insulin resistance that you know back to the bouncer knocking on the the the door of the muscle cell if
00:18:50
one bouncer wasn't enough or one molecule of insulin wasn't enough the body will say okay well let's send 10
00:18:56
molecules of insulin so High insulin is both a consequence of insulin resistance
00:19:02
but it's also a cause and this is reflective of a fundamental principle in
00:19:09
all of biology that if there is too much of a stimulus a cell if it's capable will try
00:19:17
to become resistant to that stimulus this would be like a funny analogy of in
00:19:23
in in my in the bikman home my darling wife is home with the children that is
00:19:28
what she wants to do she she is full-time mom when I'm home and I try to be home as much as I can it's funny for
00:19:35
me to note the difference in how quickly we each respond to our children I will hear my child saying mom mom mom and
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she's not responding mom has heard this for so much that she's become kind of
00:19:49
selectively deaf to when my children are demanding her attention I'm not as around my children quite as much because
00:19:55
I'm working during the day and so when I hear that it's a very fresh signal to me
00:20:00
I've not heard it so much that I've become deaf to it and so I will respond even though I'm in the other room
00:20:06
because I'm so much more sensitive to the clamoring for attention this is like
00:20:12
the body in response to insulin if there is always insulin it's always going up
00:20:18
always going up the body will start to say the muscle cell will start to say boy insulin you are knocking on my door
00:20:24
all the time this is getting old I'm not responding anymore I'm not going to listen as much as I was before so in
00:20:30
that sense insulin too much insulin becomes a cause of insulin resistance
00:20:35
and back to what I said earlier I could take you into the lab start infusing you with just a little drip of insulin to
00:20:41
increase your insulin and over just a few hours you would become demonstrably
00:20:46
less sensitive to it than you were before we started but again as I take
00:20:52
that away give your body a few hours and it's back to normal in every one of those instances it's a fast onset and
00:20:58
it's also a fast solution if we can take it away if we can take it away but if we can't take it away does it become sort
00:21:04
of chronic yeah so that especially all of these can contribute to a more lingering insulin resistance but
00:21:10
especially insulin where I focus on that one the most because of not only its
00:21:16
relevance to the slow lane but also just how present it is where 70% of all
00:21:22
calories globally are carbohydrates and now perhaps with the best of intentions
00:21:28
our experts are telling us that we should be eating six times a day and so
00:21:33
we eat we wake up in the morning insulin has finally been coming down while we've
00:21:38
been fasting overnight insulin gets to take a little bit of a break we're fasting then we break that fast by
00:21:44
eating breakfast and in the UK as it is in the US by and large this is going to
00:21:49
be a very starchy sugary breakfast it's toast with some Jam or it's cereal or
00:21:55
it's Bagels that is going to be that is almost pure glucose and so what do we do
00:22:01
we wake up we eat breakfast we Spike our blood sugar levels and Insulin has to come up insulin will take longer to come
00:22:07
down than the blood sugar will it will wait in the blood to make sure that all the blood sugar has gone back to normal
00:22:13
so depending on how much carbohydrate we ate for breakfast it could take our insulin levels three or even four hours
00:22:20
to come back down to normal long before it's had a chance to come back down to normal we've had a midm morning snack of
00:22:27
course we need to go get a sugar coffee and another Bagel or something and so
00:22:32
after just a couple hours we do it again and once again before insulin has had a chance to come back down we have a
00:22:38
starchy carbohydrate heavy lunch then an afternoon snack and then a carbohydrate
00:22:43
heavy dinner and then of course we have to have an evening snack before we go to bed so the average individual is
00:22:48
spending every waking moment in a state of elevated insulin and thus the signal
00:22:54
never really goes away because they they never give themselves a break but one of
00:22:59
the consequences of that I mentioned which is that it directly causes insulin resistance but when insulin is high it
00:23:07
starts to have a signal on the fat cell and that then brings us to the slow insulin resistance where you have
00:23:14
something happening in the fat tissue that begins to set the stage for insulin resistance in the entire body and it
00:23:20
takes longer to settle in but it takes also longer to go away that's why I call this one slow insulin resistance now in
00:23:27
the case of insulin most people so the the the the key with the yeah I'll
00:23:33
explain it this way first so the most relevant feature with fat tissue contributing to insulin resistance is
00:23:39
the size of each fat cell when we typically think of fat we would maybe say okay Steve has um I'll do this in
00:23:47
kilos for the UK audience Steve has 10 kilos of fat on your entire body that's probably too much for you Ben has 20
00:23:55
kilos and yet it's possible that I'm healthier metabolically than you um and
00:24:02
that's because it's not the mass of fat that matters most it's the size of the fat cell that matters this is why women
00:24:10
despite universally being fatter than her male counterparts are healthier with regards to insulin resistance and every
00:24:16
single metabolic problem it's because women as a result of her particular sex hormones have more fat cells but they're
00:24:23
smaller so she has more fat but smaller fat cells and small fat cells are
00:24:29
healthy insulin sensitive anti-inflammatory fat cells but the
00:24:35
bigger the fat cell gets the more it initiates a Cascade of events or a series of events that creates insulin
00:24:42
resistance and am I right in thinking we have the same amount of fat cells for our whole life pretty much that's a
00:24:47
really really safe assumption for most people yeah for most people the a fat cell um sometimes students will hear
00:24:54
that fat cells are Immortal that is not true but they're longlived fat cells will live about 10 years and so
00:25:01
typically by the time if you think of if you look at a newborn during infancy
00:25:06
childhood and puberty the number of fat cells is going up up up up up once they
00:25:11
finish puberty so mid to late teens for a young woman late teens or even early
00:25:17
20s for a young man usually at that point the number of fat cells they have is going to be very static this is
00:25:22
something people don't really understand and I actually discovered it from during this podcast and speaking to so many experts about this that that we pretty
00:25:29
much especially as an adult have the same amount of fat cells really regardless of what we eat yes and it's
00:25:35
actually just the fat cells we have shrinking or grow expanding exactly
00:25:40
that's exactly right now there are differences across which by the way makes lipos suction a pretty bad
00:25:46
idea in fact it in fact it makes things worse please let's make sure we come back to that okay I'll write down lip
00:25:51
because it really becomes the person ends up their vanity ends up really ruining their their their future
00:25:59
metabolic outcomes but there are differences across ethnicity like um this is a little oversimplified but not
00:26:05
much on one end you'd have Caucasians kind of northern European Caucasians on the other one end you'd have East Asians
00:26:12
like uh Chinese Japanese uh Korean East Asians and and then if you look at that
00:26:18
same spectrum of people making fat cells through their life an East Asian will be
00:26:23
making fat cells and then stop right about here about sort of so very few fat
00:26:28
cells relatively speaking across all the ethnicities they have very few fat cells a Caucasian on the other end of the
00:26:35
spectrum they went way higher and so this guy let's say American Ben versus
00:26:41
Chinese Ben overly simplified but but here we are um so much of fat Mass isn't
00:26:48
the number of fat cells even though American Ben has more it's the size of the fat cell so I could be the same
00:26:55
percent body fat really as Chinese knees Ben um but that would just be because my
00:27:01
fat cells were just that much smaller but this is the problem then if you have
00:27:07
let's say American Ben and Chinese Ben both gained 10 kilos of pure fat over
00:27:12
the next 10 years very easily done most people do that quite often Caucasian Ben just doesn't look as
00:27:18
good in his Speedo um which is a pasty Caucasian he's not going to look particularly good in that Speedo anyway
00:27:24
but I just am bulging a little more than I was before but otherwise I'm healthy my blood pressure is fine my blood sugar is fine everything's normal put that
00:27:32
same 10 kilos of fat on Chinese Ben hypertension type 2 diabetes fatty liver
00:27:39
disease infertility um and that is because Chinese Ben had fewer fat cells
00:27:45
to start with and so those fat cells as the body was told to store fat those fat
00:27:50
cells were getting much much bigger much sooner and the fat fat cell promotes
00:27:57
insulin resistance very very readily and so that logically moves into this the question of what
00:28:03
makes fat cells grow and it is two essential variables that we only ever
00:28:09
look at calories and yet if you take a person with type 1 diabetes and say I
00:28:15
want you to eat 10,000 calories but don't give yourself your insulin injection they cannot gain weight it is
00:28:23
it is literally impossible for the type 1 diabetic to get fat if they are
00:28:28
skipping their insulin injections in fact this is so known that if you take let's imagine a young woman who would
00:28:34
maybe have more pressure to be thin than her male counterpart although it's happening more in males too imagine a
00:28:40
young girl who gets diagnosed with type 1 diabetes at the age of 13 or 14 very impressionable time she's very worried
00:28:47
about how how she looks and how thin she is she learns that wait a minute I can
00:28:55
eat whatever I want and all I have to do is not eject my insulin and I'll be as skinny as I want and it works it works
00:29:01
so well that it's actually a formal eating disorder called diabulimia so this the fact that this
00:29:08
exists is absolute proof that the growing and the shrinking of the fat cell is more complicated than just
00:29:13
calories being high or low because like i' said earlier when I talked about hormones hormones are a way for the B
00:29:20
for the very tissues of the body to know what it ought to do with energy and so a
00:29:25
fat cell will have energy all around it and if it doesn't have insulin to tell it what to do it won't do anything with
00:29:31
it or maybe to make this more direct back home in my lab my students my
00:29:38
students are growing fat cells in Petri dishes these fat cells are swimming in a little sea of calories lots of glucose
00:29:45
lots of fats and yet they stay really small until we add insulin the moment we
00:29:52
add insulin into that little petri dish if we check those cells four hours later they're immediately fatter if we check
00:29:58
them 4 hours later they're fatter still now they know what to do with the energy
00:30:04
they have so with slow insulin resistance it develops when fat cells
00:30:09
get really really big it's like a a because they have to tell insulin insulin you continue you you are telling
00:30:15
me to keep growing I can't keep growing I'm so big that I'm going to pop I mean literally the fat cell can get so big
00:30:21
that it degrades its membrane it's like a water balloon that a naughty little boy has overfilled and it's about to
00:30:27
burst the fat cell doesn't want to burst and so it tells insulin insulin you are
00:30:32
trying to make me grow you're telling me to grow I can't listen anymore I'm becoming insulin resistant to stop
00:30:39
growing so insulin makes you fat oh very much now if you so so a moment ago I
00:30:45
said that the big fat cell is two variables you must have both you must have both a signal to tell the fat cell
00:30:51
to get big which is insulin it is the there's no other signal that can do it you can in a human just simply take away
00:30:58
the insulin like type 1 diabetes it doesn't matter any other hormone in the body it does not matter they cannot get
00:31:04
fat they could again they can eat thousand they could eat 10,000 calories
00:31:10
of chocolate cake they cannot get fat not only can they not get fat they can't hold on to their fat because if there's
00:31:16
no insulin to tell the Fat Self to hold on to it or get big it has to shrink it's breaking down its fat so the body
00:31:22
goes into such a dramatic fat burning state in the absence of insulin that keeping fat fat becomes impossible so
00:31:29
the insulin signal is necessary to tell the fat cell what to do but the fat cell will say Okay insulin you're high you're
00:31:37
telling me to grow but what am I going to grow with that's where the calories come in now the fat cell will say hey
00:31:44
fats and glucose in the blood insulin has told me to get big and so I need to pull you in to help me grow you're going
00:31:51
to give me the bulk and if you have one without the other it is death so if I'm
00:31:58
in 2,000 calories and I have a different insulin sensitivity to you so we both eat 2,000 calories and I'm insulin
00:32:06
resistant doesn't that mean that I will you'll store more as fat oh okay yeah
00:32:12
yeah so so your body now it would partly depend on there are people where you you if your if all of your fat cells had
00:32:19
reached its maximum point then you're done you're not going to gain more fat you're just going to become more and more and more insulin resistant okay
00:32:25
fine so you kind of start limiting yourself but there are studies in humans to show that if you give humans
00:32:32
isocaloric D meals so the exact same number of calories but they in the same
00:32:38
amount of protein but you differ those meals based on the amount of carbs to the amount of fat so let's say two meals
00:32:45
exact same calories 2,000 calories or that's in one meal that's too high a th000 calories in one meal one version
00:32:52
of this is the conventional way of eating which is lower fat higher carb
00:32:58
the other meal same number of calories but it's lower carb higher
00:33:04
fat this lower carb higher fat version will have a lower insulin
00:33:10
response and they they will store less fat from that meal they're met and someone would say well where do the
00:33:16
calories go you can't this it's the laws of thermodynamics you can't destroy energy the metabolic rate will go up so
00:33:24
when insulin is low if you have someone going a full day eating the same number of calories but
00:33:30
lower carb calories their metabolic rate will be almost 300 calories higher in
00:33:35
that day a metabolic rate is the yeah that's the total amount of energy that it just costs you and I to just live
00:33:40
okay you RIS going through the day but that's but that's a significant amount like if you and I were to go exercise and say let's go burn 300 calories we
00:33:47
got to be on the stair stepper for an hour or something so it's 300 calories but at the same time if your insulin is
00:33:55
low you're burning so much fat that start making ketones and I I don't intend to get onto that topic quite yet
00:34:01
but suffice it to say every molecule of a ketone has a has a caloric load
00:34:06
roughly similar to glucose and one of the and and what the body when it starts making a lot of ketones it starts
00:34:13
eliminating the ketones so every time someone is breathing out ketones they're literally breathing out calories or
00:34:20
they're urinating and they're urinating out ketones if they have higher ketones in their blood they're urinating out
00:34:26
calories because ketones have energy and so this is the way that if insulin is low it becomes impossible for the body
00:34:34
to hold on to its energy it is so determined to spend energy that it will both increase metabolic rate and it will
00:34:41
make the energy the calories be wasted in the breath and in the urine and in
00:34:46
the form of ketones because ketones have calories ketones are energy now we're just dumping them out into the universe
00:34:53
it's worth before we talk about how to keep my levels low so that I can benefit from
00:35:00
all the health benefits we've talked about it's probably also worth just spending a little bit of time trying to understand the evolutionary basis of
00:35:06
insulin resistance there are some theories that are very interesting that attempt to explain why is it that we
00:35:13
became so fantastically different from let's say our closest animal relatives other primates like chimpanzees or or
00:35:20
Apes what was the difference that had us become so different than them one of the
00:35:25
leading theories is a is a Theory called the expensive tissue hypothesis and it
00:35:31
actually does have something to do with ketones in the expensive tissue hypothesis as the theory goes our
00:35:39
earlier ancestors deviated in this kind of animal family line because we started
00:35:45
eating more meat we started eating food that was so nutritious so nutrient-dense
00:35:51
so loaded with good calories and all of the fats and proteins that we need that
00:35:57
it allowed two very distinct changes to occur in US compared to other primates
00:36:02
one our intestines became significantly shorter so if you compare the human digestive tract to any other primate
00:36:10
animal if we are a primate um then if you look at the intestines they're fantastically different particularly the
00:36:17
large intestine or the colon because our ancestors as the theory goes began
00:36:23
eating meat we didn't need the colon as much um because the colon is a place for
00:36:28
food to ferment and so if you're eating a lot of plant matter like other primates do you need a much much larger
00:36:36
colon so we started eating food that was so nutrient-dense our colon shrunk considerably we didn't need to waste
00:36:42
energy on a big busy colon at the same time as we were eating food that was so
00:36:48
nutrient dense and so loaded with good fat it allowed us to have more time to
00:36:53
be curious and explore and so at the same time our int in were shrinking because we didn't need them to be so big
00:37:00
our brain was growing and it's because it had so much nutrition including
00:37:05
ketones so ketones are an extraordinary fuel for the brain in fact one of the
00:37:11
reasons why a baby that is born premature will be more likely to have
00:37:17
learning disorders later in life is because premature baby didn't have time to get very fat and fat baby is healthy
00:37:25
baby and fat baby gets into ketosis let's say you and I were to fast
00:37:31
straight for 2 days if you took a six-month old baby that baby would be in
00:37:36
a deeper state of ketosis in two hours than you and I would be in two days
00:37:41
because the baby is burning so much of its beautiful chubby fat and the more the body burns fat the more it makes
00:37:47
ketones and the tissue of the body that appears to benefit the most in response to ketones is the brain
00:37:55
the brain the moment ketones hit the blood stream the brain immediately starts taking in ketones for a fuel very
00:38:02
often I have students who have had a professor perhaps with the best of intentions but ignorant nonetheless tell
00:38:09
the student that the brain the main fuel for the brain is glucose that the brain prefers glucose and I show them just one
00:38:16
or two papers to prove that wrong immediately and it is reflected in in in
00:38:21
this idea which if if to use some convenient UK units if blood glucose is
00:38:27
5 Millar that's a concentration a way of measuring an amount of of something blood glucose may be 5 Millar or 80
00:38:34
milligram per deciliter for the American audience um that would be a normal glucose and if you and I were to fast
00:38:41
for 24 or so hours we may get up to about one Millar of of ketones and yet
00:38:47
even then the brain has already switched to get the majority of its energy from
00:38:52
the Ketone and so don't tell me that in this Dynamic the brain prefers this one
00:38:58
because this one's five times higher than this one and even in that scenario the brain is already getting more than
00:39:04
half of its energy from the Ketone so all of this is my long-winded way of saying when we look at the principles of
00:39:10
evolution one of the leading theories is this idea that we began eating essentially a meat heavy diet that again
00:39:17
is so nutritious that it allowed our brain brains to grow maybe one final point on this although it is a bit of a
00:39:22
barbed comment people may find this somewhat amusing or disappointing or frustrating the title of a book just
00:39:29
published which is that vegetarians have smaller brains this is seen in humans
00:39:35
that the less a human eats meat then the smaller the brain becomes the brain is
00:39:41
so dependent on the nutrient density that comes from animal sourced foods that it will suffer um when it doesn't
00:39:48
get them interesting I mean that's a controversial thing to say it is and you can cut it out but it really is it's a
00:39:55
real thing and why does depression go up so much when people stop eating animal Source Foods it's because you are
00:40:01
depriving the brain of what it needs what is it exactly you're depriving the brain of in that situation yeah yeah so
00:40:07
at least among other things at least it would be the the essential omega-3 fats so there are three Omega-3s and you
00:40:13
humans can only we can only get one from Plants but it's one that the humans don't use we need the other two and they
00:40:19
only come from animal Source foods and you could supplement absolutely right and yeah you can but but that that so
00:40:26
the the solution in that regard is the vegan must be educated enough to know what they're deficient in and then
00:40:32
wealthy enough to afford the supplements to make up for it so is that the the only evolutionary sort of hypothesis
00:40:40
towards why we developed this insulin resistance oh yeah in fact it's funny that you bring the question up again
00:40:46
because I realized I didn't quite answer it that way so insulin resistance why would it exist at all it would probably
00:40:52
be a way for the body to know when it was needed to hold on to energy a little
00:40:58
better so now I say that now and and someone would think well but you just
00:41:03
why would I want to hold on to energy in a way where it's causing hypertension and Alzheimer's disease and increasing the risk of heart disease not all
00:41:11
versions of insulin resistance are negative so there is um there is what
00:41:17
all the insulin resistance that you and I have been talking about is pathological insulin resistance or
00:41:22
harmful insulin resistance insulin resistance that serves no good purpose and it's making us sick however there is
00:41:31
insulin resistance in human development which is physiological or helpful it's
00:41:36
supposed to happen and that is the two PS of physiological insulin resistance
00:41:42
puberty and pregnancy because in both of those instances as we outlined earlier
00:41:47
when the body's insulin resistant insulin is high that's not always bad because insulin wants things to grow it
00:41:55
is like a fertilizer in the body now sometimes it's misplaced and results in problems like increasing the risk of
00:42:01
cancer for example but in other instances if you have a young child who needs some explosive growth during
00:42:07
puberty well then that's really helpful insulin's telling the body to store more energy to build up tissues including
00:42:14
muscle and bone but also including fat so in pregnancy insulin's playing a role in growing the placenta sure is the
00:42:21
breasts yes so in the woman after she's finished puberty the only other time of growth she'll never have will be
00:42:28
pregnancy and and so those are the two instances where the body has become insulin resistant to take advantage of
00:42:34
the heightened scenario where it can grow because the woman's body needs to more fat goodness yes yes so her body
00:42:40
not only needs to grow tissue Mass like the uterus has to get much bigger she has to grow a placenta she also needs to
00:42:46
become a little insulin resistant to give a little more glucose to her baby because she is after all now living for
00:42:52
two people and so as as her body becomes insulin resistant actually facilitates
00:42:58
the growth of the baby a little more rapidly but as you noted it helps her store more fat and progesterone is
00:43:04
another hormone that even accelerates that process but basically it's her way
00:43:10
of her body's way of saying hey I am committing to Growing another human and
00:43:16
it's going to be metabolically very demanding and so I'm going to have as much extra fat or much as much extra
00:43:23
energy as I can in order to ensure that if there's any sort of scarcity in food
00:43:28
that happens during the course of the pregnancy I'll have enough energy to get through it all and then maybe I'll even
00:43:34
have enough to continue to feed the baby with lactation after the baby's born what is gestational diabetes yeah it's a
00:43:42
great question gestational diabetes is essentially type 2 diabetes of pregnancy
00:43:48
so it's perfectly timed question because if you look at the average woman um who
00:43:53
is very healthy very insulin sensitive at the beginning of her pregnancy so glucose is normal and insulin is
00:44:00
normal over the course of her pregnancy she stays normal healthy pregnant woman
00:44:06
which is to say she has physiological insulin resistance she doesn't get diagnosed with gestational diabetes
00:44:12
though which means her glucose is normal but to keep her glucose normal because she is insulin resistant but for a
00:44:18
purpose to help her body grow her insulin levels are high and then the glucose is still in a normal range and
00:44:25
then in some women especially if she has a family history of type two diabetes
00:44:30
the insulin resistance goes too far now she has high insulin like all pregnant
00:44:35
women do but she's not able to keep her glucose levels in check so if I'm eating
00:44:41
loads and loads of sugar throughout a pregnancy that will compound the problem absolutely so then she will go from the
00:44:47
normal insulin resistance of pregnancy into the insulin resistance of diabetes so it really is like type 2 diabetes but
00:44:54
a microcosm of it a mini verion that was really instigated or initiated because of the pregnancy combined with a
00:45:01
bit of a genetic predisposition combined with her eating the worst possible way does that then impact the future baby oh
00:45:08
for sure it does yeah so think about it's almost like the baby is devel literally developing in a hyperglycemic
00:45:16
hyperinsulinemic environment so the baby's get the baby gets hardwired to want to continue to exist
00:45:23
in a state of high insulin and high glucose after the baby is born and so so yes The Offspring of mothers who have
00:45:29
gestational diabetes are significantly more likely to gain weight and be chubbier or fatter than their
00:45:36
counterparts and to later develop type two diabetes yeah a resounding yes I read in your book that these infants
00:45:41
have a 40% higher chance to be obese and have metabolic complications in their teenage
00:45:46
years and Beyond yes I mean a significant thing and I I say that with all of the sympathy I can for the mother
00:45:51
who may be struggling with this but it is certainly a motivation for Mom to just be mindful of what you're eating
00:46:00
one of the things that that I saw the other day on social media which I wanted to ask you about was this I got a
00:46:06
picture of it here um it was someone online that posted this photo and they
00:46:12
said well this graph and they said we need to figure out what's going on here
00:46:17
um this is the graph I'll put it on screen for anybody that's watching but also it'll be linked in the comment section below um it essentially shows
00:46:24
that over the last let's say 20 20 years there's been a really significant rise
00:46:29
in cancer amongst women but when we look at cancer amongst men it's pretty flat
00:46:35
MH um and this is cancer incidence by age and gender up to 49 years old and I
00:46:42
was wondering if you had any thoughts on why this is happening yeah yeah yeah a few thoughts come to mind um whenever I
00:46:49
see these kinds of reports I always make sure I look firstly at the what are they actually measuring so just to set the
00:46:55
stage this is the number of women who are being diagnosed with cancer so not dying from cancer but it's going up so
00:47:02
one one simple explanation although perhaps the most disappointing could be that more women are going in for testing
00:47:09
younger and so we're just seeing kind of an artifact of more women are just going in sooner and they're detecting a
00:47:15
problem that they wouldn't have otherwise detected you know for 10 or 20 years which is a good thing you want to
00:47:21
detect cancer as soon as possible so that's the boring answer that it could be a reflection of just more women going
00:47:27
in for ultrasounds or MRIs or mamory scans whereas men don't ever get tested
00:47:33
for anything which is why we die more from everything possibly but to give a
00:47:38
more exciting answer this is very very likely almost entirely driven by breast cancer um breast cancer is the main
00:47:45
cancer for women um by far and so if I had to guess I bet almost all of this
00:47:51
increase in cancer incidents is because of breast cancer why might that be going
00:47:56
up I would suggest there's probably a couple instances one um although people
00:48:02
might not appreciate this is that one of the best ways for a woman to reduce her risk of breast cancer is actually having babies it's very well known um very well
00:48:09
documented that if a woman um has a f has babies and breastfeeds her risk of
00:48:15
um breast cancer goes down so yeah in fact it's very meaningful I actually don't know um the reasons for it it
00:48:21
could be the changes in estrogens during lactation phase I've just I've just actually done a quick search here to I
00:48:28
put a picture of that graph into Ai and asked it the same question and it said pretty much what you said it said there's a rising breast cancer incidents
00:48:35
according to cancer research UK the other one that it came up with is obesity Trends oh yeah I promised I was
00:48:41
going to talk about that I wouldn't leave that sorry for interrupting there no no no problem and then the other one
00:48:46
was delayed childbearing that's what I'm saying which is what you were saying yeah so as child rates as child birth rates are going down it does increase
00:48:53
the risk of breast cancer now as I'm a cell biologist right I like to understand a direct mechanism and so as
00:48:59
much as I invoke the perhaps lower rates of child birth among women I don't know the mechanism so I'm sort of loathe to
00:49:05
describe it the mechanisms I'm very familiar with are the metabolic um which is if you take a breast tissue that is
00:49:13
tumor tissue and compare it to like if you take a breast tumor and compare it to the normal tissue right next to it
00:49:20
like that it would have shared its Origins with the cancer from the breast will have seven times more insulin
00:49:27
receptors than the normal breast tissue so the idea of this tracking quite
00:49:32
nicely with obesity rates going up over the past 20 years I wouldn't say that it's the Obesity per se but I would say
00:49:39
it's the entire metabolic milu which is the insulin resistance that as much as the high insulin is promoting fat cells
00:49:45
getting bigger that high insulin is also accelerating the growth of the tumor cells because again the main one of the
00:49:53
main mutations in breast cancer is a Sevenfold so a seven times increase in
00:49:58
the number of insulin receptors and Insulin wants to tell things to grow so it's no surprise that almost every tumor
00:50:04
that's ever been measured for having insulin receptors will have a lot more it's basically telling its neighboring
00:50:11
cells insulin's going to come by and it's going to tell us all to grow I want to grow more than you and that's what
00:50:17
cancer is cancer is growth unregulated growth insulin tells things to grow so
00:50:22
the connection between obesity with the rising incidence of breast cancer is very very likely a consequence of the
00:50:29
rising incidence of insulin resistance as you guys know whoop is one of my show sponsors it's also a company that I have
00:50:36
invested in and it's one that you guys asked me about a lot the biggest question I get asked is why I use whoop over other warable technology options
00:50:44
and there is a bunch of reasons but I think it really comes down to the most overlooked yet crucial feature it's
00:50:49
noninvasive nature when everything in life seems to be competing for my attention I turn to whoop because it
00:50:55
doesn't have a screen and will armed the CEO who came on this podcast told me the reason that there's no screen because
00:51:02
screens equal distraction so when I'm in meetings or I'm at the gym my whoop doesn't demand my attention it's there
00:51:08
in the background constantly pulling data and insights from my body that are ready for when I need them if you've
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been thinking about joining whoop you can head to join. woop.com CEO and try whoop for 30 days risk-free
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and zero commitment that's join. whoop.com CEO let me know how you get
00:51:28
on you know one of the big subjects you touched on at the start was the was Alzheimer's and Dementia yes and I have
00:51:35
heard several people on this podcast tell me that they think of Alzheimer's as type three
00:51:43
diabetes worldwide there is a new case of dementia every 3.2 seconds um it seems like I don't know if
00:51:51
this is true but is Alzheimer's and Dementia On The Rise oh yes yeah it is in fact it went from not being even on
00:51:56
the radar to being a top 10 killer um now it's interesting how people even die from Alzheimer's disease it's a very
00:52:03
kind of vague death but yeah Alzheimer's disease is one of the top 10 diseases now um certainly in the west um and and
00:52:10
I would argue it's because it has a metabolic orgin now one of the interesting things about Alzheimer's disease is we have
00:52:17
spent billions of dollars on Alzheimer's research trying to identify the the
00:52:24
plaque so so just to set the stage here so that people listening can appreciate this this paradigm shift that's occurred
00:52:31
in Alzheimer's research originally and even in many people still people thought
00:52:36
that Alzheimer's disease is the result of these plaques accumulating in the brain these kind of little proteinous
00:52:43
little thick things that are preventing neurons from sending the signals throughout the brain for the brain to
00:52:48
think and and and have normal cognition and and yet there are those of us and I
00:52:53
am proud to say I have long been one of them who has said that the plaque based Theory doesn't make sense we have had
00:53:00
drugs that have been available for human use for years that have effectively
00:53:05
reduced plaques in the brain and yet did nothing to improve cognition so that is
00:53:10
an immediate challenge of the plaque based theory of Alzheimer's even further
00:53:16
even Beyond older than that evidence when you would look postmortem or look
00:53:21
at tissue donor people who passed away you would look at the brains of people who died with confirmed Alzheimer's
00:53:27
disease at the time of death and look at the brain of someone who died without any evidence of any cognitive decline or
00:53:34
any compromised thinking whatsoever and you would be just as likely to find plaques in both brains so the so whether
00:53:41
the brain had Alzheimer's disease or not you would still see plaques in the brain so the whole idea that plaques mattered
00:53:47
has long been controversial and just to put a fine point on it before transitioning to the metabolic Origins
00:53:53
about two or 3 years ago they found out that the very first published papers
00:54:00
that implicated plaque as a cause of Alzheimer's disease were based on fabricated data so the scientists who
00:54:07
published those first reports that led to the entire theory that Alzheimer's diseas is plaque based were called out
00:54:14
as fraudulent and and indeed all of it was fabricated so the entire idea that Alzheimer and and we have spent billions
00:54:21
of dollars on studies to try to how determine how do plaques CA cause Alzheimer's disease why when we reduce
00:54:29
plaques it doesn't appear to help the disease because the plaques had nothing to do with it that's just something that
00:54:34
some brains have some brains have more of these little specks than other brains and they don't contribute to Alzheimer's
00:54:40
disease at all now what did what kept rising to the top and I would hope now
00:54:47
is the dominant theory is that people with Alzheimer's disease almost always have some detectable instance of insulin
00:54:54
resistance if not full-on diabetes type two diabetes now I will say personally I
00:54:59
don't like the term type 3 diabetes because it makes it sound like it's a
00:55:05
whole new version of diabetes to say it more succinctly and accurately it is
00:55:10
simply insulin resistance of the brain and the brain is a very hungry organ it
00:55:17
is in what I teach is is a tri a trinity of high metabolic rate organs that there
00:55:22
are three organs in the body whose metabolic rate is so high that that just really sets it apart from everything
00:55:28
else and the brain is one of them the brain has a very high metabolic rate so this is a very hungry organ that needs a
00:55:35
lot of energy all the time but the brain is unique in that it primarily will only use two fuel sources and I've mentioned
00:55:42
them namely glucose and ketones but glucose in that section of
00:55:48
the brain that gets compromised with Alzheimer's disease the glucose can't just come straight in it needs someone
00:55:54
to open the door for it and that is insulin of course just like we described
00:55:59
with the muscle cell where in order for the glucose to go into the muscle insulin had to come and knock on the
00:56:04
door if you will and then the muscle being a polite responsive host would open and allow the glucose to come in
00:56:10
the brain is similar that in that section of the brain it has doors that
00:56:15
need insulin it's locked until insulin comes and opens them so even though glucose levels may be high in the blood
00:56:22
like in type 2 diabetes you would think well the brain can just get all the glucose it wants and yet it cannot
00:56:29
because it has insulin regulating the entrance of the glucose and if the brain is insulin resistant there's not enough
00:56:35
glucose coming in and thus the brain is forced to rely on the only other fuel that it can rely on namely ketones but
00:56:44
the same person who's eating all the time to keep their blood glucose high all the time has so much insulin in
00:56:49
their blood that they're never making enough ketones to fill the Gap you know and mind the gap in the brain brain has
00:56:56
an energy gap now and and where where the brain needs you know an amount of energy I'm kind of acting it out for
00:57:03
those that are watching but the brain has a certain energy demand that it needs and if there's a lot of glucose in
00:57:08
a healthy insulin sensitive person glucose will fill all of that need but as the brain becomes progressively
00:57:14
insulin resistant it cannot get all of its energy from glucose and thus there's
00:57:19
an energetic Gap and in the absence of ketones there's nothing to fill that Gap
00:57:24
and the Brain says well I don't have enough energy to keep functioning as well as I did before so I have to reduce
00:57:30
my function which manifests as a reduction in the ability to think and process in other words cognition goes
00:57:37
down what's so interesting is I just got finished describing a scenario that
00:57:42
scientists refer to as brain glucose hypometabolism or a reduction in the
00:57:49
amount of glucose the brain is using there are scientists that measured this we don't in my lab because we don't do
00:57:55
these kinds of techniques but you can actually Infuse people with the glucose that you can take pictures of and see
00:58:01
how much the brain is taking it in and metabolizing it in Alzheimer's disease the brain is not getting as much glucose
00:58:07
so they call that a hypo or reduction in metabolism of glucose and as much as you
00:58:13
and I are describing that scenario as relevant for Alzheimer's disease you can essentially open up the book of
00:58:18
neurological disorders and see the same thing depression has a brain glucose
00:58:24
hypom metabolism to it my migraines have a brain glucose hypom metabolism
00:58:29
epilepsy um and Parkinson's disease so all of these disorders of the brain of the central nervous system the one thing
00:58:36
they all have in common is the brain isn't getting enough energy from glucose and another way of saying that
00:58:43
is the one thing all of those seemingly unrelated brain problems have in common is that they all have some degree of
00:58:48
insulin resistance but then it's no surprise that they all benefit when ketones can swoop in to save the day
00:58:56
um but that only can happen if the person is giving their body a break from the insulin long enough to actually
00:59:03
start making ketones really really interesting on this point of Alzheimer's because I
00:59:08
don't think people have spent enough time talking about the link between insulin resistance and Alzheimer's um
00:59:15
and one of the things I was I was looking at there was how many people with Alzheimer's have meet the criteria
00:59:22
for insulin resistance and some Studies have it at 4% there's a study I found
00:59:27
here that has it at 70 to 80% um which I wanted to site
00:59:32
um exact percentages vary but one example is a study in the Journal of Neurology in 2011 that found insulin
00:59:39
resistance at approximately 40% of individuals with Alzheimer's um but another study in Alzheimer's patients
00:59:46
sometimes found it to be as high as 70 or 80% for instance research by Dr Suzanne Damon M at Brown University has
00:59:54
drawn attention to the concept of type three free diabetes yeah again I don't love the term but I appreciate the use of it
01:00:01
which is it does suggest a metabolic origin but even you look at those ranges Stephen you'd say well one was 40 one
01:00:07
was 80 boy what a difference I suspect a lot of that is just how did they measure insin resistance right if they were
01:00:13
looking at the glucose like so many do you're just going to miss a lot of people yeah it's quite hard to I think
01:00:19
there's different criteria right for how one defines someone as insulin resistant well yeah and that's just that's right
01:00:25
that's because there's not enough training which is at the beginning of the conversation you asked my mission one of my missions is to help people
01:00:31
learn what to look for what do they need to be looking for yeah they need to be looking at insulin so is that easy to
01:00:37
measure well it is technically easy to measure it's just that we have we don't have enough systems in place to allow to
01:00:44
enable it like again um if if someone listening in the UK were to go to their GP and say can you measure my insulin in
01:00:52
many instances they literally can't get it done the system just isn't in place to take it to the lab and and measure it
01:00:58
now some do I know some physicians in the UK who do so and they have developed their own way of getting it done and
01:01:04
they're incredible Advocates of this whole idea but it is harder in the UK in Canada um where the system is such that
01:01:12
they have said out of ignorance but perhaps well placed or or well intentioned they will say well insulin
01:01:18
isn't a marker that matters it is and if you're measuring insulin resistance just to put things back to where we had
01:01:24
talked about it earlier many people with insulin resistance have normal blood glucose levels it's the insulin that's
01:01:31
high and so I would say if a person can get their insulin measured get it measured in US units if it is anything
01:01:38
above about 10 Micro units per M that's a warning in UK units if it's anything
01:01:43
above about 40 picamoles that's a warning insulin is high you could have insulin resistance and you could be
01:01:51
skinny oh yes and have insulin resistance yes that's especially depending on the ethnic
01:01:56
like if someone listening to this is East Asian and they say well I'm quite thin I don't have insulin resistance you
01:02:02
very well could um it it depends even in in young women a a group out of Northern
01:02:08
Canada which is of course pretty far north they found that even in young healthy weight women with
01:02:14
PCOS they if they compared them to their identically matched other women without PCOS they were more insulin resistant
01:02:22
than the other group so so anyway that's my way of saying even if you look at yourself and think
01:02:27
well I'm kind of lean I'm not instant resistant you very well could be okay so I've got a friend who's a woman MH who
01:02:35
has PCOS yeah and one of the things that she often says to me is that she gains
01:02:40
weight easily is this true oh for sure and in fact I wouldn't be surprised if she does because the fact that she has
01:02:47
PCOS is not absolute evidence but very likely evidence that she has insulin
01:02:53
resistance which would mean at any given moment her insulin is at the risk of being a little higher than her
01:02:59
noninsulin resistant counterparts so if she goes and gets the test done I bet her insulin would be High um and so all
01:03:06
that would mean is which is good I mean knowledge is power and my hope would be
01:03:11
that as someone goes and gets their insulin measured and there are a handful of other tests they could also look at but that's the most succinct then it
01:03:18
would be all the more impetus or encouragement to say okay I heard I listened to step and Ben I really do
01:03:24
need to start making some Chang and even in PCOS there are reports that document the
01:03:31
absolute reversal of the disease with nothing more than just dietary changes I was looking also a second ago because we
01:03:37
mentioned ethnicity a few times and it says the research I was looking at says that East Asians have East Asians have
01:03:43
fewer fat cells and they're more resistant to obesity related metabolic issues well that's second part of that
01:03:50
statement is is not true they are more resistant to obesity but they are like if it's an interesting dichotomy I got
01:03:57
you yeah so they're you like to find a Japanese man who's as fat as the average American boy you're going to have to
01:04:04
look it's hard it's hard but to find a Japanese man who has is just as much likely to get diabetes type two diabetes
01:04:11
very easy Africans have more fat cells typically yeah so so on that ethnicity
01:04:18
if now there's a lot of kind of wiggle room here but on one end we'd have Caucasians blacks would be right nearby
01:04:24
African ethnicities would be quite close um to the to the kind of northern European ethnicity and then we would
01:04:30
move through and and I don't mean to miss anyone here but on the other end it would be East Asian and then sprinkled
01:04:37
through that would be um uh Latino Latino would be somewhere in the middle
01:04:43
kind Hispanic and then other Southeast Asian and then East Asian kind of on the worst end or the least sensitive or the
01:04:50
most resp sensitive to their fat the most sensitive to their fat this actually is a concept that has been
01:04:55
presented called the personal fat threshold which is this really interesting idea born from a group in
01:05:02
Australia suggesting that across every individual body which of course is heavily influenced by both ethnicity and
01:05:08
sex like we' mentioned earlier a body is going to have a rate at which it can store fat in a healthy way and then once
01:05:16
that threshold is met any further pressure to store fat will start creating insulin resistance and that
01:05:22
threshold is essentially how big how how many fat cells do you have and how much room do they have so if you have more
01:05:29
fat cells you have a higher fat threshold you can get fatter before it starts to hurt you does your fat
01:05:35
distribution also matter here because it does different races this research is telling me have different fat
01:05:42
distribution it's saying that Africans have better fat distribution lower visceral fat and less metabolic risk
01:05:49
because of that yeah yeah yeah Caucasian moderate fat cell quantity more prone to subcon Fat accumulation subcutaneous
01:05:56
which is that's the fat around the orans yes so Caucasians so so let's say northern European African both store
01:06:02
more of their fat subcutaneously which is the fat just beneath the skin or the fat that you can pinch and jiggle that
01:06:08
has an ability to expand more because there's nothing really to limit it um however the other place for people to
01:06:14
store fat is their visceral atopos which is the fat that is tucked within the abdominal cavity so tucked around the
01:06:21
organs it's sort of surrounding the kidneys and the intestines and the liver that is an unhealthy place to gain fat
01:06:28
but in East Asian all things equal is putting much more fat there than they
01:06:33
are subcutaneously the advantage of subcutaneous fat is which is the fat on the outside yeah yeah so the the fat
01:06:39
benath the skin yeah yeah the loose belly fat the fat that can pinch and jiggle that fat has a greater ability to
01:06:46
make new fat cells so as much as earlier you and I said fat cells remain static for the most part they do there's a
01:06:52
little bit of wiggle room where it can go up and that's purely subcutaneous and
01:06:57
Hispanics have higher fat cell quantity more visceral fat yes and increased risk
01:07:02
of obesity related conditions and so the problem with visceral fat is this is such a finite space there's so little
01:07:08
room within the core of your body that if we allow those fats to multiply it
01:07:13
could theoretically start physically compressing on tissues right and so those fat cells only grow through
01:07:20
hypertrophy which is the thing we talked about earlier with slow insulin resistance subcut cutaneous fat cells
01:07:26
are more abundant but smaller visceral fat cells are fewer but much larger and
01:07:32
so any ethnicity including Hispanic or Asian that promotes relatively more fat
01:07:38
storage in the visceral space is going to suffer from the consequences of that fat much sooner and again it still comes
01:07:44
back to size the bigger the fat cell the sicker the fat cell according to Alzheimer's disease International the
01:07:50
total number of people living with dementia globally is expected to reach 139 Million by 20 50 which is up from
01:07:56
around 55 million in 2020 which I imagine is in part related to people
01:08:02
living a bit longer they once did as well although although the past few years life expectancy actually turned
01:08:07
down for the first time in the history of modern world so who knows if it will continue to go up but yeah it could be
01:08:15
people are living longer I mean one of the effects of modern medicine is that people live longer with
01:08:21
disease um Alzheimer's included but it's absolutely a consequence further of our
01:08:26
overall metabolic milu that we put ourselves in a position where we are making our brains insulin resistant and
01:08:33
thus they're going hungrier and hungrier there's a study you talk about um which you've cited before that shows that if
01:08:40
you move visceral fat from an obese animal to a lean animal this immediately
01:08:46
caused insulin resistance yeah in the animal that received it okay yeah so
01:08:51
just to be clear if if if we took what they did in the study just just to reflect why or that different Depot of
01:08:58
fat are harmful and so the the human body has two distinct fat Depot and you and I described them subcutaneous which
01:09:04
is the fat beneath the skin or visceral which is the fat tucked within the organs of the abdominal space and if you
01:09:11
move subcutaneous fat which is like the belly fat the belly fat and and from one
01:09:17
animal to another you couldn't do this in humans if you move belly fat if you will or subcutaneous fat from one animal
01:09:23
to the other the animal is very healthy it's no problem subcutaneous fat is inert it really is just sort of hanging
01:09:29
out there and minding its own business but in that same study if you move the visceral atap POS over now all of a
01:09:35
sudden that animal that got that extra dose of visceral fat is going to become sicker it's going to become more insulin
01:09:41
resistant and diabetic because you've increased its visceral fat the amount of fat that it has in that space the body
01:09:49
wants to limit the amount of fat that it has there because if the fat again if the fat grows too much you can
01:09:55
physically start compressing and squishing organs that you need to be functioning like the kidneys and the
01:10:01
intestines have you seen Brian Johnson I have I don't know him personally but you've seen the documentaries and stuff
01:10:07
made about him and the the work that he's doing what do you make of what he's doing to extend his age because you know one of the subjects I think is linked to
01:10:14
this is the idea of longevity yeah and aging and he's become a bit of a poster child for the subjetive longevity right
01:10:21
right well I want to address this because this is a real person so I want to address it very politely and diplomatically I think that I want to
01:10:28
distinguish the difference between longevity research and science which is a very real living breathing field and
01:10:34
I'm proud to know individuals who are longevity scientists and distinguish them from um longevity you said poster
01:10:42
child so the the gurus of longevity and that's not the same thing so what I say
01:10:47
I don't mean to it to be an indictment of longevity research but I don't mind if people hear a bit of an indictment in
01:10:54
my voice of the modern longevity Guru approach so
01:10:59
these individuals and he is certainly the most um wellknown they do have the advantage of never really being able to
01:11:06
be proven wrong you know so there's an inherent problem here but I will say
01:11:11
that the the application of being a longevity um expert or not a scientist
01:11:18
but a guru and I don't mean for that to be negative but it does have a bit of a negative sound to it is that you have to
01:11:24
rely on what I would call weak evidence now what do I mean by that uh so all of the approaches to
01:11:32
longevity nowadays rely on either correlational studies or basic research
01:11:38
or animals and insect studies and then extrapolating that results or assuming those same results will apply to the
01:11:44
human so let me briefly just mention my concerns with correlational research so the longevity Guru will
01:11:51
say correlational evidence suggests that people who eat meat um die more well a correlational study
01:12:00
is by my estimation some of the weakest evidence that you can ever generate a correlational study would just have
01:12:06
someone come to your home and say Stephen can you please answer this survey about what you eat you answered
01:12:11
the survey you may lie you may not remember you may have things that you don't even think about including like
01:12:18
for example that you're part of a very um well put together religious organization and I actually use that
01:12:24
example very deliberately because people who are known to be part of good tight
01:12:29
Social Circles like a formal religious group always live longer than people who don't maybe you're really lonely
01:12:36
loneliness is a greater contributor to death than cigarette smoking and it's not even close so there could be things
01:12:42
on that survey that you just cannot capture and yet we end up making a conclusion and so all of that
01:12:49
correlational evidence is deeply flawed research and yet that becomes the basis
01:12:54
for the long longevity Guru to determine diet so if I'm trying to extend my
01:12:59
longevity yeah trying to live longer then exactly what should I be thinking about yeah so my view on longevity is a
01:13:07
metabolic view no surprise I am a metabolic scientist and I don't mind someone sort of smirking at me declaring
01:13:13
that or admitting it but I'm somewhat Justified just by way of setting the stage the earliest the birth of the
01:13:21
modern longevity research uh at if if it didn't start it was heavily influenced by the work of a
01:13:27
woman named Cynthia Cynthia Kenyan k n y o n Cynthia kenion was one of the kind
01:13:34
of she really did in my mind kind of give give birth to the modern longevity
01:13:40
Focus what her lab found using an insect model and this is again a problem with
01:13:45
the longevity gurus is that they rely on insect data um for example but it was compelling what she found I think it was
01:13:52
worms she found in worms that if they restricted the glucose that the worms
01:13:57
were eating they would live 50% longer or some some fantastic increase in the
01:14:03
how long the animals lived that kind of gave birth to the idea of fasting being beneficial but it also allowed her lab
01:14:11
to start playing around with some of the genes of these little insects and when they started knocking down or
01:14:17
underexpressing some of the genes involved in insulin they didn't have to restrict the
01:14:23
food the animals just lived longer and so that touches on this metabolic aspect
01:14:29
and everyone nowadays is really interested in autophagy autophagy is a term for a cell essentially cleaning
01:14:37
itself out which is typically associated with long fasting yeah that's yeah yeah in fact yes so that is partly why
01:14:43
fasting has been so embraced within the F longevity Community it's because if
01:14:48
you can promote longevity or autophagy rather if you can promote autophagy the cell keeping itself CLE cleaned out that
01:14:56
is thought to be a key contributor to longevity so autophagy equating to longevity I don't disagree with that I
01:15:04
think that probably is a very valid view then the question comes well how can I
01:15:09
control autophagy well there is a humble hormone that comes from the pancreas
01:15:14
that has a very powerful effect on autophagy called insulin so as much as people are fasting what's the value of
01:15:21
fasting in reducing autophagy it's because insulin comes down now what becomes interesting is what happens if
01:15:28
you were to put someone allow them to eat calories but the calories are such that they're insulin is staying low and
01:15:35
they're making ketones in other words a ketogenic diet you also enable autophagy
01:15:40
there was a very welldone animal study finding that they didn't have to restrict calories and fast the animals
01:15:47
they could let the animals eat as much as they wanted but it was a ketogenic diet they lived significantly longer
01:15:54
than their other litter mates that were eating the normal high carb Chow similar to what humans eat nowadays and so
01:16:02
autophagy probably does matter for longevity all the more reason to keep your insulin in check because insulin is
01:16:08
a powerful inhibitor of autophagy so as much as we have longevity gurus who are
01:16:14
taking thousands of dollars worth of supplements I can't help but look at that and think just control your insulin
01:16:21
that within every cell there's this battle there's a yin-yang of growth and death or building and breaking to say it
01:16:27
a little more politely in fact that is metabolism the very word metabolism
01:16:33
encompasses anabolism which is anabolic or building up and catabolism or
01:16:39
catabolic which is breaking down the key to a healthy growing living cell is this
01:16:45
nice ongoing balance of build and break build and break you have to build something up and then modestly break it
01:16:52
down and then you build some things up again and autophagy is a very important part of that breaking cycle within the
01:16:58
cell that hey it's time to get rid of some old parts and now we'll rebuild some of that again now we're going to
01:17:04
break down these parts and rebuild it insulin is the key to that process if
01:17:09
insulin stays high for two long you never allow the catabolic or the breakdown this is one reason why insulin
01:17:16
is so facilitative to cancer insulin wants things to grow cancer is a disease of growth we don't ever let the cancer
01:17:23
start to break down insulin won't L it in part you've um repeatedly talked about ketosis ketones we'll eventually
01:17:30
get there we're kind of teasing the audience a little bit yeah we are yeah but rightly so I mean ketones are a very
01:17:36
vilified misunderstood part of the body and to my great Delight um it's getting it's getting a sort of new appreciation
01:17:43
well I'm currently on the keto diet as well so I am incredibly interested to understand a like what's going on in my
01:17:49
body but be I I'm quite compelled by both the pros and cons of doing it and I want to talk about the cons and the pros
01:17:56
um because they both exist one thing you say in your book why we get sick is that
01:18:01
the longest living humans are also the most insulin sensitive yeah so you're telling me that the longest living
01:18:07
humans are the ones that are able to Stave off that insulin resistance yes yes so there are keep their insulin
01:18:13
levels lower that's right yeah in fact most of the longevity research was sort of a final point on this um is that when
01:18:20
you look at these studies that look back in time and say okay what is it about these people what variables tend to go
01:18:28
along with the longest lived humans one of them is that they're insulin sensitive and their blood glucose levels
01:18:33
are in fact a very well done study just last year out of Sweden I think it was just one year ago they looked at all and
01:18:40
Sweden is meticulous in its in its recordkeeping which is an advantage and and fairly homogeneous society so it
01:18:48
kind of eliminates some confounding variables but they attempted to document what the what were the variables that
01:18:54
were just the most consistent theme of people who lived very long one of them was good glucose control and this next
01:19:01
one is very controversial because they found that they also the longest lived people had high cholesterol levels and
01:19:08
isn't that funny it is one of the most consistent themes of longevity research that the longest lived people have
01:19:13
higher cholesterol and yet we live in a world that hates cholesterol and the moment cholesterol goes up we put them
01:19:19
on a cholesterol lowering medication we could be doing the perfectly wrong thing to to help these people live longer so
01:19:26
that was and and then low uric acid and there's a handful of other little variables that fit into this sorry they
01:19:32
found that some of the longest living humans had high cholesterol levels that's right that's what the Sweden study found for example the paper just
01:19:38
published a year or so ago what were some of the most consistent themes they had good glucose control and high
01:19:44
cholesterol I'm a great defender of of cholesterol it is a molecule of
01:19:52
life and and so many so much depends on on it mitochondria for example mitochondria have to have a cholesterol
01:19:59
molecule in them in order to work like the very Powerhouse of the cell and the more you lower cholesterol through say
01:20:05
drug interventions the more you compromise the mitochondria um the sex hormones all sex
01:20:11
hormones are built on cholesterol it's no surprise if someone takes a cholesterol lowering medication their
01:20:17
sex hormones go down this is why some men experience such terrible loss of libido because he's becoming low
01:20:23
testosterone because of the war on cholesterol but there good and bad cholesterol right well that's as The
01:20:28
Story Goes yes and yet I think that's overly simplified um where people will say LDL cholesterol is the bad
01:20:36
cholesterol and yet that gets included in these studies of longevity so I I think the good and bad aspect of it is
01:20:42
not entirely fair or accurate we need LDL and LDL is just as much a component
01:20:48
of the immune system LDL actually helps the body fight infections so it's also an unsung hero of immunity
01:20:55
there is research suggesting that in very old age high cholesterol levels do not always correlate with higher mortality and in some studies may even
01:21:02
be linked to longer life exactly which is bizarre yeah well you say that and
01:21:08
yet maybe our anti-cholesterol view is the bizarre one yeah and so as a cynic
01:21:14
who's very familiar with biomedical research I sometimes will look at clinical markers and say why are we so obsessed with glucose why not insulin
01:21:22
why are we so obsessed with cholesterol why not triglycerides which is another lipid that can be measured that is far
01:21:28
more predictive of who's going to have a heart attack or not and I think it's because we have chosen markers in modern
01:21:36
medicine that we have well-designed drugs so it's a really really good way to sell a lot of drugs so there's no
01:21:43
drug that's going to address insulin so let's not measure it but there are lots of drugs that will lower glucose so
01:21:49
let's measure glucose because then we can diagnose the problem and then we can give them a drug and make a lot of money
01:21:55
that's a cynical view but I don't think it's unjustified similarly with cholesterol why look at LDL when
01:22:01
triglycerides another lipid marker are a much better indicator it's because we don't have a drug that effectively
01:22:08
lowers triglycerides you can with diet but we do have drugs that very effectively lower
01:22:14
LDL one thing that really surprised me when I was reading your work is there was a study done in Bulgaria which
01:22:22
proved that smoking causes in insulin resistance in humans by having seven
01:22:28
healthy nonsmokers smoke four cigarettes over an hour for 3 days what did they
01:22:33
find in that study yeah so they found that if you took healthy non-smoking people and had them start smoking they became insulin resistant I believe I
01:22:40
invoked that study in the section where I was talking about inflammation um where when you cigarett
01:22:46
smoke that elicits there's a lot of junk coming in and there's a powerful inflammatory response and that
01:22:51
contributes to insulin resistance is this vaping as well oh so that is a very good question I have in fact published
01:22:58
now multiple papers with a very good friend and colleague who is a lung expert at my University a guy by the
01:23:04
name of Paul Reynolds Paul and I we have published reports together looking at cigarette smoking and the inflamatory
01:23:10
and insulin resistance effects that come from that and now we've even started looking at the molecules the hyper
01:23:17
heated molecules from vaping and they're they're terrible in fact yes very
01:23:23
similar results if you were to take a comparable amount of the chemicals from normal cigarette
01:23:29
smoke with its filter versus vaping The Vaping ones are probably worse chemical
01:23:34
for chemical in terms of their insulin yeah in terms of their inflammatory effect
01:23:40
the damage to the airway and the insulin resistance that comes from it that's horrifying it is in part because of just
01:23:47
how common it's become does smoking make us fat Ah
01:23:54
that's a a great question it doesn't because it replaces other interests so if the cigarette smoker ate the way
01:24:01
everyone else was eating it would but because the cigarette smoke satisfies a
01:24:07
craving they have less of an interest in food what's so interesting about cigarette smoking is again as I said you
01:24:13
begin to smoke other things don't tempt you as much like the cookies and the cakes but one of the ways the smoker
01:24:19
helps kick the habit of cigarette smoking is actually eating candy like will literally start carrying around
01:24:25
little candies in their pocket so that they feel a craving for cigarette smoking they will take out a little candy open it up and pop it in their
01:24:32
mouth and so it's no surprise that very commonly when a person quits smoking they gain significant weight they end up
01:24:39
trading out their addictions if you will um and unfortunately in humans all of
01:24:45
the study of addictions with food people only manifest an addiction to one type of food and that is carbohydrate there's
01:24:52
no evidence of addiction to fats or proteins you published a study in 2024 which found that exposure to De diesel
01:24:58
exhaust gas was associated with increased fat Mass yeah enlarged fat
01:25:03
cells insulin resistance and increased levels of inflammation and that was published in the international Journal
01:25:09
of molecular Sciences yeah that was one of the studies I just was referring to with regards to my colleague Paul Reynolds Paul and I we that was one of
01:25:16
the papers we published looking at these inhaled particulates the reason I was interested in this field of study in the
01:25:22
first place was just to continue continue to kill the caloric model of obesity so our and this touches on an
01:25:30
earlier part of the conversation overwhelmingly if you ask someone why do we get fat well because you eat more
01:25:36
calories than you burn why do you lose fat because you eat fewer calories and I have long just been frustrated by how
01:25:43
naive that view is Yes Energy matters but again the fat cell must be told what to do with the energy that it has that
01:25:50
of course points an obvious finger at insulin which is the strongest of all signals but what we found in that study
01:25:56
is that even something as seemingly unrelated as diesel exhaust particles mind you we did not do this study in
01:26:02
humans full disclosure we did the study in animals where we could perfectly control how much diesel exhaust they're
01:26:08
getting um so we have this mechanism through in Paul's lab where you can aerosolize these particulates and know
01:26:14
exactly how much the animal is breathing and then at the end of the study after even though they ate the exact same
01:26:20
amount of food the animals that were exposed to the diesel exhaust particulates had fatter fat cells and
01:26:26
more insulin resistance than the animals that had just been breathing normal room air so what we're breathing in
01:26:31
theoretically could then be determining how fat we're getting yeah yeah in fact yeah this evidence would suggest that it
01:26:37
goes beyond Theory so our evidence would state conclusively that yes what you breathe does matter then theoretically
01:26:43
we would say well how much does that apply to humans that is where it would get into the realm of theoretical but the evidence certainly suggests yes the
01:26:51
very air we breathe matters and you see this at a popul level look in areas where there are now there are
01:26:57
confounding variables here here I am invoking correlational research and I was just criticizing at a moment ago
01:27:02
with regards to longevity but you look in areas where they have higher pollution levels where the particulates
01:27:07
are higher in the atmosphere and those same areas are always fatter and more
01:27:13
diabetic interesting but but of course that's correlational so it's hard exactly yes
01:27:20
thank you for pointing it out and but again as much as you and I are citing the problem with the correlational study
01:27:25
there we need to always cite the problem with correlational studies when it comes to informing nutrition policy like don't
01:27:31
eat eggs because they cause diabetes but when you actually look at the studies you find nothing of the sort what about
01:27:36
other sort of environmental toxins and their impact on insulin resistance MH yeah so there are the ones that you
01:27:43
inhale a handful of inhaled particulates will matter we have shown in my lab alone with my with my collaborators
01:27:50
diesel exhaust will do it cigarette smoke will do it and more we a funded Grant right now to look at the effects
01:27:56
of vaping so apparently stuff we breathe will matter to some unknown degree
01:28:03
things that we drink will that are non-caloric so there can be like people
01:28:08
have heard of the microplastics microplastics are things that you can they are so small that you
01:28:14
drink them and they will absorb through the intestine and get into the bloodstream for reasons that are unknown
01:28:21
to me at the moment one of the sites where those micro particles will go is the fat cells and once there they will
01:28:28
directly promote the growth of the fat cells so that's actual microscopic segments of plastic but separate from
01:28:35
that are molecules that can come from Plastics and soaps and detergents like BPA or diethyl sbol Dees that's actually
01:28:44
an estrogen mimetic kind of what we referred to earlier with regards to other endocrine disruptors but there are
01:28:50
other chemicals that a person can drink um or inhale like mentioned earlier but
01:28:55
that will directly impact the growth of fat cells or promote to tell mimic what insulin wanted to do which is tell the
01:29:02
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01:31:03
on so let's talk about ketosis and ketones um the diet the keto diet is
01:31:10
becoming increasingly popular from what I've seen it's actually the diet that I'm on at the moment how does that play into
01:31:17
everything we've talked about yeah yeah so it it this is an opportunity for me to do a little bit of um B nutrient
01:31:24
biochemistry or a little discussion of metabolism so that people appreciate what ketones even are and where they
01:31:30
come from so the the entirety of the human body is a metabolic hybrid in that
01:31:35
the body is largely burning fuel from two sources it is burning blood glucose
01:31:41
or sugar blood sugar or it's burning fat those are the two main fuels for the
01:31:46
body my extension now the brain was an exception the brain is glucose or ketones and but I'll get to where the
01:31:52
ketones come from the rest of the body isn't really relying on ketones as much it's fats or glucose or blood sugar
01:32:00
insulin is what decides which fuel is used so as much as the metabolic engine has two fuel sources insulin will decide
01:32:08
which one is opened and which one is closed if insulin is high the body is sugar burning and you can measure this
01:32:14
in the whole body level by measuring the amount of O uh oxygen and CO2 that the body is producing because different
01:32:20
biochemistry or the burning of the fuels will produce a different amount of CO2 so if I'm burning glucose I might be
01:32:25
producing more CO2 yes yeah so we could hook you up to something called an indirect calorimeter and measure that
01:32:32
your reer the respiratory exchange ratio the balance between CO2 and oxygen would
01:32:37
go higher so we we increase your insulin like if I infused you with insulin in the next few minutes we would see that
01:32:44
your reer would go up and we' say boy you're sugar burning or we allow insulin to come down and then the re R goes down
01:32:52
which is reflective of fat burning so it's insulin that determines whether the body is sugar burning or fat burning now
01:32:58
when insulin has been low for about 16 or so hours something interesting starts
01:33:04
happening at the liver so the liver with insulin being low is burning a lot of
01:33:09
fat including its own fat that the liver can store the liver can store fat but also fat coming from fat cells because
01:33:16
if insulin is low the fat cells are just leaking out fat to be burned by the body
01:33:22
and because insulin is low the liver keeps burning it and the liver essentially Burns continues to burn so
01:33:30
much fat that it it fills its own needs it meets its own needs and says to itself hey I don't need to keep burning
01:33:37
fat I have all the energy I need I'm I'm doing great but it can't stop burning
01:33:42
fat because insulin is low and if insulin stays low fat burning keeps going and so because the body doesn't
01:33:49
have enough glucose well it's acting yes so in this sense it's doing it to help replace the glucose that isn't coming in
01:33:55
that's the value of the Ketone so as the liver is continuing to burn fat it essentially gets to a point of fat
01:34:01
burning where it's burning more fat than it needs and that excess if you will is what becomes ketones so ketones are kind
01:34:09
of a metabolic release valve for the liver cell to say I I can't I don't know what to do with all this fat burning
01:34:15
okay I know what I'm going to do there's not a lot of glucose coming in and so the brain may start to get hungry so I'm
01:34:22
going to start making ketones and so ketones are nothing more than a
01:34:27
product of a lot of fat burning and anyone who even fasts for 24 hours you
01:34:33
wake up that next morning you're in some degree of ketosis lest anyone think it's an extreme thing people are going in and
01:34:39
out of ketosis ideally often now why do I say ideally it's because ketones are
01:34:45
as we've already outlined perhaps the best fuel for the brain the brain thrives on ketones you can take a person
01:34:53
with early stage Alzheimer's disease and have them go through a series of cognitive tests and they do horribly on
01:34:59
them like one example is you ask the patient with Alzheimer's to draw the face of an analog clock a circle with 1
01:35:07
two through 12 and then some hands on it and it is utter chaos this is published
01:35:12
reports you then put them into ketosis ask them can you please draw the face of a clock it's still sloppy but it
01:35:20
is absolutely the face of a clock you ask them when they're not in ketosis to
01:35:25
try to tie their shoelaces they can't think through the puzzle of tying the shoelaces ask them to do it again when
01:35:31
they're in ketosis all of a sudden they can tie their shoelaces more than that they can get themselves dressed all of
01:35:37
these are published case reports it's just my long-winded way of saying the brain thrives when it has ketones as a
01:35:45
fuel source but the benefits don't stop there my lab published a report finding
01:35:50
that when humans were in ketosis which is just a term term for ketones being elevated we pulled out small pieces of
01:35:58
belly fat and measured the metabolic rate of that belly fat and we found that in ketosis the metabolic rate of that
01:36:04
belly fat was three times higher than when the people were not in ketosis what
01:36:09
does that mean yeah so that means that the fat was suddenly behaving in a much more energetic way that fat tissue has a
01:36:16
very low metabolic rate and then all of a sudden when the ketones came into them they started getting much more active
01:36:22
and they started burning more energy which is going to be very helpful for someone who wants to lose fat if your
01:36:28
fat cells now have a three times higher metabolic rate that means that the fat cells are starting to act a little bit
01:36:35
more like your muscle cells and they're just burning more energy so does that mean that I'm going to lose fat faster
01:36:40
what do that mean absolutely and that is what happens there are very well done controlled studies to show that if you
01:36:46
control for all calories when a human is in ketosis their metabolic rate goes up
01:36:51
your body your whole body is just burn more um it it's just everything's kind of been turned on a little more the the
01:36:58
the the furnace of the metabolism has just been it's have a little more fuel kind of stoking the fire so ketones will
01:37:04
increase metabolic rate of fat tissue we found a paper that we published documenting how we took muscle cells and
01:37:12
kind of insulted the muscle cells to determine how tough the muscle cells were when we incubated the muscle cells
01:37:18
with ketones they were much more resistant to injury so the the ketones
01:37:24
act to protect muscle tissue and in a way that is reflective of a function of ketones ketones are a defender of muscle
01:37:33
ketones are basically the way to tell the brain saying brain you think you need a lot of glucose and if you don't
01:37:39
get enough glucose you would start stripping the protein from muscle to turn it into glucose but I'm here as a
01:37:46
ketone so you can eat me instead and not and leave the muscle alone so we
01:37:51
published again a direct report finding that ketones actually make Muscle more resistant to injury and this could be
01:37:57
why you're seeing more and more Elite athletes using ketones as an actual ergogenic Aid or like a supplement to
01:38:04
help them better be better so at my University at BYU just this year our men's and women's cross country team
01:38:11
took the national championships the best college runners in the nation pretty impressive one of the things they do is
01:38:18
they take these Ketone drinks before they train and before they they race
01:38:23
some more and more of the Torrance teams take Ketone supplements because it is
01:38:28
just another fuel it is something that the body can burn that that we always
01:38:33
say well if once you start running out of glucose you're going to Bonk or you're going to hit the wall well what
01:38:39
if you don't really use glucose because you're burning a lot of fat and a lot of ketones instead and that keeps your glucose kind of untouched or you're not
01:38:46
you're not relying on the GL and we see this in humans if there's a human that is adapted to a ketogenic diet they they
01:38:53
burn fat at a higher rate than was ever thought humanly possible that that fat
01:38:59
is basically fueling all of their muscle movement during the exercise session rather than relying predominantly on
01:39:05
glucose the body has adapted it's burning fat for fuel and when available it's burning ketones for fuel and it's
01:39:12
leaving the muscle as sort of a last resort when it really needs a big kick I've seen these keto drinks little
01:39:19
they're almost like little shots well there's a bunch of different types if you look at the Spectrum ketones you on
01:39:24
one end you have the cheapest most readily available although less effective called Ketone salt where it
01:39:30
takes a molecule of Ketone and binds it to a mineral like calcium or magnesium um not as effective and it's a lot of
01:39:37
mineral so people will find that they might get a lot of plaque on their teeth yeah maybe increase risk of kidney stones so comes with some consequences
01:39:44
then you have the Ketone Ester which often comes in shots yeah then you have the bioidentical BHB or the bioidentical
01:39:51
Ketone one company which is original Ketone um they make it now these ones
01:39:56
are more effective you take a little bit of these and you will get an increase in ketones they're a little more expensive too but as the space is becoming more
01:40:03
competitive the price is coming down and what exactly does it do so if I took a shot of bi identical Ketone drink what
01:40:11
would go on in my body and how would I how would that impact my cognitive performance or athletic performance yeah
01:40:18
yeah so it would result so you're drinking it in you're immediately absorbing it from your gut yeah so if
01:40:23
you were not in ketosis let's say you had and I'm not encouraging people to do this you had just eaten two bagels and a
01:40:30
cup of sugary coffee you're no ketones undetectable because insulin has come up it's inhibited Ketone production and
01:40:37
then you drink a shot of the Ketone within an hour we would detect your ketones they would have gone up maybe to one Miller which is a pretty significant
01:40:43
bump yeah and they're capable of that kind of movement and maybe you do so because you're thinking I really need to be sharp right now would that make me
01:40:50
sharper well that's where we have to speculate there's no I my lab published
01:40:55
animal evidence suggesting that yes indeed it makes you sharper that we had these animals navigate mazes and
01:41:01
recognize objects and when the animals were on a ketogenic diet they were much sharper they were much quickly much
01:41:08
better at solving problems and remembering solutions to previous problems it's one of the I ask this in
01:41:14
particular because as my team know because I've said it to them a lot over the last couple of weeks since I've been on the keto diet and I've been literally
01:41:21
pricking my finger to check yeah my keto levels and the highest I've gotten to is like 2.5 which is high is
01:41:28
it high that's not problematic right I mean that is just proof positive that you're in ketosis which itself is proof
01:41:35
positive that you're burning a lot of fat yeah and three that your insulin levels are low not dropped off my body
01:41:40
like I've never seen in my life exactly yeah it's crazy so the power there is like if you'll allow me to kind of
01:41:46
springboard off of that comment the power of so so if someone is listening to this and they're thinking okay I need
01:41:52
to shrink my fat cells yeah unfortunately they don't realize that there's two variables to what caused
01:41:58
their fat cells to grow in the first place they have no awareness of the value of insulin in this in this um um
01:42:04
formula all they do is pay attention to the calories and so the average individual is looking down the road of
01:42:10
this fat cell shrinking journey and they're thinking okay what I have to do is just cut my calories and what do they
01:42:17
do to cut their calories they do the exact wrong thing and before I even answer that let me just present the
01:42:23
scenario let's imagine that step and I everyone listening is invited Steven and I are hosting a buffet we have the
01:42:29
world's best chefs it is going to be a table filled with the most delicious foods you can imagine you're in our
01:42:35
invitation we say come hungry because you're going to want to try a little bit of everything everyone listening ask
01:42:41
yourselves what would you do to come as hungry as possible you'd probably do two things or think how did you go to your
01:42:47
Thanksgiving or your your Christmas dinner as hungry as possible you would eat a little Less in some period of time
01:42:55
before the event and you would exercise a little more and it would work you would be very hungry that's why the
01:43:02
traditional advice given for weight loss doesn't work because we tell people eat less exercise more sure you may be lose
01:43:09
a little bit of weight in the short term but all that does you've given them the perfect recipe to promote hunger and
01:43:15
hunger always wins as a good example uh in the US we have a game show maybe
01:43:20
there was some version of this in the UK called The Biggest Loser it was essentially who can lose the most weight
01:43:25
and it was through a punishing Regiment of caloric restriction eat less exercise more that is like the perfect embodiment
01:43:32
of that approach they were starving and they were exercising to insane degrees and oh my goodness did they lose a lot
01:43:38
of weight and yet you never see them again they don't do a reunion tour 5 years or 10 years later because they
01:43:45
gain it all back do do you know they gain it will they do in fact a paper published in the US from the National
01:43:51
Institutes of Health doc mented not only the degree to which they gain weight back but also how it almost literally
01:43:57
breaks their metabolism that normally a person's metabolic rate is connected to their body mass a bigger body has a
01:44:04
higher metabolic rate a smaller body has a lower metabolic rate this is just human physiology and no surprise when
01:44:11
someone loses weight there's less of body and so metabolic rate goes down as they gain weight back metabolic rate
01:44:17
will typically go back up as well except for the contestants and The Biggest Loser they started with a high metabolic
01:44:24
rate because of a high body fat level they lost a substantial amount of weight
01:44:29
no surprise metabolic rate went down substantially but it this is such a dramatic change that as they started
01:44:36
gaining weight back metabolic rate did not come back with it it stayed lower
01:44:42
than it should have normally it's connected sort of one to one wherever body weight is going metabolic rate is
01:44:48
going except in these people that method of dramatic weight loss through such
01:44:53
severe restriction which is based purely on the caloric theory of obesity leads
01:44:58
to such it leads to significant hunger so no surprise if a person's attempting to shrink their fat cells or lose weight
01:45:06
if the first step is I'm going to cut my calories and they don't address their High insulin they're never going to lose
01:45:12
weight in the long run they're going to step right back to where they were because if they start cutting calories
01:45:17
but insulin is still high that's going to make them very hungry because insulin wants to be storing energy
01:45:23
a do a professor from Harvard named David Ludwig found this if you have people eating a lower calorie meal that
01:45:29
spikes their insulin it makes them much hungrier than a lower calorie meal that
01:45:35
doesn't Spike insulin so that's the key anyone listening if you're thinking I need to be on a fat cell shrinking
01:45:41
Journey let the first step of that journey be I'm going to lower my insulin
01:45:46
which means which means I'm going to control my carbohydrates I'm going to stop eating carbohydrates that come from
01:45:52
bags and boxes with barcodes and while I am restricting those carbohydrates I'm
01:45:57
going to focus more on protein and fat so control carbs prioritize protein and
01:46:04
don't fear the fat that comes with those proteins fat and protein together is a a
01:46:11
a miraculous combination of helping you feel full and it is literally giving everything you need there are such
01:46:17
things as essential proteins there are such things as essential fats so focus on those and that will be the key to
01:46:24
helping insulin come down then as you have found you haven't and when you're hungry eat if you're not hungry don't
01:46:30
eat but what the person will find as they're lowering their insulin all while their metabolic rate is going up they're
01:46:37
learning how to burn their own fat for fuel because remember the metabolic hybrid that metaphor that if you want to
01:46:43
lose fat you need to burn fat you're not going to lose fat if you're always burning glucose it's fat that you need
01:46:49
to burn and as you start burning more fat you realize that it's like the hump on a camel that hump exists because it
01:46:56
is a big source of fat for that animal to be using its own fat for energy we have our own version of that so where
01:47:04
you think about the average individual who's chubby they have hundreds of thousands of calories waiting to be
01:47:10
burned in those fat cells it's just that their chronically elevated insulin is never letting them burn it and so as the
01:47:17
person starts making these changes in their diet to lower insulin they now can finally start relying on their own fat
01:47:23
for fuel so it's no surprise that their hunger starts to come down let that be the natural way in which you're
01:47:30
controlling your calories don't control your calories because you're forcing yourself to be hungry and eat less
01:47:36
control your calories because you simply aren't hungry so I have to I'll overlay this with my own sort of anecdotal
01:47:43
experience so I every year do a keto diet for usually for about 8 weeks M
01:47:48
this time it's going to go on for a little bit longer um in the reason in part why it's going to go on a little bit longer so I've just learned more
01:47:54
about what's going on in my body and also because I podcast now and do a lot of speaking on stage and those kinds of
01:48:00
things I see tremendous variance in my ability for my brain to articulate what I want to say the same way it's like
01:48:06
it's absurd yes I I was saying this the other night to the the team that with me here in Los Angeles and I've tried to
01:48:12
say it to so many people as someone that can spend nine hours a day trying to
01:48:18
think of the next question to ask or trying to remember the research or on stage in front of people trying to
01:48:24
deliver a story or a point I get to see variants which I've never been able to
01:48:29
explain yeah um where some days I'll go up on stage I'll be in a podcast and
01:48:34
it's like my brain and my mouth aren't connected and then on other days specifically when I started doing ketosis or having a ketogenic
01:48:42
diet it just flows yeah it just flows so well and I was saying to my team it feels like I'm looking at the world like
01:48:48
this these days like I've got this intense for anyone that can't see me I just stretched my
01:48:53
thist focus on the the other thing I've noticed with my diet is I I get hungry
01:49:00
but not like I used to get hungry and then very quickly after I start eating I stop mhm I don't seem to be
01:49:08
like doing like these I used to kind of binge a little bit yeah I used to have like a longer eating sessions and my
01:49:14
Hunger goes very quickly um I also found that I didn't have these like fluctuating energy levels throughout the
01:49:20
day I don't crash anymore I used to get like slumps oh for sure and I don't slump anymore and then the other thing
01:49:26
which a lot of people will care mostly about is the the fat so like belly fat I have never seen anything that has
01:49:32
stripped belly fat off me faster and I'm talking in a matter of weeks that I could you know count on one hand yeah
01:49:41
than doing the ketogenic diet and if I I could literally show a picture of my scales because I have the digital scales
01:49:47
on the screen and it's just trundling along and then there's this Cliff Edge where it goes directly down and it and
01:49:55
so much so actually that one of my concerns for the ketogenic diet is how the hell do I keep my muscle oh that's a
01:50:00
great question because my girlfriend to her credit when I did ketosis the first time she was like I've never ever seen
01:50:07
you look like this when I took my top off but also it was quite clear that my
01:50:13
my muscles had got smaller I was lean as but my muscles were smaller yeah so with with with caution this time I did
01:50:19
ketosis again and I've been thinking how the do I keep my muscles yeah yeah okay so first of all let me just add a
01:50:25
hearty amen I'm an advocate of a ketogenic diet although it can be applied differently across different
01:50:30
people but I would say anyone would benefit from having some modest period of time of elevated ketones at least in
01:50:36
some portion of the day now how do you maintain muscle mass in the midst of
01:50:42
such obvious weight loss I can only speculate now there are peer-reviewed
01:50:47
studies that I can cite which do support the idea that a human can be on
01:50:52
autogenic diet and have a total maintenance of muscle and strength that is published so we know it's possible
01:50:58
although that isn't that doesn't seem to be what happened with you I would suspect that there were two
01:51:06
things two things happening possibly now I'm speculating here and I'm pretending to be your coach or your expert here one
01:51:14
could have been that you had relatively lower energy during your workouts because of a slight degree of
01:51:20
dehydration and then the other one would be calories which which I'll come back to in a moment I just wanted to put it out there so when insulin comes down one
01:51:26
of the other one of the many effects in the body is that another hormone comes down called aldosterone which is one
01:51:34
we've never invoked yet but low insulin leads to lower aldosterone when aldosterone comes down the kidneys
01:51:40
become much uh begin to eliminate salt and water much more rapidly now that's
01:51:47
not problematic but it does mean that a person does have to focus more on hydration and salts so if someone's
01:51:54
going on this strategy and they exercise fairly often you need to be much more
01:51:59
focused on your hydration literally drinking more because you will be urinating more which
01:52:05
is partly why people's blood pressure gets so good so quickly and just to
01:52:11
pause on that point there if if someone is on one or two blood pressure medications and they adopt a ketogenic
01:52:16
diet they usually have to stop their medications within two days because their blood pressure goes to normal so
01:52:22
quickly that if they stay on the medication they're going too low so one could be that you were actually working
01:52:28
out a little less intensely because of the dehydration but then two it's possible that you were eating
01:52:36
too few calories to actually maintain muscle muscle is a hungry organ it is
01:52:41
metabolically expensive for the body to keep that muscle on and as you start to get leaner and leaner it gets harder and
01:52:49
harder for the body to defend that muscle in fact that the difference between fasting and starvation the
01:52:55
longest known evidence of a fast was a man in the UK who fasted for 384 days
01:53:02
literally not eating or drinking a single calorie he was under medical supervision getting vitamins and
01:53:07
minerals and water and he was went to live on went on to live a perfectly healthy life um so but what was the
01:53:14
difference why was that not starvation starvation is when you run out of fat so
01:53:19
you might have gotten to the point of so lean that you didn't have enough fat to burn to make enough ketones to fuel the
01:53:26
brain if you don't have enough fat to burn to make enough ketones and the brain is saying all right well I wanted
01:53:32
to switch to ketones so that I could spare the glucose but I can't there's not enough
01:53:38
ketones here so I have to rely 100% on glucose but if you're not eating glucose
01:53:43
now the body has to start stripping the protein from muscle and it sends those amino acids to the liver then the liver
01:53:50
is so capable it will turn those Amino acids into glucose so it turns my muscle into glucose to feed the brain so my
01:53:57
comment then getting finally getting to my answer is in your version of a ketogenic diet with your level of muscle
01:54:03
mass and your inherent metabolic rate based on your body size and your activity you probably ought to eat more
01:54:09
fat I wasn't actually doing the blood test at that point I'm doing it this time around but I wasn't doing the blood
01:54:16
test so I can actually see my keto levels yeah so maybe I wasn't even in ketosis cuz I wasn't having you might have been but it could have that you
01:54:22
were simply not eating enough calories that I have to so this is an instance where that's what I'm trying to do this
01:54:28
time I'm trying eat more fat like every time you're making a steak put butter on there and when you're drinking a cup of
01:54:33
coffee as crazy as it sounds I drink yerba mate every morning I will put a big dab of butter like a big dab of
01:54:40
butter in my tea and I'm sipping on it while the world's still asleep and the kids haven't woken up yet and so I know
01:54:46
because I want to keep my muscle as a guy who's almost 50 um I I find that
01:54:52
when during my strict ketogenic phase and I'm currently in it as well every January I go to kind of a carnivore diet
01:54:58
to and I mostly do it to one lean down but also to check any addictions and habits I don't like feeling addicted to
01:55:05
things and and my wife will comment and even as an almost 50-year-old it's fun to see my six-pack coming I don't want
01:55:11
to lose my mass my muscle mass because you have to work so hard to get it yeah and what I find is if I increase my fat
01:55:19
I always get plenty of protein but if I increase my fat content I have an easier time maintaining my bulk are there any
01:55:26
downsides of following a ketogenic diet that we need to be aware of the only downside I can articulate so in fact I
01:55:33
didn't even finish because I distracted myself mentioning some of the benefits of ketones but ketones are further
01:55:39
anti-inflammatory like they directly reduce inflammation in the body by inhibiting inflammatory processes and
01:55:45
they also improve antioxidant defenses so it helps reduce oxidative stress so ketones do have benefits that go beyond
01:55:52
beond even what we've taken the time to articulate if there's any negative to a
01:55:57
ketogenic diet it could be that you start you acutely or you temporarily
01:56:05
become less metabolically flexible now that's me invoking a term we haven't brought up yet but metabolic flexibility
01:56:12
is is a term to refer to the body's ability to when it eats glucose to burn
01:56:17
glucose when it's not eating glucose it burns fat so you're shifting between the
01:56:22
two metabolic fuels that we outlined earlier when someone has been adhering to a ketogenic diet for some time it's
01:56:29
almost as if their body is stuck in fat burning mode and that if you and I being
01:56:34
in such adapted ketogenic State as we are if we were to go to lunch and eat two bagels and a sugary
01:56:41
drink it would take us a very long time to clear that glucose from our blood um
01:56:47
much longer than otherwise like let's say we go out with the production team they're eating a normal higher carb diet
01:56:52
all things equal same body size same activity their glucose levels would come up and down in 90 minutes for perhaps
01:56:59
yours in mine may take 180 minutes to come back down so the person may say
01:57:04
well gosh Stephen and Ben are no longer burning glucose very well and that's true in that one moment um our bodies
01:57:12
had almost forgotten what it was like to burn a bunch of glucose because we had adapted to fat burning so what about the
01:57:19
gut microbiome oh yeah CU cuz I tell someone who is a nutritionist that I was doing a keto diet at the moment and they
01:57:26
said oh you're poor gut ah yes well what a naive um thing to say if I may gently
01:57:33
reprimand your friend there's no evidence to support that there's any harmful change in the microbiome in fact
01:57:39
a paper was just published that looked at a man who went from a normal omnivorous human diet with abundant
01:57:45
plant matter to a purely carnivorous diet literally zero carb and they
01:57:51
documented prely no change in his microbiome none whatsoever but is he
01:57:56
eating plants no well he had been eating plants so the case study was a person
01:58:01
eating a normal diet of of plants and meat a normal omnivore diet and a do and
01:58:07
then looked at the microbiome and then adapted to a purely carnivorous diet purely meat and the microbiome didn't
01:58:13
change at all what's the time period months I think the problem with the microbiome the reason I don't take
01:58:19
microbiome research too seriously as a scientist is that it is a big black box
01:58:26
you you you came from the UK to London uh to to to LA to California if we took
01:58:32
a microbiome sample analysis of your time in the UK now it would be different
01:58:37
now even though you're eating the same but you're drinking different water you're breathing different air things I
01:58:43
was just on a plane from Utah to California give me a day or so I would have some sort of shift in my microbiome
01:58:50
so the microbiome can change in resp response to all kinds of things the idea that you somehow have decimated your
01:58:57
microbiome because you aren't eating fiber is absolutely false that is that is completely false now there might be a
01:59:03
change in some of the population of your microbiome more of one less of another
01:59:09
but there's no evidence to suggest that's problematic your microbiome is intact those bacteria do not die they're
01:59:15
just simply metabolizing other things maybe they're relying more on short chain fatty acids maybe they're relying more on amino acids they're not eating
01:59:21
as they're not eating fiber but there's still stuff in the meat or the eggs that
01:59:27
the microbiome will eat but if if if eating lots of plants does give me a
01:59:32
more diverse gut microbiome then if I stop eating plants I'm going to have a less diverse gut microbiome yeah but but
01:59:39
Stephen but even then there's a bit of an assumption built into the question because it's do we know that the
01:59:45
microbiome will be less diverse the case study I just mentioned found that in this one single man it didn't change his
01:59:51
microbiome at all it was the exact same populations in all the same proportions because isn't the
01:59:57
aren't the plants like feeding the bacteria yeah yeah so the the fiber is so fiber will but again it's not that's
02:00:06
not the only thing bacteria can eat bacteria can eat fats bacteria can eat
02:00:11
amino acids they can eat glutamine for example they um they can even meat will
02:00:16
have a little bit of glucose in it where the muscle has something called glycogen and so there's you know Trace Amounts of
02:00:23
glucose and even the meat that you're eating so I do not look at the argument
02:00:28
that you know you're destroying your microbiome that has no that has no scientific support you may be changing
02:00:35
your microbiome but who's to say that's a bad change maybe it's a better change you certainly are feeling better you're
02:00:42
thinking better you're getting leaner your insulin sensitivity is improved cognition is improved I would argue if
02:00:47
there is a change in your microbiome it's probably one that's for the best
02:00:53
and no one can prove that wrong as much as I just stated that comment in a speculative fashion it's speculative
02:00:59
because there's no evidence this is why I look at the microbiome and just say yeah it appears to matter but in ways
02:01:05
that we don't know but the the you agree with the argument that if I sat here now
02:01:11
and I ate a wide range of plants for the next
02:01:17
let's say six months when you analyzed my gut microbiome it would be much more diverse I'm not agreeing to that I don't
02:01:24
know if that's true um and again I would cite that one case report I just
02:01:29
mentioned now which is the a man who did this they reported that the microbiome was identical that there was no
02:01:36
significant change is that that's just one man there it was one man it was a case report which is not a randomized
02:01:42
clinical study so um but even still I with my
02:01:47
speculation um heavily handed here I would say probably more plants would result in a more
02:01:55
diverse microbiome but I would say but then the
02:02:01
next step is a harder one which is is that good or bad I don't know maybe all you're doing is promoting the growth of
02:02:07
bacteria that make more gas because they're fermenting the fiber and you just have more flatulence as a result of
02:02:13
it people dietitians will say well a diverse microbiome is a good microbiome
02:02:18
well prove it h how do we know that how can you prove that to me as a basic
02:02:24
scientist I want to see the hard evidence because what I can prove is
02:02:29
that we can take humans who are overweight and diabetic and hypertensive eating a standard American or Global
02:02:35
diet and put them under a ketogenic diet which is going to be a much simpler diet and yet every clinical
02:02:41
marker gets better and so if someone were to say yeah but sure you reversed your diabetes and your hypertension but
02:02:47
you're poor microbiome I would say well I don't care about my microbiome I care about the human and so if there's less
02:02:53
diversity but every single clinical marker has gotten better perhaps more diversity is not what we want in our
02:02:59
bacteria I'm and I'm speculating but s is the person who states that yes I I'm
02:03:05
not aware of um research that links the two um but I I could always have a look
02:03:12
but um I would I I was always under the assumption that a more diverse microbiome is a healthier person yeah I
02:03:18
don't know yeah but but do you do you feel healthier now um feel healthier I
02:03:25
certainly feel and it's only been a short amount of time so I don't know what what my health might look like if
02:03:30
I'd done this for like two years right because then there could be a really sort of deeper change to um I know comp
02:03:38
for more than two years and they're they're great because some of the some of the changes that occur in our health
02:03:43
take time now you you show this a lot in your work with insulin resistance that if you're insulin resistance for 10
02:03:50
years your brain think I read in your work is like it ages it ages by an
02:03:55
additional two years is that it accelerates the aging and I wonder the same thing with like my gut microbiome if I'm if my gut microbiome is not
02:04:04
diverse so I have a very sort of um narrow diet or you know I'm not getting not eating my plants could it take me a
02:04:11
couple of years to really understand the net negative impact that that has on my overall health it it's entirely possible
02:04:18
yeah yeah I would just I would just ask that we be careful with the assumptions that if there is an an increase in
02:04:26
diversity with more plant matter that's an if um is that change beneficial are
02:04:33
the bacteria that we're now promoting the growth of are they better for us or are they just bacteria that exist in
02:04:38
order to handle more fiber and again the outcome being that perhaps it's just making more gas um you know the more
02:04:46
plants you eat the more gas you have to produce by fermenting more fiber what if those bacteria are only existing to just
02:04:52
eat the fiber and not actually improve the human host at all so
02:04:59
ketosis possible to live in a it's I think one of the important points on ketosis is when I do my blood keto test
02:05:06
I fluctuate wildly after I've gone for a run my Ketone levels are super high sometimes later at night I'm just on the
02:05:12
verge of ketosis sometimes um and I think that's interesting because we don't have to live in this necessarily
02:05:19
deep state of ketosis the whole time we can fluctuate a little bit and maybe my
02:05:26
thought on it is that a person would benefit from some state of ketosis on on
02:05:31
a frequent basis if for no other reason than to really give the brain a heavy
02:05:37
dose of just straight energy um not that everyone needs to be as strict as perhaps you and I are being at the
02:05:42
moment um but I would say the more a person has a disorder or a disease that benefits from ketosis the more than they
02:05:48
ought to focus on it like if someone has Type 2 diabetes if they adopt a ketogenic diet they will
02:05:54
be off all of their diabetes medications in months all of them um if someone has
02:06:00
epilepsy if there or migraine headaches if some of the from 19 13 I think was
02:06:06
the first published report on this if there's someone who suffers from migraines as long as they're in ketosis
02:06:11
they may never have another migraine again I mean it is completely Curative or preventative for the disorder same
02:06:17
with epilepsy that many forms of epilepsy so depending on the person they would benefit from being in ketosis
02:06:23
forever for everyone else who's just sort of a normal individual who wants to be lean and keep their brain healthy and
02:06:30
happy Etc I would say it's generally prudent to just control your carbs be
02:06:35
mindful of the type of carbohydrate you're eating and as I said earlier just try to focus on the carbs that don't
02:06:40
come from bags and boxes with barcodes I'm actually quite liberal in my view
02:06:46
when it comes to whole fruits and vegetables I'd say eat them enjoy them liberally but then ALS make sure you're
02:06:52
getting some good protein and fat because there's no such thing as an essential carbohydrate that sounds
02:06:57
controversial but humans do not need we have no requirement for carbohydrate we
02:07:03
do have requirement for fat and protein what about artificial sweetness one of
02:07:08
the things that I am tempted by when I'm on a ketosis diet is like
02:07:13
the soda zeros of the world or the diet sodas of the world what impact does that
02:07:19
have on my insulin levels Etc yeah great question question there is such a breadth of of diversity when it comes to
02:07:25
sweeteners from artificial to Natural to another rare sugar more and more you
02:07:31
know these all these random I'm not random but a very broad spectrum of molecules that we have developed or
02:07:38
found that taste like sugar but don't have the effective sugar so on on the good end are things like that have been
02:07:46
shown to have no insulin effect and so you know I appreciate everyone listening letting me kind of stay with that as my
02:07:52
framework because people are going to go on and criticize all kinds of other things about other sweeteners and that's
02:07:58
just too broad that's a topic for a whole book with regards to just insulin on the good end where they have no
02:08:05
effect it would be one as common as aspartame so like diet drinks not the zero drinks but the diet drinks will
02:08:13
have aspartame as the sweetener is it a difference there is a difference and I'll get to that other one in a moment
02:08:18
so I should be having D instead of zero well I personally go to diet rather than zero um but
02:08:24
that's because Aspartame is the so sweetener in the zero in the diet rather
02:08:29
and it has no effect on insulin so to arrol sorry arrol is a little right
02:08:35
around Aspartame is generally a good one but monk fruit extract Stevia and
02:08:40
especially allulose those are inert when it comes to insulin you know alose
02:08:45
Stevia monk fruit extract um aspartame no effect orthol no effect but ariol
02:08:53
that ending o is reflective of a class of sweetener called a sugar alcohol and that does not
02:08:59
mean it's alcoholic that just refers to the actual chemical structure that puts it in the alcohol family once you get
02:09:05
into the sugar alcohols you start to get a little problematic where ariol is a good one
02:09:11
enyl is generally a good one but then you get to things like malol and manitol and they do have an insulin effect and
02:09:18
what what's what kind of foods have those yeah so often like you can get manitol in like artificially sweetened
02:09:25
chocolate sometimes for reasons that I don't know I don't know why the food formulator puts them in some things and not other things the the problem I
02:09:33
chuckle because it becomes so apparent with some of those artificial sweeteners like the sugar alcohols is that as you
02:09:40
eat them you taste it sweet in your mouth and it doesn't have any caloric value in the body because it stays in
02:09:47
the intestines uh and this is something that is largely unique to the sugar alcohols
02:09:53
where as it stays in the intestines it starts pulling in water from the body
02:09:58
which starts to create a fairly inconvenient degree of flatulence and diarrhea and so a person will know if
02:10:05
they've eaten too many of those types of sweeteners because their intestines will tell them so so but also on that
02:10:12
Spectrum kind of in the middle is the one that's in the zero drinks which is one called sucrose and while sucrose is
02:10:20
generally not a problem with insulin it is a sweetener that has been shown to cross the bloodb brain barrier and so
02:10:28
the reason I avoid the zero drinks and refer or go to the diet drinks is that
02:10:33
aspartame does No Such Thing aspartame just gets divided into amino acids we just digest it and absorb amino acids
02:10:40
sucralose will go can cross the bloodb brain barrier and I don't know what it's doing there but I don't want it there
02:10:47
and so I avoid the zero drinks because I don't want that sweetener
02:10:52
but but personally and when I'm adhering to this diet a diet soda is my actual
02:10:58
Indulgence where I want something sweet um and yet I don't want the Metabolic Effect of it one thing you mentioned
02:11:05
earlier which I've been thinking a lot about is salt and I think a lot about salt because I went to the doctor many
02:11:10
years ago and I think I was using this like Maggie seasoning that I put on my food and the doctor said to me that my
02:11:15
salt levels were too high and I and then I've heard since then from other people that were
02:11:21
actually probably not getting enough salt in our diet yeah so I'm interested to hear that your physician would have
02:11:26
said your salt is too high that is very rare that that gets measured sodium I think you yep they could have measured
02:11:32
sodium and that could have been higher they absolutely could have it's just not common so salt has be has earned a
02:11:38
terrible reputation because of a series of studies that implicated salt consumption as a cause of high blood
02:11:45
pressure and and really briefly as a as a momentary physiology professor that is
02:11:52
a real effect if you and I were to go eat salt our body for the next several hours afterwards would retain its water
02:12:00
in order to balance out the salt so that we didn't get too salty so we would retain water in order to keep our salt
02:12:06
at a normal level and so that could be reflected by an elevated blood pressure um however
02:12:14
multiple huge Studies have found that if you go to a population of humans that have high blood pressure and you tell
02:12:21
them you need to cut your salt in order to correct your blood pressure they may at most move their blood pressure by one
02:12:28
or two points it has an absolutely negligible irrelevant
02:12:33
effect um it's because salt is not a key contributor to blood pressure it's actually insulin resistance insulin
02:12:39
resistance will force the body to hold on to Salt insulin resistance will force the blood vessels to be very constricted
02:12:45
all of which play together to make for a very high blood pressure so as much as we have been telling the world that we
02:12:51
should be cutting back salt no we should have been telling them to cut back on what spikes your insulin refined
02:12:56
starches and sugars but with regards to Salt it's interesting for me to note
02:13:01
where did that whole view come from within the United States decades ago there was a study that was published and
02:13:09
they called it the DASH diet dietary approaches to stop hypertension Das the
02:13:15
DASH diet and in the DASH diet one of the critical change ches was to tell
02:13:22
people to eat less salt and when they found that when people adopt a dash diet it's amazing
02:13:28
their blood pressure goes down However unfortunately they also tell people to do lots of other things with the DASH
02:13:34
diet like when they tell someone to go on the DASH diet they also tell them to eat less sugar and less refined starches
02:13:41
and sugars well it's possible indeed I would say it's absolutely the case that
02:13:47
what's actually lowering their blood pressure isn't that they cut their salt back it's that they were cutting their
02:13:53
refined starches and sugars back and it's that that had the main effect and the cutting the salt was just some
02:13:59
innocent bystander but to put a fine point on it in human studies if you have
02:14:05
humans cut back their salt considerably they become insulin resistant so take a healthy group of
02:14:12
humans say you need to eat less salt and they do so if you measure them a week later while they're adhering to this
02:14:18
they will be significantly more insulin resistant than before they ever cut back their salt it's one of the ironies of
02:14:25
the whole scenario where a physician may be telling a patient with high blood pressure you need to cut back your salt
02:14:32
and they end up eating less salt and yet their their blood pre their blood pressure gets worse it's because the
02:14:39
main contributor to high blood pressure is insulin resistance and by telling them to cut back on their salt you made
02:14:44
them more insulin resistant and that whole mechanism is because one of insulin's many many effects is to want
02:14:51
the body to hold on to salt in water and so if you start cutting your salt all of
02:14:56
a sudden insulin says well there's little salt coming in I need to do what I can to retain whatever salt we do have
02:15:02
and so it starts retaining salt and water more in order to try to offset the lack of salt coming in and while insulin
02:15:10
is going higher and higher the body's becoming more and more insulin resistant so salt restriction can cause
02:15:17
insulin resistance in humans you talk about four pillars to eating in your book while we get sick
02:15:25
you outline these four essential pillars to develop a strategy for maintaining low insulin levels and combating insulin
02:15:32
resistance what are the four pillars yes so when it comes to controlling insulin resistance the key is to manage
02:15:38
macronutrients and the best way to manage macronutrients is going to be a strategy that helps lower insulin
02:15:44
lowering insulin is the key to both slow insulin resistance and fast insulin resistance so the more the strategy
02:15:51
lower insulin the more effective it's going to be and there are poor there are four pillars so the first one control
02:15:58
carbohydrates second prioritize protein third don't fear fat and then fourth
02:16:05
after the first three have been taken care of four frequently fast so with the
02:16:11
first one very briefly by control carbohydrates I mean that it is time to focus more on whole fruits and
02:16:17
vegetables eat them don't drink them and then don't get your your carbohydrates from bags and boxes with barcodes that
02:16:23
the more you're opening up a package and getting your chips or your crackers or your cereal or your bread the more
02:16:29
you're going to be spiking your glucose and your insulin keep that on the shelves at the grocery store focus on
02:16:35
whole fruits and vegetables that's going to be the key for number one control carbs now while you're eating fewer
02:16:43
carbohydrates you need to eat something and so prioritize protein I would say
02:16:48
particularly animal Source protein which is the best source of all of the amino acids that humans need and then with
02:16:55
those proteins will come fat don't fear that fat that's number three fat is very
02:17:00
satiating when combined with protein when fat and protein come together we digest it
02:17:06
better sometimes people will find that if they just have a scoop of whey protein it can be very upsetting on
02:17:12
their stomach it's because we're not supposed to eat protein alone in nature that never happens in nature protein
02:17:18
always comes with fat that's how we eat it we digest it better and human Studies have shown that when a human eats pure
02:17:25
protein there's some degree of muscle growth albeit microscopically minuscule but when we eat protein with fat we have
02:17:33
significantly greater muscle growth than we do with the protein alone so that is the three pillars that Encompass the
02:17:41
macronutrients or the big parts of our diet but once a person has done that then they are well positioned to adopt a
02:17:49
strategy a structured strategy of fasting and that can be there are as many ways to fast as there are people
02:17:55
who want to do it there's no right way or wrong way my goal by invoking that
02:18:01
fourth principle and and I do think it should come last once you've learned how to eat better food your your your body
02:18:07
has adapted to burning its own fat for fuel but it can take the it can take uh
02:18:12
intermittent fasting where it's one meal of the day you're fasting through um it can do where people do alternate day
02:18:19
fasting there are countless different ways to do it even if I'm in ketosis then you don't need to do it as much
02:18:24
because you're already lowering your insulin so if a person's already in ketosis in fact if a person were in
02:18:29
ketosis and frequently fasting um depending on how lean they are it's going to become extremely difficult to
02:18:35
retain muscle yeah so those are the four pillars it will be an extraordinarily effective way to address insulin
02:18:42
resistance but the problem as I started at when I that I mentioned is that while
02:18:48
these concepts are simple that does not mean they're easy because humans show
02:18:53
addiction addictive Tendencies to only one macronutrient not fats not proteins
02:19:01
all of the evidence of the neurobiology of addiction in humans points to carbohydrates and and so as much as I
02:19:07
lay out this simple plan it can be difficult and this is why this self-discipline required is
02:19:14
difficult enough that it's why people find that they have to result in you know relying on drugs for these kinds of
02:19:20
things physical activity exercise useful for
02:19:26
keeping my insulin levels in check yeah yeah I'm really glad you brought up exercise I'm
02:19:32
an enormous advocate of exercise the best exercise to improve insulin sensitivity is the one you'll do and so
02:19:39
if someone listening to this is an 80-year-old grandma and um if she if her form of exercise is walking around the
02:19:45
street down around the block with her girlfriends but then if someone else has the ability to go cross country skiing
02:19:51
or CrossFit do it so the best exercise is the one you'll do now having said that the better exercise is the one that
02:19:59
you'll do that keeps muscle um muscle building work is going
02:20:04
to be minute for minute a more effective way of improving insulin sensitivity than than any kind of aerobic activity
02:20:10
and that's because muscle is the great consumer of glucose um and back to the in fact not
02:20:17
only does muscle eat the most glucose from the blood but it's it's also how it eats the glucose when it's exercising so
02:20:24
earlier we talked about how insulin kind of comes and knocks on the door of the muscle cell and then the muscle cell
02:20:30
will open the door and allow the glucose to come in thereby lowering blood glucose unless the muscle is exercising
02:20:37
when a muscle is exercising and I'm kind of mimicking the contraction and relaxion relaxation of a
02:20:43
muscle when the muscle is exercising it has its own way of opening those doors
02:20:49
so there's an insulin independent method where the muscle cell
02:20:54
essentially tells insulin insulin I know normally I have to wait for you to come and open these doors but I'm so hungry
02:21:01
during this exercise that I'm not going to wait and so the doors just open so the Contracting muscle has its own way
02:21:08
to rush to pull the glucose in which means of course that a person's going to have an easier time controlling their
02:21:15
blood glucose which in turn would mean a better time controlling insulin but the
02:21:21
more muscle a person has the easier it is and this could be one of the reasons
02:21:26
why if you look at longevity and look at the markers of muscle strength versus the markers of
02:21:33
cardiovascular aerobic fitness the aerobic fitness markers are terrible predictors of longevity it's muscle and
02:21:40
strength that predicts longevity for multiple reasons including just the very Act of living and moving but also
02:21:47
because if you have more muscle you're going to control your glucose better which means you're going to control your
02:21:52
insulin better then you're back to these variables that people use to predict or what are the most accurate indicators of
02:21:58
longevity it's who has the best glucose control more muscle helps that happen there's a big debate around
02:22:06
whether we should be calorie restricting and low fat diet whether we should be calorie restricting in a moderate fat
02:22:12
diet or calorie restricting and a low carb diet what's what's your take on that
02:22:18
yeah I am unabashedly in favor of carb carbohydrate restriction um I I would say for two reasons um that one reason I
02:22:26
think that carbohydrates should be the macronutrient that is most scrutinized is because it's the one we eat the most of 70% of all calories consumed globally
02:22:33
come from carbohydrates that is the one that has the biggest insulin effect for and
02:22:39
that's a problem for all the reasons we've discussed but two carbohydrates are not essential um this is
02:22:46
controversial people don't like to acknowledge it but there is literally no biological need that humans have for
02:22:53
carbohydrate um the in the United States a report decades ago from the Department of Agriculture looking at the needs of
02:23:01
human nutrition there's a quote there and I'm not going to get it exactly right but I'll get it pretty close it's stated in
02:23:08
this document that the lower limit of carbohydrate consumption in humans is zero in other words there is no such
02:23:16
thing as an essential carbohydrate now I'm not saying well let's not eat any of them no
02:23:21
but I am saying why is that the one we focus the most on as 70% of all calories
02:23:27
globally are coming from that one you're telling me that we most of what we eat comes from what we don't need why not
02:23:33
put the focus on the things we do need there are such things as essential fatty acids let's eat fat there are such
02:23:40
things as essential amino acids so let's eat protein and make sure we get what we need and then on any remainder of the
02:23:47
plate we can get some other things that we want to nibble on like plants why don't we just sack all this off and just
02:23:53
take as zek then ah yeah great question so the the I have uh I have kept my
02:23:59
finger on the pulse of the whole field of gut derived hormones which is what we talk about with these weight loss drugs
02:24:05
almost since their beginning my dissertation work was in a lab one of the first funded labs to look at these
02:24:10
drugs although in the context of diabetes and then it's blossomed into
02:24:15
the context in the use of obesity this this is the class of drug GP receptor Agonist first of all what is glp1 gp1 is
02:24:24
a hormone that we all make from our guts our small intestine will make glp1 we're
02:24:30
making it all the time to varying degrees some things we eat will result in a higher glp1 sometimes it'll be a
02:24:37
lower glp one like for example a paper just published a few months ago found that if you have people eat the exact
02:24:43
same meal of calories but lower carb or higher carb the lower carb version of the meal will increase glp1 three times
02:24:51
higher in the blood than the high carb version of the meal which means that they'll feel yeah so then the B what so
02:24:57
what's the point who cares about glp1 one of glp 1's main effects is to tell the brain that we're full okay so more
02:25:04
glp1 more satiety yeah yeah more gp1 less hunger which is very impactful in
02:25:10
fact I would be remiss if I didn't mention a study that was published in humans a while ago they took obese
02:25:16
humans and lean humans and had them eat fat and found that like pure fat and
02:25:21
they found that the glp1 response was the same whether you were lean or obese you had the same amount of glp1 that
02:25:28
would suggest that whether you're lean or obese both of your brains and both of these populations will have the fat and
02:25:35
have the same sense of I'm full it would because it was matched with glp1 however
02:25:41
when they had these same groups eat pure carbohydrate the lean group had a robust
02:25:47
glp1 response big glp1 in other words words they would eat the carbohydrate
02:25:52
and say I'm full cuz gp1 would tell them so however in the obese group they ate
02:25:57
that exact same amount of carbohydrate and they had an almost negligible glp1 effect they were still hungry in other
02:26:04
words they would eat the same amount of carbohydrate as their lean counterpart and then just say okay what's next I'm
02:26:09
still hungry and so it is prudent to focus on glp1 glp1 is a powerful hormone
02:26:16
that does have an effect on human health what I feel in to comment on is the
02:26:22
negative side effects because the only thing we hear about is social media influencers extoling the benefits and
02:26:29
hey I'm on this weight loss drug and I've lost 50 pounds someone has to be the voice that says yeah but what about
02:26:35
this and there are some significant but whatabouts when it comes to these um
02:26:41
weight loss drugs one of them is the loss of muscle mass or lean mass you've
02:26:47
mentioned a couple papers from the New England Journal of Medicine a paper a couple years ago from what was called
02:26:52
the step five trials looking at these drugs they found that for every six
02:26:57
pounds of fat a person was losing on these drugs they were losing four pounds
02:27:02
of fat-free mass or lean mass so 40% of the weight they were losing uh on these
02:27:09
drugs is coming from lean mass like including muscle and bone so there are
02:27:14
now case reports of young healthy women who were overweight who go on the drug for some period of time and after they
02:27:21
get diagnosed with osteoporosis where they have eroded their bone health they're losing lean
02:27:26
mass so again they've eroded their bone health yeah so 40% of the weight that
02:27:31
people are losing on these drugs appears to at these high doses is coming from lean mass so fat-free Mass including
02:27:38
muscle and bone the reason I find that so troubling is that in the UK at two
02:27:44
years on the drug 69% of people get off the drug they don't want to be on it
02:27:51
anymore and now imagine this individual imagine if you will a 60-year-old woman
02:27:56
who's been on the drug I take that age and that sex on on purpose because it's so hard for her to to grow new muscle
02:28:03
and bone let's say she's been on this drug for a year and she's lost 20 kilos
02:28:09
well 40% of that will have come from her lean mass and 60% of it came from her
02:28:15
fat then when she gets off the drug now all of a sudden her lean mass
02:28:21
her muscle and bone that's never coming back the muscle and bone that she has lost is gone forever probably at that
02:28:27
age because we can't after the age of 60 good luck developing new muscle and bone
02:28:32
but what can come back rapidly is the fat mass and so at two years she decides
02:28:39
to get off the drug which again about 70% of people do they're going to gain that fat back but they're not going to
02:28:45
gain their muscle and bone back that is a significant loss that may be depending
02:28:50
on their age gone forever I was scrolling on Twitter the other day and I
02:28:56
saw a video going viral which is now being reported in a bunch of news
02:29:01
Publications it was yesterday that I saw um this video going viral and I'm going to play this video to you it's from a
02:29:07
singer called Avery and she talks about her experience with aenc I just L the
02:29:14
doctor's office I went to get a checkup because I've been off of OIC for 2
02:29:19
months now and I just wanted to see if my body was in better condition if there were any permanent damages kind of in
02:29:27
shock right now because I wasn't expecting this but um I guess o zumic
02:29:33
can cause bone density loss and I didn't think that that would happen to me
02:29:39
because I was only on it for a year um but I have significant bone loss
02:29:45
I have osteoporosis and um osteopenia so that AR there's like several of them that I
02:29:52
have I wasn't expecting that but that's what happens if you
02:29:58
um if you use OIC uh for weight loss and you lose too much weight yeah I wonder
02:30:04
she's so lean I wouldn't be surprised if she had it even worse than normal
02:30:10
because we see it has become I don't mean to suggest this is the case for her
02:30:15
but you do see people using these weight loss drugs who are already very lean
02:30:20
I mean I've got a picture of her here and she does look incredibly lean already but see this is what people are
02:30:26
doing they're basically using it to facilitating eating disorder in the people who are lean um this has become
02:30:31
so common that there are complaints saying that you know lean healthy people are getting the prescription and people who are obese and diabetic aren't
02:30:39
because of shortages the more the the leaner I've seen this I know someone
02:30:44
personally who is already a perfectly lean healthy woman and then she now looks sickly
02:30:50
um and what caused it well she wasn't lean enough and when you take enough of
02:30:56
that drug that you just have no more hunger because of how it's acting at your brain you do just stop eating and
02:31:03
the malnutrition at least in part is going to cause a loss of lean mass um
02:31:09
but that also play it is even further exacerbated by the mental health
02:31:15
problems where there was a paper recently published with the use of these drugs finding that people when they
02:31:20
begin the drug their risk of Suicidal Thoughts doubles it goes up by over 100%
02:31:26
and their risk of major depression triples and this so as much as we talk
02:31:32
about these drugs and we say the drug helps you control your
02:31:37
cravings What It's hap what it's doing is perhaps reducing your craving for
02:31:43
everything that while you are eating less food which is resulting in the weight loss you also are not interested
02:31:49
as much in exerc SI as you used to be which is going to make it even easier for you to lose your muscle and bone you're also less interested in Hobbies
02:31:56
like going to play pickle ball with your friends or going out and drinking with the boys um so there is this kind of
02:32:03
what's reflected across all of their interests is that their cravings for everything starts to decline on the case
02:32:11
of that girl mentioned there Avery I've Just Seen she's uploaded a post that says thanks my record label told me I
02:32:16
was fat they dropped me I got addicted to a Zen oh my gosh I got addicted to his zek and now as a result I have
02:32:22
osteoporosis and my bones are as fragile as wafer cookies yeah it's heartbreaking
02:32:28
um so now that obviously you know these are claims that she's alleging now we don't know the full picture of her
02:32:34
health and there might be something more yeah but we do know based on that one report that 40% of weight loss is coming
02:32:40
from fat-free mass and so it is in people's best interest to be mindful of that tendency and that if they're going
02:32:46
to explore the use of the drug to do so responsibly and and I want to mention
02:32:51
that um kind of caveat or angle to everything because I don't want someone listening to me thinking all right Ben
02:32:58
says I should never touch this and it is uniformly evil and bad I'm not saying that I find that I have to speak a
02:33:04
little more boldly about the negative consequences because nobody talks about them what would she have done if she
02:33:10
knew about them for example no one knows about these kinds of negatives because people want to sweep them under the rug
02:33:16
now I believe there is a use case for these drugs although different from how
02:33:22
it's being used currently in my mind the best use of these drugs is to help someone learn how to control their
02:33:28
carbohydrate addiction because it will help you control your addiction sweet
02:33:33
Cravings goes down significantly within six months of the person taking the drug
02:33:39
so I think in addition to getting proper education and if I may be so bold I would say it's those pillars I mentioned
02:33:46
earlier control carbohydrates prioritize protein and don't Fe fat all the more
02:33:51
reason prioritize protein and fat to help preserve your muscle and bone
02:33:56
muscle and bone are not made of carbohydrate they're made of M of protein and fat eat protein and fat lift
02:34:02
weights to keep any of that lean mass you can keep the Integrity of your bones intact but take advantage of the drug
02:34:10
helping reduce your cravings for sweet things especially I would say find the lowest effective dose you can where you
02:34:18
are able with a little bit of self discipline where you're not assigning all of the self-discipline to the syringe that you're going to inject into
02:34:24
your tummy there is value and learning to deny yourself something you know you
02:34:30
shouldn't be doing there's life lessons to learn there and so enough of the drug
02:34:35
that makes it a little easier for you to overcome your carbohydrate addiction at
02:34:40
the same time you're learning how to eat well you're learning how to eat properly by managing your macronutrients and
02:34:47
lifting weights and then over time ideally I would say you find that you
02:34:52
are able to reduce the dose of the drug and then eventually get off of it entirely it's worth saying that I I did
02:34:58
also search to see if there was a link between a zenek and bone density and there was no clear Link in the studies
02:35:04
that have been done I I don't know whether there's been a lot of studies done but it says in the studies and reviews semaglutide generally shows no
02:35:10
harmful effect on bone mineral density although rapid weight loss itself can sometimes affect bone health yeah so I
02:35:15
actually think it's an artifact that's a term that we would use as a scientist to say that it's it's an it's an effect
02:35:21
that's happening without being a main effect so I don't believe the glp1 drug is attacking the bone I think it's
02:35:28
because the person has just stopped eating and stopped moving remember what I said earlier people find that they're
02:35:33
just less interested in doing stuff like going to the gym for example um and so
02:35:40
that is probably combining where a little bit of malnutrition combined with a little less physical activity means
02:35:47
you're accelerating some lean mass loss one of the things that this podcast has taught me is that
02:35:53
liposuction is dangerous do you agree with that statement I do from a metabolic
02:36:00
perspective I absolutely do um liposuction is not dangerous to fit into
02:36:06
the clothes you want to wear but it's deeply problematic for metabolic health and that's because as a reminder it's
02:36:12
not the mass of fat we have that matters most when it comes to metabolic Health it's the size of our fat cells so let's
02:36:18
imagine an individual who has more fat than they want in some particular part of the body the best way to help reduce
02:36:27
that fat is to shrink your fat cells so that's very important for people to realize when you lose weight you're not
02:36:33
killing fat cells you're not you're not getting rid of them you're shrinking them and small fat cells are very
02:36:39
healthy fat cells they are literally anti-inflammatory they're releasing hormones that fight inflammation in the
02:36:45
body and they're very insulin sensitive which helps the body by extension be very insulin sensitive so very healthy
02:36:52
small fat cells are healthy fat cells the problem with lipos suction is that you are going in and rather than
02:36:58
shrinking the fat cells you are sucking them out now let's say like a study that
02:37:03
was done in the US in women they found that when women had lipos suction from
02:37:09
their buttocks and hips area um which is where most women gain their weight which is because of sex hormones telling her
02:37:15
body to store that weight there they may look at that fat on their butt and hips and say there's more than I want I'm
02:37:21
going to suck it out so they do but they don't change their habits so they're still eating the same way they were
02:37:28
before essentially now they have fewer fat cells but the body wants to store
02:37:34
that same amount of fat based on how they're eating in other words there's enough insulin telling the body to store
02:37:40
a certain amount of fat and there's enough calories to fuel that fat storage but the the fat would be saying hey we
02:37:48
don't have all these fat cells in the buttocks and hips like we used to let's go somewhere else and so it's no
02:37:53
surprise that over the ensuing years after she's had lipos section not only does she not experience any Improvement
02:37:59
in any health marker nothing gets better with regards to her health and that is
02:38:05
again reflective of the fact that it's the size of the fat cell that matters maybe she has lost 10 kilos of fat that
02:38:11
might be a little much for liposuction six kilos and you would say well you have
02:38:16
six kilos of less fat clearly you're healthier and yet they're not at all nothing has gotten better and then if
02:38:22
you follow them over the years they cannot gain that fat back on their butttocks and hips because it was
02:38:28
literally sucked out and adults have a hard time making new fat cells so it's no surprise that they start storing more
02:38:35
fat in an area that wasn't sucked out namely their belly and so a woman who's
02:38:41
gone through lipos suction yes she will have lost fat by lipos suction at her butttocks and hips but if she doesn't
02:38:47
change her lifestyle habits the body will take those six kilos and say well I need to store those now somewhere else
02:38:53
because you're eating in a way that makes me want to store that much fat and so her remaining fat cells that are
02:38:59
intact get bigger and store a bigger burden and so over time it's no surprise
02:39:04
that Health outcomes can start to get worse by having fewer fat cells she's increasing the burden that the remaining
02:39:12
fat cells have to carry not only does that result in a dist a change in where she's storing fat namely storing more on
02:39:18
her abdomen but all the fat cells will get bigger and thus metabolic Health can
02:39:24
get worse we have a closing tradition on this podcast where the last guest leaves
02:39:29
the last question for the next guest not knowing who they're leaving it for and the question that's been left for you Ben is who in your life gave you a
02:39:35
chance or believed in you when no one else did what a fun question um thank you
02:39:44
um probably my wife uh frankly I just adore her I think about so when we were
02:39:51
newlyweds uh we got married quite young if you'll allow me to be a little El personal for a moment we both really
02:39:59
wanted a family we knew that we wanted to be uh mom and dad and she really
02:40:04
wanted to be an atome mom just full-time mom which I loved I benefited my mother
02:40:11
um who died when I was quite young she was a full-time mom and most of my memories come from her being home when I
02:40:19
was would come home from lunch or I had a tummy ache and she would come pick me up and I I mean I thank I thank God for
02:40:25
my for my mother of course but also for the time I had with her because I had so little um and we both really wanted
02:40:33
Cheryl to be able to be full-time mom mom is just that special that meant as a
02:40:39
young newly married husband I was anticipating a future where I would be the sole provider for the family and it
02:40:47
was very daunting very um scary for me as a 23-year-old
02:40:53
that's how old I was when we got married and I worried how am I going to provide for my family and I would look at the
02:41:00
trust that my beautiful wife had in me and I felt inadequate and I I have
02:41:06
moments where I remember young Ben in his early 20s as a newlywed and how
02:41:12
scared I was in how my wife's ongoing devotion put us in a position where both
02:41:19
make a wonderful amount of money to provide for the family and help secure our future and then at the same time
02:41:25
still have a schedule that lets me be really home to go home early and help one of our daughters with her
02:41:30
homeschooling which I do to always not go into work until I've made breakfast for the kids and we've had some family
02:41:38
time so um much of all of it is just this the support of my wife because at
02:41:44
any moment if she would have said no I'm done you got to go get a job right now I
02:41:49
would have I love her and respect her enough and even rely on her Insight that I would have done it but she just really
02:41:56
believed that okay Ben you're not dumb I didn't marry you for your looks I think you've got something I'm going to trust
02:42:03
you and that trust was it was both humbling and scary but also very
02:42:08
empowering and it's given us a beautiful life Ben thank you my pleasure it's been tree ey opening and you've answered so
02:42:13
many of the questions that I've had for so so long especially as it relates to ketosis and the broader link between
02:42:20
insulin infertility pregnancy PCOS all of these kinds of things which are topics of conversation amongst my
02:42:26
friends and people that I love Ben thank you my pleasure thank
02:42:32
you isn't this cool every single conversation I have here on the Diary of a CEO at the very end of it you'll know
02:42:39
I asked the guest to leave a question in the Diary of a CEO and what we've done
02:42:45
is we've turned every single question written in the Diary of a CEO into into these conversation cards that you can
02:42:52
play at home so you've got every guest we've ever had their question and on the
02:42:57
back of it if you scan that QR code you get to watch the person who answered
02:43:03
that question we're finally revealing all of the questions and the people that
02:43:09
answered the question the brand new version two updated conversation cards
02:43:14
are out right now at thecon conversation cards.com they've sold out tce twice instantaneously so if you are interested
02:43:21
in getting hold of some limited edition conversation cards I really really recommend acting quickly
02:43:27
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02:43:46
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