Written by Christopher Kelly
Jan. 12, 2016
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Christopher: Hello and welcome to the Nourish Balance Thrive Podcast. My name is Christopher Kelly and today I'm joined again by Dr. Tommy Wood. Hi, Tommy.
Tommy: Hi.
Christopher: How was your Christmas? We're recording this on December 30th. So tell me about your Christmas. What did you eat?
Tommy: What did I eat? So I was with my dad just outside Oxford in the UK. We ate a lot of turkey, ham. I did quite a bit of the cooking myself or I sort of at least helped out, make sure we're getting the turkey right. But also Christmas pudding which is like a very dense fruitcake if anybody hasn't had that.
Christopher: Yeah, I have. For sure it's got all sorts of weird things in it that maybe we shouldn't be eating.
Tommy: Actually, I've got a couple of people in my family who can't eat dairy or eggs for various reasons. So my stepmom actually made a vegan Christmas cake. So there was some probably vegetable oil or something in there that we're trying not to think about. And a good whoop of gluten. But I think at that time of the year I don't really worry about that at all. I think it's the important traditions and everybody sits around the house a little bit and I enjoyed it very much. So I have no problem with that.
Christopher: Awesome. I had kind of visions of you being in a lab somewhere in Oslo, just you and the mice for Christmas.
Tommy: No, I did my escape for a couple of weeks.
Christopher: That's awesome. And I'm so lucky here. My wife is obviously a fantastic cook and she did a big meal on Christmas eve and we had the last of our pig that we bought from a local farmer and it was all like super duper squeaky clean AIP Paleo because of some of our guests. And then on Christmas day, Julie's mom made this prime rib that must have cost $5,000 because it was like bigger than my quad. It was ridiculous and it was done roasted like this salt roast thing, absolutely incredible piece of meat. And then, of course, all the side dishes are all totally Paleo as well. So very lucky.
Tommy: Sounds perfect. I saw some great photos actually. That's some very impressive pork.
Christopher: Oh, yeah, yeah, yeah. This pork has been fantastic. I think it's the best thing in the world to go down to the Farmers Market and actually meet the farmer and -- I don't know. You just seem to get better quality meat that way, I think.
Tommy: Yeah, absolutely. Absolutely.
Christopher: I didn't get you on today to talk about Christmas although that is fun. I think I've really only got two questions for you but they're quite big ones. The question is: What is insulin and what does it do? So it's a two-part question, which is I know is annoying. As an interviewer, I've realized this, you can't ask seven-part questions because you only get an answer to the last part. So maybe I'll try and keep you on track. So why don't we start by talking about what insulin is?
Tommy: Okay. So I think without saying that the reason why -- So you and I have talked about this quite a lot and also we're part of an online group run by Marty Kendall which is all about optimizing insulin and he's done a lot of work looking at trying to minimize the impact of diet on insulin or managing insulin in various diseases, so metabolic disease particularly is very important. And what is increasingly apparent is that not that many people really understand what insulin does. And I gave a talk about this a while back. I've talked about it with people since.
It just seems that the basic idea is that insulin is just what your body uses to stuff glucose into cells. I mean, that's what I was taught in medical school. So you eat carbohydrates, blood glucose goes up, the body releases insulin and that insulin sort of stuffs the glucose into the muscle cells or the liver cells.
Christopher: Right. And that's the answer I would have given you probably only six months ago.
Tommy: Yeah. And that's what most people are still working from. But actually, what it turns out, and this is something that I maybe spent the last few months sort of looking into a bit more and more on the side because it sort of becomes such a hot -- insulin has become such a hot topic. Actually, insulin really isn't very good at pushing glucose into cells. It's pretty much the last thing that it does compared to lots of things that it does.
But basically, what it is, is it's a short peptide hormone, which is basically a small protein that's released from the pancreas, beta cells in the pancreas, in response to various stimuli. So blood glucose going up is one but there's also -- it can go up in response to the body just expecting food. So you see food and your body releases insulin because it knows that it's going to need that insulin to start moving things around the body and deciding where energy is going to go.
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And that's basically it. it's a small hormone that's released from the pancreas and then the idea is it sort of helps what people say -- a lot of people will say nowadays that it's sort of it's there for nutrient partitioning which basically means that it sort of helps decide where things go. So where the carbohydrate, fat and protein go. And that's part of its main job is deciding where those kind of things end up.
Christopher: Okay. So if insulin's primary role is not for stuffing glucose into cells, what is its primary role?
Tommy: So, I think, the best way to think about it -- So if you're thinking about insulin as something that stuffs glucose into cells then it's kind of that view is of insulin being, say, anabolic, so as in building stuff up. So you're kind of pushing things in the direction of, instead of breaking things down you're trying to build them up or potentially for storage. So pushing, so the traditional thought is that blood glucose goes up, insulin comes out, pushes insulin into the muscles and then you store that glucose as muscle glycogen.
But actually, the main thing that insulin does or its first role is rather than being pro storage or pro building up it's actually anti-catabolic. So it's anti-breaking things down. So it's stopping breaking down muscle tissue to provide amino acid. It's stopping breaking down glycogen that's already stored. Or it's stopping you breaking down fat. So we talk a lot about if you keep your insulin levels high all the time then that could prevent you accessing body fat if you're trying to lose weight. And that's one of the sort of tenets of the insulin hypothesis of obesity.
If insulin is high all the time then you never, you can never access your stored body fat because one of its main jobs is to stop you breaking down body fats. And the way it does that actually is sort of the first thing it does -- So the way I like to think about it in terms of the order of importance of what insulin does is the order through which it travels through the body. So if you release insulin from the beta cells of the pancreas, the first thing it does is it affects the alpha cells of the pancreas which release glucagon.
So glucagon is thought to be the opposite of insulin in that it promotes the breakdown of muscle tissue, promotes the breakdown of fat, promotes the breakdown of glycogen because it's basically signaling we don't have enough energy on board so we need to release some of those stuff that we got stored.
Christopher: Right. So glucose is gone, glucagon.
Tommy: Exactly. Glucose is gone so then glucagon gets released. And so the first thing that insulin does is it turns off glucagon. It stops glucagon being released from the pancreas. Because the glucagon would then go out into the body and start telling it to sort of break things down, release glucose from the liver. Because that's where a lot of our store is in that sort of intermediate times when we're fasting and we haven't eaten then we use glucagon to sort of help regulate how much is released or how much energy is released from stores in the body so that we can then use them up as necessary.
So the first thing it does it turns off glucagon. And then you only need -- You actually only need very small amounts of insulin to do that because it's literally, it's happening in the cells next door to each other. So it doesn't need to go out into the body to do that. It happens very locally. Then the next thing it does is it goes to the liver. So insulin then goes to the liver and it says, okay, so we can -- We don't need to be releasing glucose, we don't need to be breaking down glycogen, we don't need to be turning amino acids into glucose and to fuel ourselves and we basically have enough energy on board or enough energy is coming in so we don't -- the liver doesn't need to control kind of the excess. Because that's what happens next.
And then if insulin goes up to the body the first thing it does is it tells cells to stop breaking down fats and to start taking in, taking out fat from the blood, so fatty acids from the blood. They've actually done some really nice experiments of this where basically if you take -- They did this in the upper arm and you can look at veins, your arteries going in to the arm and veins coming out of the arm and then you can either look at the deep veins which are mainly the blood coming out from the muscle and the superficial veins which are mainly blood coming from the fats.
And it's not exact but it's kind of rough. And you can kind of see that based on what, where your insulin is, if your insulin goes to about ten, this is a rough, the number we talk about, so ten might be [0:09:56] [Indiscernible]. Then those, the fat and the muscle cells stop taking off from the blood, start taking off fatty acids from the blood.
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But nothing happens to the blood glucose. The blood glucose stays exactly the same because it hasn't stimulated the uptake of blood glucose yet. And it's not until the blood glucose gets to maybe 40 or 50, or sorry, your blood insulin gets to 40 or 50, so four or five times the amount that you need to stimulate fat uptake into cells that you actually start to uptake extra glucose. So that's literally the last the insulin does. First it goes to the pancreas then it goes to the liver then it talks about taking up fats and then finally it starts increasing the uptake of glucose into the cells.
Christopher: So how did this happen? So how did it that happen that everybody thinks about the primary role or the first role of insulin is to push glucose into cells? Like, I mean, that's in text books. This is text book stuff that we're talking about. It's not like a myth that's been propagated from some blog on the internet somewhere. How do you think this became the common knowledge?
Tommy: I think part of it comes from work in type I diabetes. In type I diabetes you destroy your beta cells so you don't make any insulin. And then what happens is people get very, very sick because their blood glucose remains very, very high. And then you end up going to something called diabetic ketosidosis. And this is again what people think ketone is about, is from diabetic ketosidosis where basically you just stop burning everything.
But because there's no insulin then there's nothing to tell the cells what they should be doing with various nutrients. But one of the -- But then when you give these people insulin, they obviously get -- they get much better. And the most important thing is their blood glucose comes down. So without any insulin the blood glucose goes up. You give them insulin their blood glucose goes down. So that kind of says, hang on a second, obviously insulin is saying blood glucose should go into cells.
But at least one part of that -- and this is based on -- People might have seen a recent video done by Robert Anger and he did a huge amount of work in glucagon-centric model of type II diabetes or diabetes in general. And that maybe doesn't fix the whole picture but it definitely helps you understand what the roles of, what insulin is actually giving. And so what's happening is that when you don't have any insulin you have uncontrolled glucagon release. And so that the glucagon is telling you is the liver produces much glucose as it can because there's no insulin there saying we've got enough energy on board.
And that comes from burning muscle tissue. It comes from releasing glycogen stores. You also get a huge release of fatty acids store which get turned into ketones because the cells can't listen to the message of whatever nutrients are going around because there's no insulin. And so actually the first thing, the most important thing probably in those people is that you give enough insulin to drive glucagon down and then the body gets out of that kind of emergency mode where it just basically burning everything it can just to survive.
But because of the basic glucose goes up, insulin goes in, glucose goes down, you're missing that extra step. And nobody really thought about that or people or any reason to sort of bringing that back up. And so it's probably stuff like that. And then also if we're doing work in animals or in cells you can see that insulin does increase the uptake of glucose into cells. But it requires very ,very high levels of insulin to do that. And in the context of what should be a normal diet, then maybe we're not just -- I mean, we weren't looking at the levels of insulin. They're actually the most sort of physiologically relevant.
It's very easy to kind of get that wrong because you just -- four or five times the amount of insulin couldn't completely change the effects that it's having. But it's very difficult to sort of finally tune that in the test tube. So the combination of stuff like that probably creates its own confusion.
Christopher: Right, right. And so I think it's super interesting to think that if you have really high blood sugar then it's probably coming from your liver. And if you were to inject a tiny amount of insulin then that might not be enough to start stuffing glucose into cells but it could be enough to shut down the gluconeogenesis so the glucose is coming from your liver and so you would see an overall reduction in your blood glucose from that tiny amount of insulin even though it's not working in the way that most people think it is.
Tommy: Yes. You kind of have to -- The problem is that when you're injecting insulin say in a type I diabetic you're injecting it into subcutaneous fats, usually somewhere in the abdomen maybe on your stomach. And you're expecting--
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So if you mention where insulin be coming from, it should be coming from the pancreas and first acting on the pancreas. Coming as a slow release from the fats on the abdomen, on your tummy, that's a very, very different from where the insulin should be coming from. So you need much larger doses for it to actually get to the places it needs to get to, to have the effects that it needs because it will have to basically spread throughout the whole body before it has the effect on the pancreas that you wanted to. So you actually need very, very tiny doses of insulin to have the effect in the normal physiological situation. You need to take even more if you're injecting externally because it doesn't stop by going to the place that needs it first.
Christopher: Okay, I understand. And this is kind of -- One thing I thought was interesting is you've been talking about very specific blood levels of insulin. But when I did -- So maybe some people listening they heard on an older podcast -- and I'll link to this in the show notes. We talked about carbohydrate experiment that I was going to do which involved me consuming 75 grams of carbohydrates and then measuring my blood levels of glucose and insulin at the lab and in the end I didn't have to go to the lab to do that.
I found a company, a lab called Meridian to offer this test as a blood spot and so I ended up doing the test at home effectively just by pricking my finger with a lancet and then put some blood on to a filter paper and sending that into a lab and they measured my glucose and insulin. And the thing I thought was interesting was that my insulin response was really, really tiny. So my insulin never got above seven or eight points, which is a kind of normal fasting insulin even though I just consumed 75 grams of carbohydrates. What do you think might have been going on there?
Tommy: What I like to think of it is that most people on a day to day -- So say eating a standard American diet or standard western diet. Because it's definitely not limited to America. It's everywhere. You end up relying on insulin to stuff extra glucose into cells because you get this huge sort of peak in insulin based on what you're eating. And part of that, a big part of that is the fact that you are combining carbohydrates with fats.
And we know that if you add fats to your carbohydrates, that increases the amount of insulin that you release. And the longer the fat itself and the more saturated it is, the bigger the effect it has on y our insulin. So when you're eating things of that sort of combination of carbohydrate and fat, you are increasing your blood insulin to levels that will help stuff extra glucose into tissue. But that's not something that we're necessarily adapted to do all the time.
That kind of combination of carbohydrate and fat isn't something we're used to seeing. And if we were used to seeing it then it was at a time when actually we could use a bit of extra storage because maybe in two or three months time we won't get that much food. So then it helps to kind of store that extra stuff where we can. But the way I think we should be using insulin and we should be using glucose is basically glucose should be demand driven.
So rather than the body saying you have to store this extra glucose, it should be the periphery or say your muscles particularly saying this is how much glucose I need so this is what I'm going to take. So rather than it being -- So then it's a demand problem rather than a supply problem. So the moment we got lots of supply but we don't have enough demand and what should be happening is that you -- your muscles probably take about on average 75% of blood glucose goes into muscles. And a lot of that is going to be based on how active those muscles are and how healthy those muscles are. So for somebody like you, Chris, when you do these tests, you also did some exercise in the middle. You did some, a couple of sprints and was it 45 minutes or an hour?
Christopher: Yes. So I rode my mountain bike. So this is part of the experiment. You can listen to the other podcast. I described the experiment on more detail. As part of the experiment I kind of tried to simulate what would be a bit like a race. I didn't have enough time to do a whole race but I did have enough time to ride my bike for an hour and I threw in a couple of 90 second race pace intervals. So certainly slightly anaerobic, certainly slightly glycolytic. So, yeah, not just does -- and if you follow the instruction on the test kit they would just have you sit quietly on the couch for the duration of the experiment and that's not what I did.
Tommy: Yes. So what would normally happen is we know that you are very insulin sensitive. And that's probably combination of good metabolic health plus you are an endurance athlete who trains a lot. So you have muscles that are primed to take up the carbohydrate that comes and are ready to use it.
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And so you have that demand. So what happens is when you took that carbohydrate, you immediately started training and you probably already have slightly depleted muscles because you are on a ketogenic diet so they've got some buffer there. And then the carbohydrate goes straight into the muscles and it doesn't have to -- It doesn't have to then push a huge amount of insulin out to them get it to be stored somewhere. You're already ready to receive that glucose and use it immediately so you don't need to then rely on insulin to distribute it.
So then what happens is you know there's kind of risk that come in, your insulin dance up a little bit, it shuts down glucagon, you probably shut down hepatic gluconeogenesis so the liver isn't producing that much extra glucose or it's not burning muscle tissue into glucose, if that's -- that will be more likely to be in a fasting situation but if you're calorie depleted then it could definitely possibly happen.
So that glucose is going directly where you need it to and most glucose up taken to the muscle does not require insulin. It will happen without insulin. And so that just happens quite naturally. And so that stuff goes where it needs to go and then you don't need to increase insulin so much that then it can sort of push extra in. So that kind of small -- That sort of just small bump of insulin I think is completely normal and we think that we're going to see it more in people who adopt to low carbohydrate diet.
And that's probably one of the reasons why maybe you walk around with slightly less muscle glycogen. A lot of these people are also very cognizant about the amount of exercise that they do or the amount of movement they do. They've got that demand there waiting for any blood glucose that comes in and they don't need these huge bumps in insulin. The problem is you get those huge bumps of insulin, what you do is you completely -- So you basically completely smash the pancreas over the head with insulin and then you smash the liver over the head with the insulin just so you could get that insulin out to the muscles to push a bit of extra glucose in.
So you're basically very early on going to be completely obliterating those early effects that insulin needs to have which actually don't need that much insulin for because you're relying on much higher dose of insulin in the muscles or the fats to have that effect. So when you're eating things like that where you don't have that demand, you don't have that need for glucose in the muscles then the insulin release that you need in order to drive that is going to really, really affect the earlier processes that insulin is needed to drive.
Christopher: Interesting. I think we're kind of -- I mean, we've talked a lot and you've given me a lot of great information here but I think there's a key takeaway message here. When I did this experiment my glucose did tap out really high. So it went up to 200 milligrams per deciliter after consuming 75 grams of liquid carbohydrate, it was. But it did come down really quickly after I did the exercise and I'm sure that at least part of that very high peak, 200, was due to the stress response of the exercise.
So I've seen this before. I've gone out and done a session of hard intervals, haven't consumed any carbohydrates whatsoever, testing my blood glucose right after and it's 150 milligrams per deciliter. It's to do with the stress response of the intervals. But I think the key message for me here is that insulin is not for driving glucose into cells. Exercise is for creating a demand for glucose. And that's what causes the glucose to go into cells, right?
Tommy: Yeah, absolutely. And you should have -- So the problem is that if you've got -- if all your cells are overloaded already and then more stuff comes in then you need to rely on much higher levels of insulin to start stuffing that glucose somewhere essentially. That's where you, what you end up having to do. But the way that it should work is that you've created that demand. And as you exercise, you will release cortisol, adrenaline, those are there to drive out blood glucose levels. And you need to do that because even if you're exercising aerobically you will have some glycolysis.
You do have some need for glucose as a substrate in the muscles because as you activate certain pathways within the exercising muscle but just increases glycolysis. So you just need some and your body will do its best to revive that. So you create that peak based on those hormones sort of releasing extra glucose so that you can supply it to the muscles. That is completely normal. And we will, in the future, you'll do a dry run with just the exercise and no carbohydrate just to see what the effect of exercise is on your blood glucose levels.
Tommy: Right. Yeah, of course. I think that would be a great experiment. I've got a number of like -- I'll publish the--
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I'll put the link to the article I published in the show notes for this episode but I've got a number of interesting experiments coming up. I interviewed Mark Newman who is the founder of Precision Analytical who makes this hormone test. And so this weekend I'm going to do a cyclocross race and then pee on a filter paper so that Mark's lab can measure the amount of cortisol and its metabolites in my urine before and after a bike race which I think is going to be really interesting to see just how stressful bike race is.
I'll link to that experiment in the show notes. But maybe just this one last bonus question I wanted to ask you about. And I kind of have seen this in myself in the past but now not at all and I don't think I really have a good explanation. So especially when people are eating a low carb diet they tend to see normal glucose levels during the day even when they're eating -- so they'll see some '80s, '90s maybe, so less than five millimole if you're outside of the US.
And then first thing in the morning they're seeing like some crazy number. Maybe even over 100. And it seems like some people are referring to this as the dawn effect. And I'm wondering whether -- especially given what we've just discussed about insulin -- whether you have kind of any insight into what might be causing this.
Tommy: Yes. So, I think, this seems to come up a lot and people talk about -- they mention low carbohydrate diet. They call it physiological insulin resistance. And one of the things that they think and one of the things that they refer to or they say this is physiological resistance is a creeping fasting blood glucose particularly -- yeah. So particularly in the morning. And I'm not really sure that has anything to do with insulin resistance at all actually.
I think we do know that blood glucose peaks, can peak in the morning because of an early morning peak in cortisol. That's what's meant to happen. Your cortisol goes up, first of all, it helps wake you up, increase the alertness. But it also increases blood glucose so that you can essentially go out and do what you need to do before you then eat later on.
Christopher: Right. And we see this in the -- especially in the new DUTCH test. It actually captures the cortisol awakening response. So the old saliva test, it would just -- You would just see this gradual decline of cortisol throughout the course of the day. Whereas Mark has designed the timing of the test to capture that cortisol awakening response. So you see the cortisol is actually quite low just before you go to bed. But two hours after you get up is actually when you see the peak of cortisol. So the cortisol spikes after you get up.
Tommy: Yeah. Obviously, you can't test for it but it should peak two to three hours before you wake up or it should start to come up two or three hours before you wake up. Because it's sort of there to get you going early in the morning. And that's one of the reasons we think why people have heart attacks, more likely to have a heart attack in the morning because of that.
Christopher: Oh, interesting.
Tommy: An early morning cortisol spike. Obviously, if you're at risk of that kind of thing. But I think a lot of potential stuff could be going on there. So I think if people aren't eating -- So first thing, anything that's going to potentially increase cortisol could be causing a problem there, so are people sleeping properly, are they addressing stresses? That's obviously going to be a potential problem. Then also anything which maybe isn't maximizing metabolic health and that -- There's loads of stuff that I see particularly in the low carb community that I think we may address well enough.
So we are taking enough magnesium or potassium which is really important for metabolic signaling, insulin signaling. Are people just eating stuff that is low carb but they haven't really looked to the quality of it? So is it full of vegetable oil or things like that? I see some low carb groups where mayonnaise is low carb. The rest doesn't matter. So are we getting enough vitamin D, omega 3s? All those kinds of things are very important for normal metabolic signaling. I think the quality of a low carbohydrate diet is important there.
Another thing that we know can happen and was at least been one interesting study on this is looking at a ketogenic diet. I mean, we know that a ketogenic diet can actually increase cortisol levels. And the reason it does that is because if you sort of say overweight or you have oxidative stress problem or chronic inflammation which is often associated with something like obesity, what you do is you upregulate the enzymes that break down cortisol.
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So you break down your cortisol very quickly so you end up having what we would have seen on a saliva test. Previously we would have seen a low free cortisol. But when you have a low free cortisol, you don't know if that's because you're not making enough or because if you're burning through your cortisol really quickly. Does that make sense? So it's either you're breaking it down very quickly or not making it enough. But before you couldn't really tell that.
But if you really look at after you adopt a ketogenic diet, or in this one study it was in obese population, cortisol goes up but it's not because you're making more, it's not because it's stressful. It's because you are no longer breaking down the cortisol really quickly. So what we know is we have seen and there's a few study that showed on the ketogenic diet cortisol can go up and people thought that it was because it was stressful but it might just be because you're actually not breaking down cortisol as quickly.
So what people might need to do actually and -- A ketogenic diet, when you're in ketosis, traditionally, we think that it's part of a buffer when you haven't got enough calorie or you're not taking enough calories because the ketones and the fat breakdown are you kind of backup energy source. And particularly people who haven't addressed other health issues. So say if they have some kind of autoimmune problem or they have some kind of infection or something like that then I think the addition of ketogenic diet might actually act as a stressor.
And we know that if you, say, have some carbohydrates in the morning you can actually bring down the morning cortisol and you could actually almost, you can actually bring down your blood glucose by eating carbohydrate because you actually blunt some of that hormonal response. So I think when people are seeing fasting blood glucose goes up, there's a lot of different things that could be going on. And I don't think it's necessarily a normal thing.
So people say, "Oh, it's just normal that your fasting blood glucose goes up in the morning." And actually it might be but there's also a huge number of reasons and things that you could be just sort of making sure you're getting right to try to bring that down because you shouldn't have a super high blood glucose in the morning to suggest that you're not getting what you need to the periphery to the brain to the muscles.
Christopher: Interesting. Yeah, I know. I did see some trace of that in myself a few months ago where my blood glucose, fast blood glucose was creeping into the 90s. But more recently in the last few weeks, it's come right down and it is now consistently in the low 80s. I've even seen numbers in the 70s which I've never seen. I've never seen a number that low for as long as I've been testing. I'm having trouble of like trying to isolate exactly what it is that might have caused this more recent change.
I guess it could be pretty much anything. It could be that I'm sleeping much better now. The only thing I can pin down with supplements is nicotinamide riboside but we discussed this offline and it seems unlikely that that's what is causing this change in fasting blood glucose.
Tommy: Yes. So for people who haven't heard about it, nicotiamide riboside is basically a precursor for NAD which is basically one of the ways that we move -- one way to think about it is one of the ways we move electrons around the cell. So NAD is something used to accept electrons from the Krebs cycle so then you can move them into the electron transport change to generate ATP. You do that by making NADH. The ratio of NAD to NADH is really important determine of a number of different processes because basically it tells you how much energy you're supplying versus how much energy you need.
So in people who have something like type II diabetes, you have a lot of extra NADH compared to your NAD. So that ratio changes. And one of the things that -- one of the reasons that might be happening is because we know that nutritional deficiency is going to affect this. So if you have a deficiency in vitamin B3 or niacin, then, which nicotinamide riboside is a metabolite of or a precursor to, then that kind of -- you sort of you end up with not enough NAD to accept all the electrons from the energy that you're taking in, from the calories that you're taking in.
So taking some nicotinamide riboside can help affect the ratio and allow you to then get more throughput, more energy throughput into the cells and then you're actually getting energy where it needs to go especially if you are deficient in the first place. So you're kind of signaling that you can take that stuff in. So if your NAD goes up compared to your NADH you will activate, say, glucose uptake into cells because you're indicating the space for more energy to come through.
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I think that could affect it. The problem is there hasn't been that much human research on nicotinamide ribosides. I'm not really convinced that it could have that much of a dramatic effect. And there are other things you've done and you've been sleeping better. As you should have got into this section of the season, you train a bit less [Phonetic]. I know previously we kind of -- you're taking creatine and beta-Alanine, which can kind of affect your energy regulation. You also occasionally eat some carbohydrate which I do think for some people could have improved gut health but definitely improve insulin signaling in the short term.
I think it's very difficult to identify which thing caused it and definitely nicotinamide riboside might help. But I would be -- just based on the -- just because [0:35:55] [Indiscernible] that much that the theory is good but it hasn't been that many -- There haven't been that many large scale studies. I'll be very, very impressed if it's just purely that.
Christopher: Right. And it's so hard to control these variables. Because you're right, I have been -- I've not really been training much at all over the last few weeks. I'm still racing cyclocross but I've not been doing any training at all. Like I've done literally three or four bike rides in the last couple of weeks or even three or four weeks. I begin to wrap up my training again shortly. It would be kind of interesting to see if I keep taking the nicotinamide riboside and the fasting blood glucose goes back to where it was before then it's probably not it.
But this seems like a good place to kind of segue into -- I wanted to talk to you today about a new program that Tommy and I have put together. It's called conciergeclinicalcoaching.com. And I will link to that in the show notes because I know the concierge can be a bit of pain to spell. But just to give you a background here, there's a lot that goes on behind the scenes with Tommy and I and I don't mean anything weird.
Tommy sends me a lot of emails. People ask me. A couple of times I was asked this. There's a podcast guest yesterday: How on earth have I done this? Have I gone from being just a kind of a lay computer programmer to having all this knowledge and being able to help with these different people and the answer is Tommy has been a huge part of that process. And Tommy typically sends me, I don't know, what do you think, probably averages out like a thousand words a day or something of email. It's a lot.
Tommy: Yeah, definitely. When there's papers that come up and things we've talked about, yeah, we're talking about particular issue for somebody, yeah, it can increase quite rapidly.
Christopher: Right. And so I'll ask Tommy a stupid question. Like can nicotinamide riboside lower blood glucose in the mornings? And Tommy will write a thousand words and he'll attach four scientific papers for me to read. And so that's what I spend a great deal of my spare time doing is reading these scientific papers. And it's an interesting way to learn. It's kind of me that's providing the motivation and then Tommy gives me the background and shows me. Tommy is a research scientist and I feel like this time you really need someone that knows what they're looking at to direct you towards the good science. And if you don't have that you're kind of left floundering a little bit I think just because of the volume of stuff that's published now. Do you think that's true?
Tommy: Yeah. No, absolutely. And this is kind of -- We're in a point, I guess, this is an existential question for all research scientists. But we're at a point where if something is published we assume that it's -- It's been peer reviewed and, therefore, it's good science. And which, unfortunately, just isn't the case. Or people are just -- I see a lot of people just basically doing whatever they can to just get whatever they think is true to be published, if that makes sense. There's so much vested interest in cognitive distance and this stuff that people don't agree with and, therefore, it's brushed under the rug and things.
We can't say that we're immune to that because, obviously, we have our own biases and the only thing you can do is just appreciate that those exist and do whatever you can to try to be as balance as possible. But it can be very, very confusing to try and talk through all the stuff that's out there.
Christopher: Right. I think it's fair to say that you're about as evidence driven as a person could be and having someone like that help you navigate the science is extremely helpful. And that's how I've learned. Like that's how I've learned all this stuff, is by reading these papers and things like Bryan Walsh's Metabolic Fitness Pro has given me the knots and bolts to understand some of the words that I see in these papers. I mean, as a computer scientist, just to see these words is just variable names, right? And then once you know what the variable represents, it's like not that hard to follow along and learn stuff.
[0:39:58]
And what I'd been toiling with for the last few months even is like how can I bring this experience to more people? So I have this unique situation where I've got the biochemist, a medical doctor, a research scientist who is teaching me in effect. And how can I bring this experience to more people? And it's difficult. And there's not really a good way I can think of to do this other than what we have now in terms of this membership site that we put together, conceirgeclinicalcoaching.com.
And really what it is a private Facebook group. I think that is the part of the site which is going to be the most popular. So once you join the membership site, it's $100 a month, you do have the ability to ask questions inside of the membership site itself. So if you don't have a Facebook account you'll still be able to take part. But my gut feeling is that all of the action, all of the good stuff is going to happen on Facebook. And so if you don't currently have a Facebook account, it might be an idea for you to get one and then not just tell anyone about it.
If you don't want to be part of that Facebook thing, you can be anonymous on Facebook, I would guess. The idea is I want to create this kind of Facebook goup where you can follow along with studies that we're looking at, the questions that we're trying to answer and then also we were thinking -- Part of this idea came from the O2 Boost program that we did where people did a blood chemistry with us and then optionally also an organic acid.
I only have 30 minutes to talk to that person after the fact about their test results. And it was obvious from the beginning that that wasn't nearly long enough to be able to explain what all the results meant. And what I really wanted was a way to keep in touch with those people and to have them digest some of what -- So this is the problem. I can't sit down with you for two hours and just snow you with everything I know.
You've really got to take it in chunks and digest it and then you'll think of questions. I'm hoping that this Facebook group, this private Facebook group is going to be a way for people to ask their questions about their blood chemistry and the organic acids and maybe whatever other else testing they've done. And an efficient way for us to answer those questions and at the same time we don't get broke.
I can't go back to a situation where I just spend all day answering people's questions on email. And at the same time there's no way for me to pay my mortgage which is obviously not a sustainable situation. Yeah, it's an idea. It's a concept. I'm hoping that either podcasters are kind of into this. And maybe if you think it's a terrible idea you should -- I would greatly appreciate you letting me know because that's a really valuable feedback. I'll link to it in the show notes and you can check it out and maybe think about joining. Did I miss something, Tommy? Do you think there's anything else we should say about that?
Tommy: I think the real -- There's a few sort of potentially -- And the reason we put it together is because you and I communicate a lot and we share a lot of information backwards and forwards. And it's not stuff that just because of context and how well we know each other, it's very difficult to just put that out there on internet. But we're hoping that we can create a community of people where this information can just be passed backwards and forwards instead of you and I just sending each other emails and we can sort of open it out to other interested parties and then you can sort of discuss things as you go and give opinions and we'll be somewhere where people can share information.
But it's not just that because there are plenty of places where you can do that. But what we noticed was something like the O2 Boost program, like you said, is that you can get some results in, you get some information about people's training habits and their diet, things like that, and then you can sort of talk them through it and come up with a plan for the future. But the problem is there's no follow up from that. Or in that program, we didn't provide follow up because we wanted to give people a good amount of information, what was a very, in the field, a very low price.
Our times didn't really cost very much because want to just try and get, help people as much as possible. But what this idea would do instead is very similar but we'd be -- You'd get continuous feedback so you could continuously ask questions, you could continually bring your results. We recommend people testing and retesting maybe every few months. You have a problem, we fix it, we follow up. And then as well as just as the Facebook group will have regular, at least once a month, depending on our popularity, like a live Q&A session.
So you can either give us questions beforehand if you can't make it live where we can answer them or you can have questions as we go and we can discuss things sort of in person and those things will be -- If there's a transcript of the Q&A that will be turned into an article we can also -- we'll also add papers and things that we think people should be reading and it will kind of allow us and other people to learn as we go and give that kind of continuity and care, if you want to call it, in terms of your own performance and health. The idea is to deliver all of that in one kind of package.
[0:45:18]
Christopher: Yeah, I know. That's a really important part that we missed actually. So we're going to do a monthly Q&A webinars. So once a month you'd have the chance to join us just to -- I have some software and it kind of looks like Google Hangout. It's like a video conference. And you have the ability to ask questions via a chat box. And then I now also have the ability to actually bring you in live into the conversation if you want to do that. If you got a camera and a mike you can actually join the webinar live and ask your questions.
I think this is going to be a powerful tool. This for me is what's kind of brought about the results that I see now. In the beginning, before I'd really done any training at all for the mountain biking cyclocross, having somebody just program my calendar, like go ride your bike for 90 minutes at this heart rate, that got me great results. And then within a year or two, I plateaued with that. I stopped seeing results. And now I've got to the point where I feel like all of the benefits, all of my games, they're coming from running blood chemistry, running organic acids, maybe do some stool testing, look at your hormones, all these biochemistry stuff, and then having someone like Tommy answer my stupid questions.
I've kind of been using that information to make maybe some diet and lifestyle tweaks, maybe taken some different supplements. I've been getting great results for that. I think that's a really powerful tool that could either complement or take the place of the traditional kind of coached athlete model where you're just given a training plan and you're supposed to stick to it for a month. I'm not sure that's such a fantastic idea. It's something for people to think about.
Tommy: Yeah. And one of the things that you haven't mentioned is the fact that you personally have got -- I'm amazed by it more every day. Like you have this huge network of people that you talk to behind the scenes and most of them have ended up on your podcast. There's a lot of people you can go to with questions because you'll never going to have the answer to everything. But know the person who has the answer to something and you have access to them because you developed a relationship with them. And that's something that I don't think anybody else really has. I think that's a very powerful tool that people will hopefully benefit from as well.
Christopher: Yeah. I know. And I never realized this. When I started the podcast I was just thinking, "Well, I guess, this is going to be a way for me to talk to people." Like if I start a podcast maybe people will listen. And now, with hindsight, maybe almost a couple of years in, I realized that the guests I've had on the show, like those are the world's leading experts in their particular subject matter. And in some cases, there would be no way for me to reach them or connect with them at all.
Earlier, Tommy and I were talking and I mentioned Joe Friel who is in his 70s and he probably doesn't want for money at all, or certainly not coaching clients and he's not coaching anyone at the moment. I now have a relationship with him where in n theory I could ask him a question. That's true of a lot of experts that had been on my podcast. I didn't realize this was going to happen. It just kind of happened organically. I realized it's such a powerful asset. Like you're saying, Tommy, I've kind of a bit of an answers man now. If I don't know the answer myself then I probably do know someone that would be able to give a better answer.
It's amazing. I think it's amazing what's happening with the internet now. It's just changing everything. Before we had libraries. You could maybe go to the local primary care physician and ask him or her a question. And now information can be just disseminated so quickly and it's an incredibly powerful tool and I really want to encourage it.
Tommy: Absolutely.
Christopher: Cool. Conceirgeclinicalcoaching.com. It's $100 a month at the moment. We're pricing it really low and I hope that people will get involved. We want to figure out whether or not it's a good idea. So the price probably will be going up especially as it's a limited resource. We're not selling cookbooks here. We've only got so much of Tommy's time that we can sell. If you're interested in this, I would jump on it now. I'm going to build in a feature which allows you to get the first seven days of access for $10 so you could at least come in, check out the Facebook group, maybe ask a question, find out what it's all about before you commit to the full $100 a month thing. Yeah, let's hope it's a success.
Tommy: Yeah.
Christopher: Cool. Well, thank you so much for your time today, Tommy. I really appreciate it.
Tommy: Thanks. That's always a pleasure.
Christopher: Don't drink too much for New Year.
Tommy: I'll try.
Christopher: Okay. Thanks then.
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