Written by Christopher Kelly
Dec. 22, 2016
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Christopher: Hello, and welcome to the Nourish Balance Thrive Podcast. My name is Christopher Kelly and today I'm with my Chief Medical Officer, Dr. Tommy Wood.
Tommy: Hi.
Christopher: We are at the Buck Institute for Research on Aging for Dr. Dale Bredesen's training course that we're very excited about. For the first time ever, I'm outside recording the podcast. It's absolutely beautiful here. Maybe I'll take a picture so I can post it in the show notes. We are outside in Marin County. There's a blue sky. There's trees. There's sunshine. There's a turkey vulture flying around over there. It's absolutely beautiful. I have to take a picture of this. We're totally so excited to be here. Why don't you tell people a little bit about Dale Bredesen and why you thought it was a good idea to come here for this training, Tommy.
Tommy: Yeah. So, Dale Bredesen is a researcher largely affiliated with the UCLA. He has a long history of really fantastic research in neuroscience, so really basic stuff looking at what affects the brain particularly in Alzheimer's disease, looking at some of the initial trafficking and underlying biochemistry in Alzheimer's disease. And he's published in like The Journal of Neuroscience. It's one of the top journals in the world essentially.
And then over the last 20 years, he's moved from doing stuff like really basic research and now he's got to this point where he used to think that it was going to be one molecule that was -- They're going to make a drug and fix Alzheimer's. And now he's here and we spent now two and a half days listening to things about stress reduction, exercise, nutritional ketosis, all these nutritional supplements and all these things, all the stuff that, I guess, we talked about normally, for a wide range of different conditions and now finding this sort of really well-respected Alzheimer's research was kind of coming in from the basic research, so I've been seeing how a lot of this stuff is really helping people with Alzheimer's disease.
And, actually, he's probably the first person to take some case studies applying protocol which include things like improving sleep, improving stress, nutritional supplementation, maybe some targeted nutritional ketosis. And actually seeing reverse, sort of cognitive decline reversal of symptoms of Alzheimer's disease.
Christopher: Changes in hippocampal volume in MRI.
Tommy: Yeah. So people going from having very -- So, the hippocampus is generally considered to be the area which controls memory production and you see people who have huge hippocampus, all of that hippocampus is essentially disintegrated over time. They gloss that mass. And then when they've done the protocol they gained it all back essentially. They've re-grown their brain, which we sort of only appreciated in the last few years how possible that was.
Christopher: Yeah. No one believes him that it's even possible. It'd be absolutely amazing. He's using blood chemistry. He's using genetic data. He's looking for mold and other biotoxins. He's looking for heavy metal exposure. He has some software that he calls Recode which I think is extremely interesting, that takes all this data from the testing and then provides a report. I would describe this software as performing a dimensionality reduction.
So, it's very difficult to keep hundreds of biomarkers in your head at once. And he reduces all of that data down to about five things that pretty much anybody can keep in their head at once, which is very, very interesting. I think it's only going to get better. My main objective for coming here was to connect with him. I want to be part of what he's doing and I want to have his attention and be able to ask him questions. So, yes, super exciting times.
I just spoke to Dale and he agreed to do a podcast interview with me. In the future, we'll go into more detail on the protocol. If you've got any questions for Dale, do send to me ahead of time and I'll have those prepared ready for that podcast. Over to you really. I mean, what does oxaloacetate do? You can get it as a nutritional supplement. Why would I want to take it?
Tommy: So, I guess, it's worth taking a step back here. We've talked quite a bit about oxaloacetate, you and I, sort of in our background workings of the things that we do. It kind of comes up fairly frequently as a nutritional supplement and, I think, most recently, it came up during the Keto Summit. One of the speakers on the Keto Summit mentioned using oxaloacetate and, I think, there's one very specific brand that's sold that's supposed to increase anti-aging, something.
They're giving that to athletes to try and improve ketosis and improve performance especially when in ketosis or when increasing ketone production, I think was the phrase that was used. You are contacted by Dr. Keith Runyon, who you've had on the podcast very recently, and he was like, "Well, that's nonsense because what oxaloacetate does is it's in the mitochondria. It binds to the acetyl CoA and then that continues in the citric acid cycle in the Krebs cycle.
And when the acetyl CoA level drops then actually your ketones drop because you're not using that acetyl CoA to then make ketone bodies. And he's absolutely correct. When somebody is saying, "I'm giving somebody oxaloacetate to increase ketone production," those two just doesn't make sense. That's not how oxaloacetate works. And when you actually look at what's being reported or what's out there and people saying sort of like anti-aging, increasing longevity, mitochondrial function, there's loads of really interesting stuff about oxaloacetate and it's really important particularly for function and performance in athletes, in making at the right time, having it in the right place. It's the way that we use up ketone bodies in the muscles.
But people are just -- I don't think taking it as a supplement is worth anybody's time. I think it's a complete and utter waste of money and, hopefully, we can go through all the different things that people are talking about and I can tell you why I don't think it's worth taking.
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Christopher: Yes. So, let's go over some of these specific claims. The first one is that it gives you some of the advantages of caloric restriction. Perhaps we need to start right there and ask the question: Does caloric restriction provide any benefit in humans?
Tommy: Yeah. And the thing is, we don't really know the answers to that question. Probably the best trial is the CALERIE trial.
Christopher: I will, of course, link to these things. If I mention something that's a noun, then it will be linked in the show notes.
Tommy: They have shown some improvement in health markers in people who are sort of calorie restricted for long periods of time, many, many years. But when people are talking about calorie restriction, they're usually talking about longevity. So, basically, if you calorie restrict you will live longer. And when you do that in most animals in the lab, that does work. That is the case. If you take a mouse eating the standard mouse chow and you make it eat less of that, it will tend to live longer.
The problem is they've done -- If we try to then expand this to humans, you would want to look at higher animal species. So they've done two main primate studies. In one of them, calorie restriction worked. So, when they reduced the calories of one group of monkeys, they lived longer. The problem is those monkeys were essentially eating the monkey version of a standard American diet. So, basically, if you're eating a standard American diet, a western diet, and you just eat less of it, you live longer. I'm not really sure that anybody is going to be surprised by that.
In the other study, they actually had the monkeys eating what's more like a natural monkey diet and then when they -- very timely controlled calorie restriction group, 30% fewer calories. And those guys did not live any longer. When you actually then try and expand this to humans, I do think there's benefit. Periods of fasting, periods of reducing calorie restriction, all of it is part of this sort of hormetic stresses that we know sort of bring us back bigger and stronger in whatever way.
But usually, if you're trying to do some intermittent fasting or some calorie restriction, fasting mimicking diets, a lot of the benefits come after you re-feed. So, there's a period of re-feeding afterwards where things sort of, where you rebuild and you sort of makeup. So, if you did some autophagy, some mitophagy, you broke down some old proteins, some old mitochondria, to rebuild those things and repair for the long term function, actually that requires to re-feed.
And I know Valter Longo, who is big in the sort of fasting world, fasting mimicking diets, sort of the thing that he's championed, he definitely talks about the need to re-feed after doing the period of restriction. You can't just restrict continuously and hope that it's going to make you live longer. I think it sort of reminds me of that famous quote, I think it was Frank Sinatra, which is that: Not smoking, drinking or taking drugs doesn't make you live longer. It just makes it feel longer. I think that's probably going to be the same with calorie restriction.
Christopher: I would refer people to my podcast interview with Todd Becker where I think Todd has a got a really great handle on this whole idea of hormesis. And everybody listening to this podcast who is an athlete is very much familiar with this idea that it's not about the damage that you do in the gym or on the bike or on the pool. It's about the recovery that comes afterwards. It might seem the same with the fasting. It's not really about the fasting. It's about the re-feeding. If you never do the re-feed, if you never do the recovery, then there's almost no point in doing it at all.
Tommy: If you're then talking about the studies that have been done on animals -- So, particularly, most of this had been done in worms, in C elegans, which is like a model species and it's really nice to work with for longevity because they only live for three weeks. So, if you can make them live 30% longer then they live a week longer and that's a study you can do in a really short nice period of time.
So, if you give them oxaloacetate they do live longer. And the reason that happens is because of the way oxaloacetate works in the cells. So, if it goes into the cytocells first, so just in the first sort of main body of the cell, what it does is it combines with NADH. And oxaloacetate takes part in what's called the malate-aspartate shuttle which is basically used to move NADH from the cytocell into the mitochondria. So, it's a way to basically link glycolysis and aerobic metabolism, the Krebs cycle. So, it's a way to kind of -- You can move electrons, reduce NADH from the cytocell and into the mitochondria so they can use them in the Krebs cycle.
And so what happens is that oxaloacetate binds with NADH, creates NAD and then makes malate which then gets moved into the mitochondria. And then people, we talked more and more about NAD, NADH, sort of the ratio between the two, and what happens there is that if you're reducing the amount of NADH and the cytocell is just making NAD, what that does is that activates all the genes what we associate with fasting and aerobic exercise.
So, if you increase NAD relative to NADH then you activate AMPK, you activate things like SIRT1, which then sort of regulate the histones and can regulate gene function and then they sort of promote some of those longevity promoting genes and pathways like FoxO3 and things that sort of are all associated with longevity. So, if you do this in worms then you just squirt oxaloacetate on them then you are in the cytocell causing the shift. You're making the cell think that it's got or you're creating more NAD in the cell and then you're having all those positive triggers. And that's what we've talked about things like nicotinamide riboside.
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We talked about the redox state of the cell in the worm. With oxaloacetate, you can definitely affect that and then it's going to make them live longer. If you then try and do it in mice, I think one of the best studies I saw was basically they took, they called them genetically heterogenous mice, and that's nice because it just means that it's just a bunch of mice. It's not like one specific mouse that's bred to do one specific thing and it doesn't really mean anything in the sort of bigger picture. And then they gave them oxaloacetate and do you know what? They didn't live any longer.
So, when you're then trying to say, well, oxaloacetate mimics caloric restriction and then will increase longevity, there's absolutely no evidence that that happens in mammals at all. And when you're sort of looking at the references on a site that's selling oxaloacetate, what they'll do is they'll say, "Well, oxaloacetate mimics caloric restriction in worms." And then they'll just reference loads of paper about the benefits of caloric restriction. So, they don't actually reference paper showing that oxaloacetate improves anything in humans or in mice or rats because that data just doesn't exist.
Christopher: What about this other quite specific claim and it's one that's very pertinent this weekend is that oxaloacetate maintains healthy neurons and protect your nervous system against the toxic effects of glutamate?
Tommy: This is really interesting thing and it's actually something that I've studied in the labs. When I did my PhD, it was in neuroscience. I was looking at the models of brain injury in rats. One of the key ways that you could create injury, if you have reduction of blood flow to the brain particularly essentially what we call a stroke, then what happens is the brain stop being able to make enough ATP and then sort of this cascade that lots of glutamate, which is an excitatory neurotransmitter gets released into the synapses.
But then also the cells can't then reuptake the glutamate because that also takes ATP. So, this glutamate just hangs out in the synapses and then it causes something excitotoxicity which is basically causes huge influxes of particularly calcium into the cells and then that causes mitochondrial dysfunction and those cells often end up dying. So, glutamate associated with inflammation or changes in blood flow or whatever is very closely linked to a number of neurological diseases both acute and chronic.
So, where oxaloacetate comes into this is in an acute setting, so if you do a model of a stroke and you give oxaloacetate, what's really interesting is that oxaloacetate actually is transaminated with the glutamate and it makes aspartate. So, people will have heard of aspartate transamiase, which you measure on a blood test. It's one of the liver function tests. And so peripherally, if you give oxaloacetate, it actually sort of uses up the glutamate by using the AST enzyme. You just create aspartate instead.
And actually then you remove glutamate in the periphery and you increase the gradient of glutamate from the brain to the periphery and then glutamate comes out of the brain. And so that is actually neuroprotective in the acute setting. I actually did this in my rats. In my model I gave them oxaloacetate for this exact reason. The problem is when you're then talking about chronic problems, so if you're talking about like brain fog, decrease in cognition, yes, glutamate is still potentially involved. But what the body is very good at doing is regulating the peripheral glutamate level.
So, if you give oxaloacetate chronically into an animal or into a human, if you can actually increase the blood level significantly, the liver will just make more glutamate to balance everything out. You can't do that for a long period of time. In the acute setting, it is possible that an infusion of oxaloacetate may be a neuroprotective thing that we can do in the future but if you're trying to take this to improve cognition, I don't think there's any evidence that that's going to be possible.
Christopher: And could you think of any reason that I would want to supplement with oxaloacetate?
Tommy: No. And the main reason is the doses that are given, I think the capsules are 100 milligrams, and in the grand scheme of things, it just doesn't really mean anything. And one thing, when we're talking about the importance of oxaloacetate, that it needs to be there to accept acetyl CoA in the Krebs cycle to make citrate. That's one of the first steps of the Krebs cycle so that you can use up -- So, acetyl CoA is made, it comes from pyruvate in glycolysis. It can come from the breakdown of ketones or it can come down from the beta-oxidation of fats.
So you need that there to accept the acetyl CoA. The problem is that where that oxaloacetate comes from, generally, it doesn't really come from just the recycling of the Krebs cycle. But when the body needs more of it, it just makes more and it comes from pyruvate via an enzyme called pyruvate carboxylase. And, basically, it does a process called anaplerosis. And it's really important when people are doing fasting for long periods of time. The reason, one of the main reasons why they use up some muscle mass or they can make some glucose from the glycerol, from fatty acid from lipid, tissue breaks down, your adipose tissue, you release some of the stored fat, the glycerol back burner, the triglycerides can be turned into glucose.
The reasons why you use both, where you use muscle mass and you use some of that glucose from glycerol is for this process, is to make more oxaloacetate so that you can actually use the acetyl CoA that's coming from the fatty acid tissues so that you can actually run the Krebs cycle. So, it's really important when you're trying to burn fats, say, if you're trying to run on fat, which a lot of people are trying to do.
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You need oxaloacetate there. And so you need either glucose source or you need a protein source just a little bit to basically keep the cycle turning. The easiest way to do that would be just to have like a very, very small amount of protein or have small amount of glucose and then that's just going to go where the body needs it. And so actually taking oxaloacetate doesn't make any difference because the body will make the oxaloacetate if it needs it.
Where people might come into a potential issue is you've got a problem with pyruvate carboxylase which does potentially happen and it's caused by a biotin deficiency which is an opposing cofactor for pyruvate carboxylase. And they're using a really high dose of biotin for some neurological diseases like multiple sclerosis because they think the part of the problem is that, basically, the person can't do the process of anaplerosis so they need to supplement with biotin, which is also important for things like making new fats so that you can make myelin, which is like the coating around neurons which also goes awry in multiple sclerosis.
So, I think there's a possibility that some people might be biotin deficient and then physically can't do the process of anaplerosis but then you just do some kind of proper nutritional supplementation. Biotin is supposed to be largely made by the gut microbiome. So, again, look at the gut, look at rates, fixing the diet. All of that stuff comes in first before you start taking a really expensive pill that isn't going to do anything.
Christopher: Okay. I have to say it's pretty amazing to watch him in action. I've not spent that much time recording podcasts with Tommy in person and it's been quite an experience here at this educational seminar for the last three days. It's all a group of doctors, right? They've all come here to be trained. Every time Tommy opens his mouth, like a small group of people form around him. And the only reason it's not happening now is because we've moved into this extra space away from everyone to record this podcast.
But, yeah, absolutely amazing. I have no idea how you manage to organize all this in your head and then recall it in that fashion. It's quite extraordinary. You, obviously, have some sort of visual mapping thing going on inside of your brain. Okay. So, we should probably go on and talk about the context for a ketogenic diet. And I think I've got some confessing up to do here, maybe some apologizing even, because I think I've not been very clear about the context in which a ketogeic diet is important.
We did the Keto Summit and that's been amazing for us both in our educational development and for us as a business and it's been wonderful here at the Buck Institute. People are recognizing my voice and saying, "Oh, you're the guy from the Keto Summit." It's great. It's all to the good. And there are, obviously, some amazing applications for the ketogenic diet but we've now seen a number of clients that have come to us to do some testing where the context was just all wrong. And the diet really hasn't worked for them. So, do you want to explain some examples of where the context was wrong?
Tommy: Particularly because we work largely with athletes or at least people who are working really hard in a number of different domains, what we tend to see is people coming to us and, again, it's performances dropping off and that could be athletic, it could be sexual, it could be cognitive. And where we're really seeing an issue is people who have switched to a ketogenic diet or low carb diet and they're trying to do some kind of really high intensity high glycolytic sport.
So, cross fitters, obstacle course races, some short distance triathletes or short distance cyclists, there's been all this stuff out there. The fantastic life of guys like Jeff Volek and Steve Phinney and all those sort of low carbohydrate diets for athletes. And then what tends to happen is these guys switch over. And with the demands of the sports that they're doing, obstacle course racing, cross fit, these hugely glycolytic sports, they're basically then trying to completely smash a pathway that they're just not supporting at all. And then what happens when they come to us, they don't have any testosterone, their thyroid are--
Christopher: Single digit testosterone.
Tommy: Like literally no testosterone. All their thyroid markers were in the floor. And then you don't make red blood cells properly so they have like a macrocytosis or their red blood cells are too big. They're anemic.
Christopher: Let's slow down and work through some of this slowly because I think that people will be able to follow along with some stuff that they tested. So, I'm looking at a blood chemistry right now and it's an example of one of these people and I hate to single someone out because there have been many examples. But fasting glucose of 68, hemoglobin A1C of 5.2, fasting insulin was actually un-measurable by the lab. They just said less than one. We don't know. And so, I mean, if I saw those numbers, if I prick my finger in the morning and saw a 68, I'd be like, "Mission accomplished," right?
Tommy: Oh, yeah. And again, if you felt really good and if you're just following your blood glucose, you'd be like, "This is brilliant. I save myself a life of type II diabetes." But then I said you can sort of dig a bit deeper and see what comes up next.
Christopher: Right, yes. So, let's talk about alkaline alkaline phosphatase because I think that's a really, really interesting enzyme that can implicate many, many things. This one is really, really low, like below even the standard reference range which we know can be problematic because most sick people do a test than healthy people do. So, talk about alkaline phosphatase.
Tommy: Yeah. So, it's become this really interesting thing that we talk about a lot. It's a super, super non-specific marker but whenever somebody comes to us and they have a low ALP you know there's something not quite right. And it could be a zinc deficiency and you often -- pretty much everybody working has a zinc deficiency.
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Because in athletes, both, maybe they're not getting enough from the diet and then you also lose a lot in the sweat. And so we're joking out here that we just need to hose down athletes with zinc. And especially that--
Christopher: And magnesium.
Tommy: Yeah.
Christopher: [0:20:15] [Indiscernible] magnesium. Just spray people down with it as they come in.
Tommy: And talking about cognitive decline, a lot of people have an overload of copper relative to their zinc. That's also really important. Some people are the opposite, obviously, so you need to kind of tailor it. So, low zinc, problems with B12, some autoimmune disease. We often see it in people that have like really messed up guts. It's just like when ALP is low, you don't often talk about -- Markers usually, if it's high it's bad. A lot of things we're seeing, if it's really down the other end of even the normal range, you're really starting to see some kind of pathology. So, it's actually really nice but really unspecific marker.
Christopher: Let's talk about thyroid because I think this is really interesting and important. Maybe some people won't know that there is a problem here because the TSH that I'm looking at is 1.5, which is bang on. I'd be super happy with my TSH at 1.5. But then when you look at the hormones that are downstream of TSH like free T3, for example, is 1.9, which is super duper low. So, what's going on here? The brain seems happy with the amount of circulating thyroid hormone and yet it's so low.
Tommy: Yeah. This is really interesting. I think a lot of it ties into both inflammation and cortisol levels. So, in this particular person, from all the testing, they have some overgrowth in the gut that are maybe part of the problem. But particularly with the elevated cortisol levels, and this is somebody who's basically not eating carbohydrates and doing super, super intensive training program and racing program in a glycolytic sport, so then they're basically going to be running on cortisol just to like get up in the morning let alone do anything else.
And what happens is when your cortisol is really high, you might have heard of deiodinase enzymes which are basically the enzymes which convert T4, which is largely made in the thyroid gland, and then convert it into the T3 in the peripheral tissues for use. And when you have really high cortisol levels, something really interesting happens which is that it down regulates the correct deiodinase in the periphery so that you don't get enough T3 floating around in the body but it up regulates the deiodinase in the brain.
So, basically, the brain is seeing enough T3 and thinks thyroid level is fine but the periphery isn't seeing it. Obviously, the periphery is where you want your [0:22:30] [Indiscernible]. So your brain might think I've got plenty of thyroid hormone but the body isn't seeing that. And so, like this guy's reverse T3 is in the normal range, which essentially means that it's elevated relative to his T3 and that's probably because of his action of cortisol and inflammation which then causes a misbalance. So, even though the reverse T3 isn't elevated, because his T3 is so low, he's got this huge imbalance.
Christopher: All right. And I wonder if there's a reinforcing cycle going on here because his cortisol production that we see on the DUTCH is completely normal. The amount of cortisol that's coming out of his adrenal glands is normal. But then we see the elevated free cortisol and free cortisol is the active fraction and that is what's elevated. And it could be that low thyroid function. He's not clearing that cortisol correctly. And then you got this horrible reinforcing cycle.
Tommy: Yeah. So, if you're not eating enough, you could probably even drop your thyroid a little bit initially and then, absolutely like you said, you get that reinforcing function, reinforcing like cycle in it especially if things, as the thyroid drops and cortisol doesn't clear properly. And we know that in people who are hypothyroid they don't clear their cortisols well and then the free cortisol goes up and then you have kind of knock on effect of again not making enough T3.
Christopher: And then what about lipids? It looks like we might be seeing a knock on effect here from the thyroid function on lipids. So, total cholesterol is 267. So, not crazy, crazy high, not the highest I've ever seen by quite a stretch. But the LDL is 169. That's getting up there to where people would be concerned, I think. Can you explain what you think about that and what the connections might be?
Tommy: I mean, it's difficult to say exactly and sort of -- I mean, the traditional levels of an LDL of 100 or some people may go even lower and total cholesterol under 200 or something like that, probably not that relevant. People are doing more and more advanced lipid testing. I don't think that's something that this person needs to do. They're otherwise fit and healthy if we sort of fix the other things that are going on.
But thyroid is really, really important for the expression of the LDL receptors. If you're trying to take LDL cholesterol up into cells and that's also going, to an extent, become important when you're trying to take up cholesterol into cells to make sex hormones. If you are hypothyroid, you're not going to make the LDL receptor. It's not going to be on the cells. So, take up the LDL and then instead it's just going to increase the LDL circulating around the blood. There's been a nice number of studies showing that people of sub-clinically hypothyroids, so their TSH is elevated but they wouldn't be diagnosed with real hypothyroidism.
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But even in those people, if you give them thyroid hormone, you dramatically reduce their risk of cardiovascular disease. Maybe the LDL is just along for the ride. It's actually because you just fixed their thyroid.
Christopher: Interesting. Interesting. And then we're also seeing some weirdness with red blood cell production. So, total hemoglobin is going to be quite predictive of exercise performance in all but the most anaerobic of sports, I would say. I think that's a fair comment, isn't it? We're always interested in hemoglobin. What can we do? Can we fix a nutrient deficiency? Can we fix thyroid function? What can we do to increase the production of hemoglobin? And here we're seeing abnormally large red blood cells. So, can you explain what that means?
Tommy: It's what we call -- And we often work within a tighter range of what people might use. So, maybe you want to be -- So, an MCV is the mean corpuscular volume which is basically the average volume of your red blood cells. And maybe you work within the range of 80 to 90, maybe a little bit outside that. This guy's is over 100. And again, depending on the lab that might just sneak inside the normal range, but probably not.
And what it means particularly when you have very large red blood cells is that you haven't been able to properly deconstruct the DNA or the nucleus that's inside the red blood cell which is kind of ejected while the red blood cell is maturing because they don't normally have those. So then those cells stay abnormally large.
And you tend to often think about macrocytosis we call it in people who have B12 or folate deficient because that's really, really important for proper handling of DNA. But you also see it in people who drink a lot of alcohol and in people who are hypothyroid. So, in this guy, we know that his thyroid, a lot of his thyroid hormones are basically in his boots. And so that's probably the cause for the high MCV.
Christopher: I'd say this guy is going to be awesome when he eats some carbs.
Tommy: Amazing. So, this is the problem. Some of the other things we see just like general anemia, so just not making enough red blood cells, and that's because testosterone is really important for that. So, that's just somebody who has very, very low levels of testosterone. I mean, there are some other things that we need to fix but in reality this guy is just not eating a diet that's geared to his training and lifestyle. This guy should actually eat some carbs.
We work with some people who have been told how carbs are evil, everybody needs to be on a ketogenic diet, ketogenic diet is the key to long life and long health. In some cases, that's absolutely true. But there is no evidence to suggest that every person needs to be on a ketogenic diet or they all benefit everybody. Some of these people, actually, you just add back carbs and it's like you've turned the light back. You switch the lights back on.
This is sort of happening more and more. There are so many good people out there in the health world but they all have a different context. So, when you're listening to one person talk about low carbohydrate diets and you listen to the next person talk about fasting and you listen to the next person talk about protein restriction, people who are listening to this podcast, out in the real world, they're taking all this information in. A lot of these people have more time to read more papers and listen to more podcasts--
Christopher: This is great. I love it.
Tommy: It's brilliant. And you talk to these people, they know as much as you do. It's just like -- it's more like a meeting of minds rather than just like--
Christopher: Yeah. [0:28:09] [Indiscernible].
Tommy: Yeah, exactly. So, we get to talk to these people, it's absolutely awesome. But the problem is when you do all of those things at the same time, so restrict carbs and you're doing intermittent fasting and then you restrict protein and then you try and race obstacle course races, it just does not work. At some point you just need to accept that you need to fuel for the performance that you want. And that's going to include eating some carbohydrates. There are a lot of people, othorexic podcast hosts out there telling obstacle racers to eat only 50 to 100 grams of carbs a day. And I just disagree with that completely. The entire--
Christopher: What would you say then is the reasonable amount then? For a guy my size, 70 kilos-ish, doing obstacle course racing, how many carbs?
Tommy: I could easily you 150, 200, 200 grams of carbohydrates.
Christopher: Which is really nothing compared to what I was throwing back in the day. Like 2011, I was probably doing between 600-800 or something like that, I would say.
Tommy: Yeah. And sort of the average diet, you look at some -- There's some studies of the Paleo diet and people with type II diabetes and in the control or in the Paleo arms, or people trying to improve people's health with, type II diabetes with a Paleo diet, they give them 400 grams of carbs a day. And that's just like a completely normal amount. So, when you're talking about somebody who's super active, super glycolytic, working really hard, telling them to eat 300 grams of carbs a day just isn't that bad a thing.
And again, if you want to try and balance the effect of improved health with performance, there's going to potentially be a tradeoff. So, if you are a person who's doing Ironman, who's doing ultra marathons, who's running an obstacle course race every weekend, that's not necessarily going to dramatically improve your health. But if it's something that you enjoy and something that you want to do, you just have to appreciate that there's a bit of a tradeoff. You just need to sort of bring everything together and make sure that everything you're doing is sort of geared to the goals that you have at that particular time.
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Christopher: Do you like my business model there? Did you see how it works? You talk about ketosis on the podcast, you do the Keto Summit, you get hundreds of thousands, literally 100,000 people a month listening to this podcast now. So, thank you so much to all the people that have shared this content. I really appreciate you. So, people then decide that this ketogenic diet is the diet for them, myself included. And then you get completely broken by it. And then you come back to me and I fix you and say don't eat the diet and then you go away again, you listen to the podcast and then you get back on the diet.
I have actually been eating some carbs for the last month, like a normal amount of carbs, not 150 grams a day. I have to say that I do not feel as good as I do when I'm in ketosis. I understand why people want to eat the diet. My afternoon concentration is not nearly as good and it's not bad but it's just not as razor sharp as it is when I've got one millimole of ketones or something.
Tommy: The thing is that -- So, a lot of people can find the way -- And sort of the ketogenic diet works for them long term. That's absolutely great. But it's that kind of -- We do talk about the fact that it is that kind of fasting or starving physiology is meant to make you mentally sharp so that you can go out and get some food. And, yes, periods of ketosis, absolutely great, but I think for most people there's always going to be a benefit from occasionally re-feeding especially if you are then trying to do some specific kind of sport. If you're focused purely on longevity, maybe you don't need to do that. But particularly for athletes, I think that can become just really important.
Christopher: Okay. So, we're saying that highly glycolytic, say, obstacle racer, cross fit, maybe a few other sports, you could probably figure them out. When are the right times to do a ketogenic diet? What are the applications that you've seen that you think right? If that happened to me, I'm in, I'm measuring ketones.
Tommy: Yeah. So, the two main ones are going to be cancer, particularly brain cancer.
Christopher: And, of course, I talked with Adrienne Scheck recently in the podcast. I'll link to it. You should definitely listen to that interview. That was a good one.
Tommy: And some of the guys like Dom D'Agostino doing very similar research. And then probably any neurological disease. I've done a lot of work in multiple sclerosis. If I got diagnosed with multiple sclerosis, I'd probably move towards a ketogenic diet, maybe some other neurological diseases. We talked about Alzheimer's, periods of ketosis. Maybe somebody who's an ApoE4 homozygous. They need to be in ketosis continually. That's a discussion that we've had here.
If there's any of those scenarios, I think a therapeutic ketogenic diet is absolutely where I would go personally. Other than that, if we're talking about trying to sort of build a lifestyle that's more in tune with our evolution then I think you could definitely get to a point where you're eating carbohydrates in longer light cycles and not eating carbohydrates when it's dark. So, most of my family came from northern Europe, so we would have some excess of the carbs in the summer and in the winter we would have eaten probably what would have amounted to a ketogenic diet. If you're trying to tailor your diet to both your physiology and your latitude, then I think something like that may be the thing that you need to go to.
Christopher: Yeah. It's a really good idea. Think about where you're from. The closer you are to the equator the more likely you are to do well on a carbohydrate based diet.
Tommy: Because that's what you have access to.
Christopher: And I've noticed -- So, we were talking about this earlier. My wife, we looked up her hereditary using the 23andMe test and she's Siberian with a little bit of Hungarian. And she just does great on a keto diet and she loves it presumably because it feels so good. I've never really talked about it in depth which is kind of we're -- We have a three year old daughter and she's still breastfeeding and I've always been encouraging her to eat some carbs. Why don't you talk about that a little bit? I'm sure most people won't know this, why you should eat carbohydrates while you're breastfeeding?
Tommy: Yeah. And I don't think that that means you need to go like down the whole huge doses of refined carbohydrate. That's not what [0:33:30] [Indiscernible]. We're just talking about like, "I'm back on the Coca Cola." Just like including some sweet potatoes or rice or whatever your sort of favorite carbohydrate, whole food carbohydrate sources. But there's some really interesting data and it's in kind of both -- So, there's cultured cells from humans so basically breast epithelial tissues.
Basically, these epithelial cells which basically line the dots of the breast and they're the ones that secrete and produce most of the breast milk. And when you have a newborn baby, you want them to be in ketosis, in fact. That is what helped us develop the brains that we have is the fact that we can go into ketosis and so we do so well in ketosis. And we can do that during the first period of life where we're basically useless lumps with a huge metabolic demand in the brain. You need the ketones to--
Christopher: Right. So, huge brains small body.
Tommy: Yeah. And just completely -- I mean, you're just the lump. And there aren't many animals wherein that's the case.
Christopher: No. You're still a fetus when you're born.
Tommy: Exactly. So, that's really important. But the way that you achieve ketosis in large part is due to MCTs, again, medium chain triglycerides, produced in the breast milk. And the way that that happens is those MCTs are directly synthesized from blood glucose. So, you can actually run glucose across these cells and then make MCTs. That's what they're designed to do. And that's so that you're baby can get into ketosis during breastfeeding.
Pediatricians and neonatologists know this. They put MCTs into various types of formula particularly with premature babies. They give them to them because they know it's a really important source of energy for babies. What happens is that if you don't have that source of glucose then you don't necessarily make those MCTs.
[0:35:03]
And this happens both in rats. So, I've read studies about the production of breast milk in rats. And it also seems to happen in humans. When I was doing my PhD, I basically had a theory which was if I can somehow increase the amount of MCTs in the breast milk then maybe that will reduce the brain injury in the young rats. Seeing these rats already eat basically 100% carbohydrate based diet, you can't really increase the glucose trying to increase MCT production so I kind of went the other way.
And thought if I basically feed the moms mainly MCT -- So, when you eat a low carb diet and you're breastfeeding then what happens is the fat content of the milk will closely represent the fats in the diet. Because you then start using some of the fatty acids from the diet going to the breast milk because you [0:35:44] [Indiscernible] your own in the breast tissue. So, I kind of thought, well, if I mainly feed the moms MCTs then maybe some of those MCTs will end up in the breast milk and then you end up more MCTs and then you're sort of ketosis.
And the reason I did that is because we tried some various things giving other ways of increasing ketosis in the [0:35:57] [Indiscernible] that didn't really work so well. And this was just kind of like some pilot project on the side of what my main PhD just because I was interested in it. And what happened was that I made like this really high ketogenic diets for rats and the moms loved it and they went into really, really deep ketosis. So, I tested the blood ketones. It was like five, six millimolar.
But then when I tested the young rats, the pups, the ones whose moms weren't on a ketogenic diet had lower levels of ketones because the moms weren't making these MCTs because they didn't have a source of glucose. The livers of the moms were just converting all of that low glucose into ketones themselves and that wasn't ending up in the breast milk. It was increasing ketones in the pups. And those guys were then, if you did like a model of brain injury, those guys actually worse than the moms who were eating 100% carbohydrate diet.
I'm really, really wary about extrapolating stuff like which, some stuff which I just did out of interest in the lab with rats to humans. But if you look at the physiology and then you look at the effects there and what's going on, I do kind of worry about people on a ketogenic diet breastfeeding. And I'm not saying that it doesn't work and I'm sure there plenty of people and we know people have done it and it's--
Christopher: Maybe you're managing some other situations that's worse, right? You've got refractory epilepsy or cancer even.
Tommy: Absolutely. And then you absolutely, you got to do the balance. But I don't see any harm in somebody who's breastfeeding particularly because you need to intake a lot of calories to cover the calorie -- Producing breast milk is very energy intensive. So, including some carbohydrates in your diet. Again, it could be Paleo diet, whole food diet, whatever. I just think if I have kids and that is definitely the road that I go down just having looked that kind of level of the physiology and what happens and what you need to do in order to increase the ketones in your baby, which is sort of the end goal of that whole thing.
Christopher: So, in summary, mommy's carbohydrates, those carbohydrates are used to synthesize MCTs in the breast tissue that then gets into the milk, goes to baby, baby uses the MCT to make ketones as fuel for the brain.
Tommy: Yeah. Absolutely.
Christopher: So, mom needs the carbohydrates in that situation.
Tommy: Yeah. But again, we're not talking the huge, huge amounts. We're just saying just fuel for the activity that you're doing and in that case the activity you're doing is breastfeeding and then you might need some carbs for it.
Christopher: Okay. I think that's a nice place to wrap this one up. It's been a bit of a head spin. You might have to re-listen to this one again and then turn the speed down to 1x so that you can follow what Tommy is saying. Well, this has been great. Thank you so much, Tommy. I really appreciate you as always.
Tommy: It's been awesome. Thanks.
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