June 13, 2019
[00:01:16] About this Podcast and Sponsors
[00:05:18] Guest Introduction
[00:09:26] What makes each DNA test different and how to choose what's right for you
[00:14:44] Characteristics of A Proper DNA Test
[00:20:02] A review of my DNA test and how it compares to my two sons
[00:23:49] Vascular Function
[00:35:06] Podcast Sponsors
[00:38:42] cont. Vascular Function: Increase good quality vegetable matter
[00:43:30] What happens when someone doesn't have 2 copies of a gene?
[00:45:49] 3 Vitally Important GST Genes and Continuation of My DNA Review
[00:57:23] Personalizing Diet And/or Supplements Based on DNA Test Results
[01:18:23] Differences Between the Hormone Pulse Report and The Genome Pulse Report
[01:28:49] About the ACTN3 Gene and Its Relation to Exercise Types
[01:32:52] The Functional Genomics Test Package
[01:36:09] Closing the Podcast
[01:38:35] End of Podcast
Mansoor: The human body does not work based on individual genes beating to their own rhythm. The human body works on an awesome orchestral masterpiece of many genes working in cascades to get the various cellular functions done. Are there any genetic underlining contributors? How resistant are the cells that line the blood vessels? Is there such a thing? And when you look at it, there is such a thing.
Ben: I have a master's degree in physiology, biomechanics, and human nutrition. I've spent the past two decades competing in some of the most masochistic events on the planet from SEALFit Kokoro, Spartan Agoge, and the world's toughest mudder, the 13 Ironman triathlons, brutal bow hunts, adventure races, spearfishing, plant foraging, free diving, bodybuilding and beyond. I combine this intense time in the trenches with a blend of ancestral wisdom and modern science, search the globe for the world's top experts in performance, fat loss, recovery, hormones, brain, beauty, and brawn to deliver you this podcast. Everything you need to know to live an adventurous, joyful, and fulfilling life. My name is Ben Greenfield. Enjoy the ride.
DNA, the magical building blocks that unite all humans. We're going to talk about them on today's show, not humans but–well, we're not going to talk about humans, but we're going to talk about DNA in a very, very profound and deep way. My guest on today's show is a super smart doc in genetics.
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Another thing I wanted to tell you about was that something that helps out this show quite a bit is for you to leave an iTunes review. So, if you enjoy this show, go leave us a quick review in Apple podcasts, or really anywhere where you tend to digest your podcast, and that helps out the show quite a bit. Some of you have been asking me about how you can get access to episodes that are eight years old, ten years old, et cetera, because this podcast has been around now for, going on around 12 years. You can download the Ben Greenfield Fitness Podcast app in the App Store for Android, or for Apple, if you just search for Ben Greenfield Fitness, there's an actual app that's just jam-packed with all of the podcasts. And it's just like a podcast player. It's pretty handy. So, if you weren't aware of that, check that out and also leave a quick review on iTunes.
You know, I'm constantly blown away by the amount of genetic data and actionable information you can get from a freaking little bit of your saliva. And what I wanted to do for today's podcast was give you an insider glimpse using some of my own genetic data, as well as a conversation with one of the guys who I think is probably on the most cutting edge of genetic testing and genetic interpretation to teach you how this goes way beyond what you might get from like the 23andMe. Your pee might smell like asparagus, or you have a high risk of a unibrow, or like the ancestry information that might show that you're a mix of, whatever, Sub-Saharan African and Southeast Asian and Northern European.
And a lot of that stuff can be useful, but to get really, really useful information on things that can help you out with your sleep, your gut function, your neurotransmitters, even your life span or your brain health, you have to take a deeper dive. You have to look at a lot more of these so-called SNPs. And that's what my guest on today's podcast specializes in. His name is Dr. Mansoor Mohammed. And he has a very impressive background in the field of genetics. He, not only studied genetics at a university level, as well as doing post-doctoral studies in Cytogenetics. He's the president of a company called the DNA Company, which does functional genomic testing and consulting, and even does like individualized supplementation programs based on your genetic profile.
But he's also widely regarded as a pioneer in the field of medical genomics. He was the Founder and President of a company called ManaGene. He was the CEO of Combimatrix, which was a Nasdaq traded company in diagnostic genomic microarrays. He was the Director of Genomics at Quest Diagnostics, which you may have heard of before. That's the world's largest reference laboratory. He has a market capitalization I think of over $10 billion, and he was their Director of Genomics there. He was also the Director of Research at Spectral Genomics, which was one of the industry's first commercial genomic microarray developers. He's done a lot and he's probably seen more freaking gene reports than just about anybody I know.
So, Dr. Mansoor, welcome to the show, man.
Mansoor: It's an honor, Ben. Thanks for having me.
Ben: Yeah. And you're up in Canada, right?
Mansoor: Yes, we are. And don't rub it in, but yes, we are.
Ben: Which area are you in over there?
Mansoor: Toronto. So, more East Coast. Toronto, but honestly speaking, I wouldn't trade it for anything else. I do miss the sun, but it's an awesome city, awesome research, awesome people.
Ben: Yeah. One of my buddies has a restaurant over in Toronto. It's supposed to be amazing. I was supposed to go there last time, but I wound up going over to that controversial meat restaurant where the guy carved the deer in the window in front of a bunch of protesting vegans. I forget the name of the guy. I went there with my friend Ben Pakulski, who's like a former bodybuilder, and we just punished a huge amount of meat. I forget the–it's like this big carnivore restaurant. The guy was on the Joe Rogan Show. I'll remember the name of it here in a second. Yeah, it's like this controversial meat restaurant in Toronto. Antler, Antler Kitchen and Bar. Have you heard of that one?
Mansoor: No, I've not. Honestly, Ben, I don't get out too much when it comes to restaurants here.
Ben: Okay. But the other one is owned by one of my buddies, Alon Ozery, and it's called Parallel Brothers. And apparently, they do a bunch of like molecular gastronomy and a bunch of super, super healthy tasty foods. That one's on my bucket list, too.
Ben: There you have it. As long as, based on our discussion today, my genes allow me to go there. I don't know. I'm going to find out. So, we'll dive into that. You guys do some very interesting tests at the DNA Company. And I'm curious, just first of all, why is it that one test might vary from company to company? Why is 23andMe different from, say, maybe Ancestry, different from, say, You? How do we interpret the difference between all these different genetic tests?
Mansoor: Excellent question. So, most folks, when we think of genetic testing, we think of SNPs, these things that you referred to earlier, single-nucleotide polymorphisms. And SNPs definitely are some of the most important contributors to a person's genetic variation. So, number one, yes, we need to test SNPs. However, SNPs aren't the only variability to the human genome. There are other genetic phenomena, things like copy number variation, CNVs, where it's not about what we'd call spelling differences, which is the analogy of SNPs, but copy number variations are where whole paragraphs of your genomic manual can be missing or duplicated.
So, that's another major one. So, when you think of looking at a genetic test, that's going to give you the fullness of variability, important variability, something that we'll probably talk about later in the podcast, which is what type of variability are we really looking for, as you noted earlier? Do we really want to find out that we've got a unibrow? I'd say, “Go look in the mirror if you want to find out if you've got a unibrow.” Right?
So, SNPs, we need to look at that. We need to look at CNVs. We need to look at INDELs. If it's not the whole paragraph that is missing by that analogy, parts of the paragraph might be missing. So, to summarize, when a person, when a consumer wants to consider a genetic test that is meaningful, they need to understand that the variations that impact the genome are beyond SNPs. SNPs are important, but you got to look at these other phenomena. Okay. That's the first thing. The second thing is–and it gets a bit of technical detail. So, what we're going to understand is how do labs go about testing SNPs. Let's just stick with the SNPs for the time being. You see, your genes can be looked at, let's say your genes or the individual instructions, the individual paragraphs in your operating manual. Okay. And within that paragraph, we all have or we all should have two copies of any given paragraph because of course, the miracle, the awesome miracle of the human genome is that it is diploid. We have two copies of the operating manual.
When you think of any cool piece of gadgetry that you buy, you're only expecting to get one manual with it. You're not going to expect to have two almost identical copies of the manual. Yet with the human being, we've got two almost identical copies of the human manual. So, at any given time, any paragraph, any discreet instruction, any discreet gene that is going to be expressed, the body, the cell is going to take a look at those two copies of the gene, one from mom, one from dad, and make a determination as to which of the two copies your cell is going to express. And there are some basic phenomena that defines, are you going to express mom's copy of the gene, dad's copy of the gene? Are you going to express both of them and have a hybrid outcome? No. Of course SNPs come into play, and that there are these spelling variations in the two copies, the two paragraphs. Okay.
Well, when we go about testing for SNPs at the laboratory level, what we're doing is we've got to find a way to “read” the paragraphs and look for these variations. What differs at the laboratory level is how many paragraphs is a test designed to query simultaneously? You see, some tests, the tests that we–for example, the DNA Company that we designed, we look at fewer paragraphs at any given point in time because why? The more paragraphs that you simultaneously try to query, simultaneously try to look for these spelling errors, the greater risks there is that one paragraph starts to look like another. And we can get some crosstalk, we can get some false information, we can get some false negatives, false positives in regard to the SNP that we're looking for.
So, now to summarize, the technology for determining and detecting these spelling differences, these SNPs is amazing across the board. Really, SNPs now, there are machineries that you can buy. You can run this in your garage if you really wanted to, and you can be pretty confident in the results you're getting. That's not the issue. The issue here, Ben, is the design of the test. How many genes are you looking at simultaneously? How many paragraphs in this 22,000 gene manual are you attempting to query simultaneously? Keeping in mind that the more that you query simultaneously, there is a greater chance of error.
So, I think that's where it comes in. It comes into the design of the test, the size of what you're looking for, not to say anything as the functional relevance of what you're looking for that. We'll talk about that later on maybe. And then of course, are you looking at just spelling errors? Are you looking at deletion errors? Are you looking at grammatical errors? These are the type of things that influence one test being different from another?
Ben: So, when you say query simultaneously, do you mean, for example, if you're looking at one specific gene rather than interpreting that gene in isolation, actually interpreting it in terms of how it might interact with the other genes?
Mansoor: My query here, we were speaking at the initial physical DNA platform, the PCR platform of that gene. When you refer to query as per interpretation, that comes later. What I was referring to, as you see, there's an actual molecular reaction. Think of a test tube. Think of that test tube having your DNA, your DNA sample. And all I'm going to do in that one test tube is I'm going to go in using a technology that will find one gene, one predetermined gene, and I'm going to ask, are there any variations in that one predetermined gene in your entire manual? Versus that, I can take a test tube with your DNA, all of your DNA, and in parallel, I can run a query, I can determine the sequence and the presence of variations, not in just one gene, I can do it for five genes simultaneously, 20 genes simultaneously.
That's what I was referring to. And the more the number of genes you try to scan looking for variations simultaneously, which of course depends on the platform that you're using, that's where you start to enter the risk of false positive or false negative results. That's at the level of what I referred to as querying at the actual platform level. And then later on, depending on the genes that you studied, then what you referred to becomes even more important. Which genes did you study? What is the impact of these genes, and how do they interact, and how do they determine each other's expression, each other's outcome? So, they are two completely different phenomena.
Ben: Okay. Got it. So, after you've gotten your hands on the saliva and you've done this simultaneous querying of the genes, what occurs next?
Mansoor: So, at that point, you now need to curate. You need to say–and this is the logic flow that should happen. Whether it happens in every test or not, obviously, that's not a comment that I'll make. What should happen is this. You should go into a test. And now we get a little into designing a test. At the end of the day, what are we doing this genetic testing for, Ben? Because really, physiologically, we almost don't care about genes. It's a pretty bold statement because physiologically, what do we want to determine? We want to determine are those cells working? What is the outcome? What is the manifestation in the person? That's ultimately all we care about.
Now, obviously, cellular function, the person that you're dealing with, their deficiencies, optimum abilities, as the case might be, do harken back to their particular version of genes. So, when you design a test, a really well-designed test should be one that says, “What is the cellular function that I'm going to be studying? Well, what is that pathway?” Because the human body does not work based on individual genes beating to their own rhythm. The human body works on an awesome orchestral masterpiece of many genes working in cascades to get the various cellular functions done.
So, when you design a good test, what you should really be designing is this. You should say, “What is the cellular function? What is the pathway? What is that system in the body that I want to study?” Let's map that out independent of genetics. Let's just say, “What are the things that influence vascular endothelial function, for example, huge contributor to vascular and cardiovascular disease? What are the mechanisms? What are the cellular processes that keep the lining of our blood vessels healthy or not? We put that on a white board. Nothing to do with genetics. We map out the players, we map out the cellular processes, and then we begin to pencil in the genes that influence the ultimate outcome.
Now, what comes out of that, when and if you approach your genetic testing this way, is the genes that you test for, per that design that we just discussed, those results now tell a story. So, when you ask me the question, “Well, what do you do when you've gotten your DNA from your saliva and you've tested it?” The answer to your question is, what did you ask of the DNA in the first place? Did you ask of the DNA intelligent questions, meaning, intelligent, judicious choice of genes? Or did you just have a shotgun approach and just say, “Let's go query 500 genes and see what comes out of it”? This then, Ben, becomes a major differentiator in the test and in the results that you're going to get when you choose a lab.
Ben: So, you're not looking at just say one SNP that says, “Well, you have, whatever, a 20% increased risk of cardiovascular disease.” You're looking at multiple SNPs that affect the entire cascade of events that could influence risk for cardiovascular disease.
Mansoor: Exactly. And you're doing it, you're taking that cascade in a meaningful–that the total is greater than the sum of the parts. Are you open, Ben, to jump into some of your results so that we can take this very point and highlight something?
Ben: Yeah. I think that using actual results and examples will help people wrap their heads around this a little better. So, let's do that. And by the way, what I'll do, I've got the shownotes all available for people at BenGreenfieldFitness.com/dnapodcast. That's BenGreenfieldFitness.com/dnapodcast. If you go over there, you can, if you want to, pull up my own DNA results. Unless you're an insurance company or you're an employer, in which case, keep your dirty, dirty hands off of my results. But other than that, you can go grab my results and follow along if you want to see what natural results printout looks like from the DNA Company and some of the stuff that Mansoor and I are going to talk about today.
So, yeah, that being said, go ahead and jump in wherever you want to jump in, doc.
Mansoor: And Ben, are you comfortable with your two little angels? I mean, I guess they're not quite little anymore, but River and Terran, are you comfortable with us doing any compare and contrast between you and them?
Ben: Yeah, yeah, yeah, for sure, because you've tested both me and my boys. So, absolutely.
Mansoor: Yeah, absolutely. And they're definitely daddy's boys. So, let's do this. Let's just step back for a moment and say, “Okay. I want to design something that would be informative about the cardiovascular function, the players, the contributors, to overall cardiovascular health of an individual.” And so often you know, we'll see a report that has meaningful genetic information, but it comes with this gene gives you a 30% increased risk of cardiovascular disease, this gene gives you a 40% increased risk of Afib or something else, cardiovascularly irrelevant.
Now, what in the world does that mean in any event? If I told you a gene result confers a 30% increased risk of cardiovascular disease, what does that actually mean to you? How do you process that? Does it mean that if you live three lifetimes, at least one of those lifetimes, you'd have a cardiovascular event? Does it mean that if I put you amongst 100 people, you would be in the top 30? What does it mean when I tell you a gene confers a gene, one gene confers some percent risk of something?
When you really take a look at it functionally, it has very little meaning until you understand what is that gene doing, what is the variation in that gene that is perturbating the responsibility, the job of the gene. So, now, let's just step back. Intelligent genetic testing should start, as we said, with looking at the overall function, penciling in the genes that are the players. And every time you're penciling the gene in your test, you should be asking, is the function of this gene known? What does it contribute to in the cellular cascade? Where is it playing? Number one. Number two, do we know that? Do we know that that function is well-established in human studies that it has the same function across multiple ethnicities?
A major point of misinformation that is out there, so many genes, Ben, with a particular job that is to be done by that gene, a version of that gene, what we would call an allele, a particular version of the SNP, but that might be defining the allele of that gene, can have one outcome in one ethnicity. And the same version of that gene can have a diametrically opposite outcome in a different ethnicity. So, just putting that, we'll come back and we'll stitch together these important points, but I want to start highlighting where people have been, when we take an overly simplistic view of genetic analysis, how misleading the end outcome can be?
Okay. So, we come back now and we take a look at cardiovascular disease. And what we want to be able to do is this. We want to say, “Which genes contribute to that vascular function? Do we know what the job of the gene is? Do we know that if there is a variation in that gene, a SNP, an INDEL, a CNV, as per all of the three things we spoke of earlier, will that variation truly impact the job that that gene was supposed to do?” Which brings us to another point. Because there is a variation in the gene, it doesn't mean that that variation necessarily impacts the function of the gene. So, testing for every variation without knowing whether the variation actually has a meaningful outcome, a meaningful change to the operation of the cell, is really just data for data's sake without any real functional outcome. Again, all of these little points, we've got to be cognizant of.
Let's go back to cardiovascular function. Here's an example of what we call a storyboard, and I'm going to quickly now summarize the Ben Greenfield storyboard for cardiovascular.
Ben: And by the way, I got two different reports from you, guys. I got this one called the genome pulse report, and then I got one called the hormone pulse report. Which one are we looking at right now?
Mansoor: We're looking at the genome pulse report for the time being.
Ben: Okay, okay.
Mansoor: Okay. But by the way, a person's hormonal status of which–Ben, forgive me, but you've got the genes of the gods as they say. So, everyone out there, yes, it's true. Ben's hormonal steroidal, how Ben Greenfield makes and processes his progesterone, his testosterone, his DHT, dihydrotestosterone is just about perfect.
Ben: Oh, gosh. Thanks.
Mansoor: So, yeah, Ben, yeah. No, it really is, and I'm not trying to be facetious. It really is. And we'll talk about that later. But let's focus in the genome pulse for the time being, and here's what the storyboard looks like.
Ben: Hold on. I'm going to grab a beer because apparently, I can get away with that. So, you keep talking, I'll be right back.
Mansoor: So, here's how it goes. Vascular function. When we talk about vascular function, we're talking about how are those blood vessels living up to and withstanding the wear and tear of every living, breathing, waking, sleeping moments of our life. Let's take a look at the vasculature and what are the cells that are getting the most punishment, so to speak, the cells that line the vasculature known as the vascular endothelium. Those are the cells that line the inside of the blood vessels.
Now, why are those cells important? Because think about it. At every given moment in time, those lining cells are subjected to whatever is dissolved in your blood. And by dissolved in your blood, we mean literally, when you swung your left foot or right foot off the bed this morning when you got up, whichever side of the bed that you're on, the quality that which is present in your blood, vis-à-vis metabolites, vis-à-vis toxins, vis-à-vis whatever it might be, is different first thing in the morning than after you've had a breakfast, after you've hit the big city, after you've sat in an hour's traffic, because after later in the day, your blood represents all of the things that were either through dietary intake, through breathing, through touching things. All of these things enter into your bloodstream.
And to the degree that the things in the bloodstream are inflammatory, they've got inflammatory properties, those pole endothelial cells, the pole cells that line the blood vessels are taking a pounding. So, one of the first things we need to ask from this what we call genomic storyboarding, from this intelligent approach is we're going to simply say, “Hey, listen. Are there any genetic underlining contributors to the resilience? How resistant or how sensitive is the corollary? Are the cells that line the blood vessel, is there such a thing? And when we look at it there is such a thing. Some amazing research over the last 20 plus years have shown that there are a couple of genetic markers on Chromosome 9. They're known as the 9p21 markers.
Okay. Now, notice I said markers and not genes. These aren't quite genes. Their DNA sequences within which there are these markers that have been found to be correlated to how resilient is the lining of your blood vessel. I like to call this your Teflon coating index. See, we want the lining of our blood vessels to be Teflon coated. We want it to be non-stick. We want it to be resilient. Except some of us are born with a Teflon coating that is–we might call it the [00:28:30] ______ version of the Teflon coated frying pan. Some of us are born with the Williams Sonoma Teflon coated frying pan. We've got a really resilient lining to the blood vessels. These 9p21 markers, Ben, were so important when they were discovered. The first publications refer to them as the heart of the human genome.
Now, let's go with this. There are two 9p21 markers, two of them, many others that are studied, but these two are really important. Each of those 9p21 markers you have two copies; one from mom, one from dad. So, we've got two 9p21 markers, each with two copies. We've got four copies of these 9p21 markers that we're going to be looking at. Now here's how it goes. Each of those copies can come in either an A version called the A allele, or a G version, the G allele, so that any given human being, anyone chose that random, might have four As, zero Gs. Another person might have two As, two Gs, and so on and so forth. And then we have some individuals with zero As, four Gs.
And here's the importance. For these two markers in that region of your genome, the more the number of Gs you have from zero to four, the less resilient, speaking plainly and simply, but that's functionally what happens, the less resilient is the endothelial lining. You see, the guys who have four Gs, all four of their markers for these 9p21 low side are Gs, their endothelium, their vascular endothelium will be more sensitive to inflammatory markers in the bloodstream. Well, Ben, that's one of the few negative things we found, or potentially negative things that we found in your profile because as you can see, you and your little angels, you all have four Gs, isn't it?
Mansoor: Both you and your boys at these two super important markers, what do they do? They influence, they contribute to just how sensitive is the lining of your endothelial, your vascular endothelial, which means to the degree that we know that it's sensitive or resilient is the degree to which if and when things are present in the bloodstream that would have been inflammatory, those vegetable oil derivatives, those toxins that are piggybacking on the foods that we eat, all the polycyclic aromatic hydrocarbons from cigarette smoke, or the VOCs, volatile organic compounds, from all of the things that we deal with in our modern buildings, and so on and so forth, okay, when these chemical and/or cellular metabolites enter into the bloodstream, depending on lifestyle choices, those things, those chemicals, some of them impart inflammatory consequences onto the lining of the vasculature.
And now we have a first differentiator. We can say the guys and gals who have four Gs, their vascular lining can't take as much of a punishment as the guys and gals lucky enough to have zero Gs, all As. Putting some statistics to this, Ben, you and your boys then belong to about, we estimate, less than 10% of the human population will have four Gs across these two markers. Okay. Well, does that mean that Ben is going to be faced with vascular disease? No, but it does mean that Ben, right off the bat, needs to know that he wants to take steps to protect that vascular lining more than the other Joe who was smoking since he was 15, drinking cognac and then here he is, the George Burns effect like I like to call it, at 80 something, still smoking, still drinking, and his blood vessels probably look like a 20-year-old. He is very unlikely to have four Gs.
Ben: Now, that would be an example of someone who's healthy despite their genetics, or I guess I should say someone who's healthy because of their genetics not because of their lifestyle if they had that double A copy of the 9p21. That would be like the person in the, whatever, the 110-year-old French grandma who smoked a cigarette and ate a biscotti and a croissant every day and yet she's got no coronary artery disease or risk of ischemic stroke.
Mansoor: Badda bing. And here's something really cool, Ben. When we talk about high vegetable, of course we can all benefit from an increased consumption. Let me be very careful. I want to actually be as accurate as I can possibly be. Most of us can benefit from increase in good quality vegetable matter, and we've all seen the studies that sometimes say, “Well, a glass or two of red wine a week can also be beneficial.” Studies, they come and they go. Sometimes another study comes out that negates these associations.
Here's an important phenomenon. Do you know that the association of improved endothelial function, the very cells that we're talking about with the consumption of increased vegetable matter, it seems like the people that have improved the vascular function with increased vegetable matter, that appears to be much more so for the people with zero Gs? In other words, the folks who have increased number of Gs, which is not to say they shouldn't have vegetable matter in their diet, but the protective effect of whatever, all of the wonderful things that increased vegetable consumption, and all of the studies that show that it is cardiovascularly protective, they benefit less from vegetable intake, which is not to say they shouldn't have it, but they benefit less than the four G carriers than the folks with zero Gs.
You know the studies that show that red wine consumption has certain beneficial vascular associations? It turns out that the folks who benefit from red wine and the resveratrols and all of the other goodies in that are also the folks with the zero Gs. Not to say that the folks with Gs couldn't benefit from those things, but in other words, having more Gs diminishes the beneficial effect, to talk about just these two dietary things that have been often studied.
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So, you could, and this might be extrapolating too much, but you could potentially say if you have all four G copies that you could potentially better handle something like a carnivore diet that's lower in plant matter and red wine?
Mansoor: It's a little stretch. We can start coloring just how much of an additive benefit these purportedly beneficial things are, vegetable consumption, red wine, which will again, I want to stress, they can be beneficial across the board to make the leap that you did, which is a sound one, a logical one. We need to look at other contributing pathways, which we'll get to shortly, okay?
Mansoor: Alright. So, we start off the storyboard. We said, “Hey, listen. If we're going to look at vascular health, we got to start with, will the player tells you how strong, how resilient is the lining of your vasculature?” Now, why did we go down that path? We went down that path for the next point, which is what would be the things in the bloodstream that would have or could have caused inflammation in the first place? We just said how resilient you are to those inflammatory things, but now let's ask a different question, an additive question, a logical next step. Let's ask, how is the body keeping the blood supply? How healthy is the body, how good, how efficient is the body at monitoring the quality of that blood supply? Because of course, what is in the blood will be the things, as we mentioned earlier, that would inflame the lining.
So, here is what we're going to do. We're going to say, “Well, listen. The most important vascular endothelial disruptive things are, and we could all list them, all of these chemicals and byproducts that we're becoming more and more aware of, whether it'd be cigarette smoke.” And you know, Ben, so many folks when I speak to patients, I have to remind them that smokers are more likely to die from vascular disease than lung disease. We all think and we all can associate with smoking and lung disease, but here's the point. The lining of your lung, the alveoli lining and the lining of your gut are designed to take much more for pounding, much more for beating than the lining of your blood vessels. The lining of the lung, the lining of the gut has a mucosal in a microbial lining that protects the biologic cellular lining, which is not present in the vascular lining.
So, we're going to say if a person, depending on environment, lifestyle, and diet, if certain things are getting into the bloodstream that are pro-inflammatory, toxic, oxidative causing, how good then is the body dealing with those things so that they would be neutralized, or conversely, if they're not neutralized, if they've not metabolized and flushed out, and God forbid you still have a four G, a more sensitive lining, now we're building up the momentum to saying this person has to watch out.
And the most important of such phenomena, Ben, is we're just going to ask, how good are your detox genes? And this is not pie-in-the-sky detox I'm going to go on a detox diet, this is the bonafide hepatic liver function that your blood is constantly flowing through your liver, and through the liver enzymes and the livers, you know well, are metabolizing, neutralizing toxins, byproducts, pharmaceutics, and so on and so forth, one of the major jobs of the liver. And one of the major genetic pathways, Ben, one of the first, I call [00:42:30] ______ pathway of the body, it's the pathway that neutralizes, gets rid of toxins in the bloodstream, is known as your glutathione transferase pathway.
So, glutathionylation is the cellular process that neutralizes the laundry list of toxins that you can think of. Think of something that is toxic, and all chances are it's going to be neutralized and removed from the body via glutathionylation, which is not to say that it's the only detox pathway, but it is certainly one of the most important. So, if glutathionylation is the pathway that is going to remove toxins from the blood, or one of the major pathways, and if said toxins would have been the very things to inflame the lining of the vasculature, and of course we've determined whether someone's a zero G, three G, four G, two G, we've got to ask how good is your glutathionizing capacity.
So, that's when, Ben, we jump over to a seemingly unrelated part of your report, the part of your report that talks about detox. And what we find is this, a remarkable phenomena, isn't it? You see, we started off this very discussion saying for the vast majority of genes, vast majority of genes, we're going to expect to have two copies; one from mom, one from dad. But for some really important genes, for reasons that still baffled scientists, some people may not have two copies of a given gene. They might not have inherited that gene from mom; they've only inherited from dad or vice versa. And my goodness, Ben, there's sometimes genes where you didn't inherit it from either parent.
Now, of course, let's stop for a moment here. If you did not inherit a gene, if that instruction, if that paragraph of which you should have two copies isn't there, period, it's not even there, talking about SNPs in that gene is completely irrelevant because the gene isn't there. More than that, Ben, talking about epigenetics of that gene is further irrelevant. You see, people get really caught up and, you know, “Let's change our genes.” That's one of the blood pressure rising statements. We don't change our genes. We might be able to alter the expression of our genes. That's epigenetics. But by god, if you don't have the gene in the first place, there is nothing to alter.
Now, when we look at your GST genes, we found, you, specifically, Ben, we found something interesting. You see, because this phenomena of detox via glutathionylation is so incredibly important, the good Lord, whatever you believe in, didn't design us with just one gene responsible for something so awesomely important, detox. So, what do we have? We've got several GST genes that are essentially duplicates of each other, that are placed in different parts of the genome doing the same job. Just in case something happens to one copy of those genes, we've got backups.
So, there are three particularly important GST genes. Each of these genes are essentially identical, essentially. They're placed in different parts of your genome, in different volumes of your genome, different chromosomes of your genome. And they're going to be responsible when toxins show up in your bloodstream to get rid of them. Keep in mind I'm going to expect that I should have two copies of each of these genes.
Now, as much as we said that each of these genes are almost identical, their order of preference, the order in which when a toxin shows up in the blood, these genes are expressed. In other words, the priority with which they do the job of cleaning up, detoxifying at a cellular level, studies suggest that they're slightly different. So, studies suggest that the big brother, the big sister of this triad is the GSTT1. Each member is going to have the prefix GST. And then each of the members were differentiated by the suffix, T1 for theta 1, P1 for pi 1, M1 for mu 1.
So, what we're going to do now is we're going to say, “Alright, let's go check for the GSTT1 gene.” And, Ben, we want to see two copies because that's the gene that is going to be one of the major players in keeping Ben's blood free of toxicants, toxicants that you can name anything on the laundry list. Why do we want this information so badly? Because we've predetermined Ben's vascular lining is a bit more sensitive than we would like.
So, we go looking for Ben's GSTT1 gene. The GSTT1 gene is on chromosome 22, volume 22 of the 23 volume encyclopedic sets of which we have two copies of that encyclopedia. So, we pull the volume 22 from mom, that you inherited from your beautiful mom. We pull the volume 22 from your dad. Okay. We look on the page of that volume that should have had the GSTT1 gene, and we found something interesting, Ben. We found that you only inherited the GSTT1 gene from one of your parents, and not the other. Ben Greenfield has one, not two, one copy of this gene.
And just so that you know, Ben, the expression level of this gene is directly correlated to the number of copies, simply stated, you, Ben, and there I say, Ben, yours truly, myself as well, I have one copy, we both produce 50% less of this important detoxifying enzyme GSTT1 than the lucky gals and guys with two copies. You could take that to the bank. Now that you just do a quick little statistics check, so that we don't feel too badly about ourselves, it turns out Ben is that it is estimated somewhere around 60%, depending on certain ethnic drifts, about 60% of the human population has one copy of this gene. So, in other words, having one copy still gives us enough detox activity for the ranking file toxic exposure.
Of course the guys and gals that is estimated that somewhere between 20% and 25% have two copies, those are the lucky buggers, those are the guys who can detoxify and keep removing toxins when they enter into the bloodstream far faster and more efficiently than you and I. About 20% to 25% of the human population has two copies. Okay. So, we were in the average. We were in the 60% that has only one copy. Okay. This means, remember, we're keeping an eye on that four G phenomena. So, we're saying, “Listen, so long since Ben has a modicum of healthy environmental practices, dietary practices, lifestyle practices, so long since he's not exceeding his toxic threshold, starting with this one gene, he's not doing too bad, he's average.”
Well, hold on. Remember, there are three of these guys. Each of them helping, acting as backups one to the other. So, let's go to the other all-important, GSTM1, the sister of the T1. And that's in your first volume, chromosome 1. The first volume of your manual is where the GSTM1 is. Keeping in mind that it's almost a duplicate of the T1, but it acts as a backup. So, we go looking now in Ben's two volume 1s on the page. It would have had the GSTM1 gene. Okay. We open mom's volume 1. Oops, Ben did not inherit the GSTM1 gene from his mom. We open dad's volume 1 to see if he got the GSTM1 from dad. Lo and behold, it's not there on either of the copies. Ben Greenfield does not have the GSTM1 gene at all. It's not there.
So, let's stop for a moment, Ben. Keep in mind, it means your entire paragraph, the paragraph that was that gene, minimally, it's just not there at all. We're beyond SNPs here. There's no SNP to be spoken of in Ben Greenfield for this gene because he doesn't have the gene, period. But Ben, yours truly as well does not have the gene. Ben, 60% to 70% of human beings, notice we said, 60% of human beings have one copy of the T1; 60% to 70% have zero copies of the M1. It tells us something important. It tells us that the M1, even though it is an absolutely important detox gene, can be lost with a plump in a large portion of the human population, assuming they at least have the T1. Alright. So, keep that in mind.
The M1, in other words, most studies suggest that the M1 is a backup. We can lose it with less consequence so long since the other functionality of detox is working. So, what does this mean? It means that Ben Greenfield, with one copy of the T1, zero copies of the M1, heck, we would have at least liked one copy of the M1. But you know what, one copy of your T1, zero copies of your M1 puts you at scraping the bottom of average. You and I have, thus far, what we call just about average, low to average glutathione detox capacity.
So, you and I now have to be that much more cognizant of our environmental choices, our dietary choices, whatever is going to enter into our bloodstream, the laundry list of toxins that needed to be cleared via glutathionylation, you and I need to be that much more weary about it. And why is it even more important to you? Because we're keeping an eye on the sensitivity of your vascular membrane, your lining, your endothelial lining.
The final player here to speed up the GSTP1 is the final member of this triad that we look at. And every human being that we can tell has two copies; you, me, everyone else. So, we do have two copies. So, now, we've got two copies. SNPs are going to be important. Are there spelling variations to the two copies of the P1, pi 1 member of this family that contributes to its efficiency, its optimability? And the answer is yes. Simply stated, Ben, you've got two copies of the P1, and both of your copies are the optimal versions. Aha, so now that puts you a little above average. So, you've got one copy of T1, zero copies of M1, two good copies of P1. Ben Greenfield, through the mechanism of glutathionylation, is just a little above average in his ability to clear things from the body. He's not going to win a gold medal here for detox. But so long since he's moderately, a little bit more in tune than others, he should be okay. And remember, that's super important considering the four G status of your lining.
Now, let's just quickly close on this, Ben. Let's quickly look at your little angels. This is why he's a father. Awesome. I mean, my god, your boys must be tickled pink, having a dad like Ben to watch out for them and to train them and to educate them because here's what's important, Ben. Both your little angels, River and Terran, both have the four G status. Okay. So, their vascular endothelia–and by the way, that's how they're born. Their Teflon coating isn't quite the robust Teflon coating that we might otherwise have liked. Fair enough.
But here's where it gets really important for River and Terran versus Ben. You see, River and Terran, they are completely deleted for the all-important GSTT1. The T1, Ben, that you have one copy of, that at least you have one copy of, the big player in that detox pathway, River and Terran have zero copies apiece. So, you see, Ben, River and Terran, from their youth, not to think schizophrenic over it, but from their youth, Ben, you need to be the dad that informs them, “Hey, guys. Dad's going to treat you. Dad and mom are going to encourage you and train you and engender in you the best lifestyle practices, environmental practices.”
Ben, you and your noble wife, artificial air fresheners shouldn't be a thing in a common place in your home. Those toxic bomb cleaning detergents shouldn't be there, especially for your boys, because those things, those artificial air fresheners with polycyclic aromatic hydrocarbons, volatile organic compounds, when they enter into the body of your boys, be it through the bronchial alveoli, the lung, be it through the GI tract, be it through dermal touching, when those toxins enter into their bloodstream, River and Terran are at a reduced efficiency and notably reduced efficiency in their ability to glutathionize, neutralize, and get rid of those toxins from the bloodstream hepatically through the liver, then through the kidney out through the bladder and urine.
And because they are endothelialy four G, you can see now the one-two punch that we've got to watch out for. You need to be the dad that says, “Hey, River, Terran, listen. I know you guys are going to be teenagers and university gurus one day, but you know what, sons, don't be the guys that are smokers. I know your buddies might try it out. But for you, you got to understand that you really just aren't equipped to handle that like some other guys might have–“
Ben: Yeah. For your genes, kid. Now, in a situation like this, for myself, like do you make targeted supplementation recommendations as well? I mean, I know that your company is associated with Youtrients that does like customized supplement packages based on your genetics. Will this be a situation where you'd say like, “Okay, we're going to include some kind of glutathione or superoxide dismutase support or something like that”?
Mansoor: Brilliant. And the answer is yes, but I must color that by saying, Ben, and the little that I know of you and that I've seen, the awesome, just holistic approach that you bring to health, which is why you are who you are, we always stress, Ben, that we want the most that we can get from whole foods. Nothing compares to that optimal diet the way in which compounds were they to be individually isolated i.e. through micronutrients and supplements versus those same compounds amidst the complexity of whole food, other compounds that work synergistically and so on and so forth.
So, the first point here, the first answer to your point is this. We encourage optimal whole food, eating good whole nutritious food. So, by the way, for the very concept of someone with poorer glutathione function, we're talking about the awesome nature of the ingredients in cruciferous veggies, those isothiocyanates, those sulforaphanes, cysteine containing foods, and acetylcysteine containing foods, whey, the whey fraction of a good grass-fed, the whey fraction of the milk of a good grass-fed animal, this chock-full of the precursors, of the things that improve glutathionylation, a little quick —
Ben: Looking at a lot of this, sorry to interrupt, looking at the full picture of a lot of this, I did notice on my results for my–I believe it was the metabolism section of the report, increased risk for lactose intolerance. So, when you're making a recommendation like that for any dairy type of foods, do you kind of couch it in light of other related SNPs related to dietary factors?
Mansoor: A hundred percent. And when we speak, you're speaking of the MCM6 gene, Ben, that you carry, the G allele, which is associated with lower lactase production. Again, one minute of diving deep, let's get geeky for a little while here for that MCM6, and then we loop back around. First and foremost, that G allele, that allele that is associated with lactose intolerance, because it's associated with adult, or as you–post-weaning reduction in lactose production is of zero benefit in individuals of Sub-Saharan ethnicity.
So, here's an example. If you're someone of Sub-Saharan ethnicity, and of course with the beautiful diaspora for modern world, these individuals can be anywhere in the world, and you get your gene results and you go, “Oh my goodness, I have got the G allele. I'm lactose intolerant.” No. That G allele and lactose intolerance was associated in the Caucasian, Western European Caucasian population. It is not associated with lactose intolerance in certain other ethnicities, including the Sub-Saharan population. But for you, there is that association. Okay. Fine.
Another point here. This gene, the G allele, which is associated with lactose intolerance, and it's bandied about. So, now we've just heard something that says, “Listen, you just can't bandy about that G allele and tell someone they're lactose intolerant unless you know their ethnicity.” Number one. Number two, that G allele, what does it do? It confers post-weaning a reduced lactase production. Now, here's the point. Notice I said post-weaning. You see, individuals that have the G allele, that is a risk, it's a predisposition, yes, to lactase reduction. If post-weaning, their culture, their diet remained rich in dairy products, for those individuals, it was as though they never weaned. For those individuals, they can have the G allele and still maintain, oftentimes, healthy levels of lactase.
So, this is critically important. This is an epigenetic phenomena that just because you've got the G allele does not mean that you're absolutely lactose intolerant. You've got to look at, did you nurse in the all-nourishing mom's milk? And then after weaning, is your culture, was it a culture replete with the use of yogurts and cheese and milk products or milk-derived products? And if the answer is yes, then lactase reduction, it was as though you never weaned. Again, Ben, the awesomeness of seeing how superficial interpretation can be given versus a really deeper dive. Okay?
Mansoor: So, coming back to it, a little beautiful tip. I learned this from a dear colleague of mine, brilliant Oxford scientist. He did–showed that, Ben, back in the Victorian era of England, the wealthy folks in London and other places of Victoria, England, when it came around September, October, November, they couldn't be found in the cities. Where would they be? They would be in these lodges in the Scottish Highlands. And what were they doing in the lodges in the Scottish Highlands? For weeks on end, they were actually being given, they were feeding on whey fractions of these healthy grass-fed sheep.
In other words, way back in Victoria, England, the whey fraction, and absolutely as you pointed out, you do still have to have other parameters of discussion; lactose intolerance, milk protein sensitivities, and so on and so forth. But just to point out, people from a long time ago understood that there were whole food components that radically improve, whether it'd be detox phenomena and other healthy things in life.
Now, to answer the final part of your question regarding supplementation. If and only if–and this is where I say I am an advocate. What we do at Youtrients, what we try to do is not promote supplementation but rather reduce it, reduce it to only if and where it is necessary to educate the population. Listen, just because something is a supplement, just because it's supposedly natural does not mean that it's once and used in 50 things under the kitchen sink in the sun all at once.
Think about it, Ben. The human body was not designed to respond cellularly to the microfractionation and condensation of 60, 50 micronutrients all at once. How does that work with the cellular functions in the body, the circadian rhythms of the body? More often than not, our body, the cells of our body weren't designed to handle supra levels of micronutrients that have all sorts of gene expression consequences. So, what we do at Youtrients, Ben, to answer your question more fully is we ask, is there a cellular function that is discernibly suboptimal or dysfunctional? And are there judiciously certain micronutrients that might improve said discrete cellular function? And then those are the places we recommend and we custom-formulate ingredients.
So, what can we do for individuals with reduced glutathione function? Well, of course here comes a really important point, Ben, that a lot of clinicians get wrong, well-meaning clinicians. They would say to River and Terran, they would say, “Well, River, Terran, you've got poor glutathione function.” Follow with me just one minute here. So, what are we going to do? Are we going to recommend that you get these glutathione IVs that have become vogue? And let me make it clear. Glutathione IVs can have some awesome properties for some individuals.
But we've got to understand something here. That GSTT1 gene that Ben and River are both missing, what is it? Is it the gene that's making glutathiones such that because it's missing, we give them more glutathione and off they go, they're happy? No. This is the gene that is controlling the use of the glutathione. It is catalytically binding glutathione to the toxin. So, in other words, what River and Terran are missing is they're missing the controller, they're missing the guidance system to zone in glutathione unto the target. That's what they're missing.
So, simply pumping them chock-full of glutathione via an IV is not the solution. In fact, will we to give River and Terran one too many IVs of smack into the serum, smack into the bloodstream glutathione? Glutathione, as you know, Ben, is one of the most awesome–first and foremost, it's a tiny polypeptide. It's just a three amino acid polypeptide with massive cellular absorption capacity. It even gets into the mitochondria because it's so small. If you overdose someone with glutathione, for whom the control of the use of the glutathione isn't as optimal, you can radically upset the redox system of the mitochondria. And then these folks get glutathione IVs, where other folks go, “Damn, that was the best thing since sliced bread.” For Rivers and Terrans of the world, they get one too many IV glutathione shots and they will feel like someone has pulled a rug from under them because their entire–for a duration of a few hours, their whole mitochondrial redox has been thrown off-kilter. Did you get that, Ben?
Ben: Yeah. That makes a lot of sense. I think it's a good point for a lot of people who just think more is better or who find out whatever they have low glutathione status, they should go out and get intramuscular glutathione or a glutathione IV or something like that, when in fact, the mitochondria might not be able to handle that. So, very good point.
Ben: Okay. Cool. Got it.
Mansoor: Okay. So, now we stitch together, Ben, but we're going to start speeding up here because again, to the listeners up there, the Greenfields, clearly part of Ben and mom, beautiful genomic profile, we're focusing here and only that which is dysfunctional but there are lots of other great things. So, Ben, we've just established endothelial sensitivity. We've layered in intelligently. Look, we've only spoken of five genetic markers thus far, two 9p21s for endothelial function, three of the GSTs, yet the sum total of the impact of what we're witnessing in actual physiologic manifestation is huge. And this raises a really important point here, Ben, that even when it comes to genetics, more is not necessarily better.
You see, Ben, we've got 22,000 odd genes in our library. If every single one of those genes were independently capable of being dysfunctional or not, and then networked into cellular systems, that would then further perturbate the dysfunctionality of any particular gene. We wouldn't survive, Ben, as a human species if we had so many opportunities for this function. Rather, yes, we've got 22,000 genes, yes, they've got these awesome important functions cellularly, but we can really distill cellular dysfunction to some landmark things. We're not looking for 1,000 points of dysfunction. What can we distill this to, Ben? We can distill cellular dysfunction to some big-ticket items. How good is that cell at detoxifying itself? How good is that cell, and here's if you were to ever ask me, Ben, how good is that cell at controlling inflammation? You see, so now you can take big-ticket items and really create informed physiologic outcomes without having to look at hundreds and hundreds of genes at the same time, because we've established there is an increased susceptibility in the vascular endothelium, meaning, an increased susceptibility to inflammation. We've just established how good are you at keeping down the things that would cause the inflammation.
Now, let's switch gears very quickly. Other than toxins in the blood, Ben, the ones that you could think, “Yeah, boy. If those things were in the blood, they would be really abrasive to my Teflon-coated blood vessels.” What else other than the point of finger at the toxins, if present in the blood, chronically elevatedly would be inflammatory? What else? Well, at the top of the list, and you know this, Ben, better than most, at the top of the list would be chronically elevated, a hyperglycemic condition to the blood with the corollary. And many people miss this point, not you but many.
Most of us, we correctly focus on the deleterious nature of chronic hyperglycemia due to poor glucose control. But we forget that chronic hyperinsulinemia, secondary to hyperglycemia, but importantly in the context of insulin resistance, because of course insulin resistance is going to define the very phenomena if the cells of our body are resistant to the chaperone. Insulin is, as you know, the chaperone of glucose to get it into the cells. If our cells were resistant to the signaling of insulin to get glucose into the cells, what does the body have to do? The body will compensate by producing more insulin.
And now we've got an individual who's going along life, going, “Heck, yeah. My hemoglobin A1c is good. My fasting glucose is good.” And what they're not realizing is unless they're looking at their C-peptide results or even an insulin challenge test results, what they're not realizing is they're going about life with chronically elevated blood insulin levels. And that is another contributor to inflammation of the vascular lining.
Now, Ben, why am I talking about that? Because this is going to be your triangulation of all of the things in the limited genes, limited genes that we looked at for you. Your triangulation of concern is precisely your four G, 9p21 status. And what that confers, you're just above scraping button barrel detox more so for your boys. And the third component is we looked at this all-important TCF7L2 gene; Tomorrow, Charlie, Frank, 7, Laughter, 2. This gene, Ben, has become the poster child in the type 2 diabetic world. Okay?
It seems that this gene controls what is known as an insular tropic hormone, GLP-1. It seems the GLP-1 is this thing that is produced in the gut when we ingest carb and glucose-rich foods. And through a cascade reaction, the activity of the TCF7L2 gene affects two things. A, it literally affects the efficiency of insulin release in the early post-prandial, and actually, prandial phase. It's affecting insulin release. But remarkably, in the post-prandial phase, this gene is involved in insulin resistance.
Now, this gene, we all have two copies of it. There is a SNP. This one has a SNP in it that is informative. The SNP comes in two versions; a G version, G as in George, a T version, T as in Thursday. The T version of the gene is deleterious. It's suboptimal. And by the way, Ben, here comes another phenomena. Yes, we've got two copies of the gene, but sometimes one of those two copies, depending on what's there in the human population, is as you well know what we call dominant. Meaning, whatever that one copy that is dominant, it doesn't matter what the other version, the other second that you got from either mom or dad is, because that one copy is dominant.
Now remarkably, Ben, the T version of this gene, which is suboptimal, which confers suboptimal response to dietary glucose in a biphasic manner, A, because it confers suboptimal prandial and post-prandial insulin release, as well as secondarily and paradoxically–well, not paradoxically but importantly, it further then confers insulin resistance. So, then you start seeing a post-prandial spike in insulin more than you would have liked in these individuals. The T version that is suboptimal is dominant.
So, hold on. Whether you are T homozygote, which you are, Ben, both of your TCF7L2 genes, you carry the T allele. By the way, your boys are heterozygotes. They are GTs. They obviously then got the G from mom, the T from you, but even though they're heterozygotes, they're still going to behave more like you because their T allele, which is suboptimal, also happens to be dominant. Now, Ben, this might, and of course this opens up a whole different discussion, but when you take a look at this gene that is actually now it confers the single highest genetic association with type 2 diabetes, secondary insulin resistance and poor insulin control, the single most important gene, which is remarkable for something as polygenic, something that's type 2 diabetes that absolutely has multiple genes contributing to the end outcome, this is the leader of the pack, that the suboptimal version is dominant.
It starts to inform us, isn't it, Ben, as to what maybe our forefathers were designed to eat? It starts to inform us that maybe we weren't quite as designed for high processed sugar or high, low–high simple carb meals because if after all the suboptimal version of the gene is dominant, it tells us something, isn't it? Now, the point here, Ben, is you're homozygote T. Your boys are heterozygote, which means that, Ben, in the context of a high carb diet, either you and/or your boys, you are at a greater risk of insulin dysfunction, which can create a non-toxic pro-inflammatory condition, environment of the blood, which would further perturbate that delicate lining, that 4G lining of your vascular endothelium.
I'm going to pause there, Ben, because now what we've just done is we've taken three disparate aspects of cellular function; endothelial quality, detox capacity, insulin productivity and function in response to diet. And look at the awesome story, functional, logical cascade that we've been able to formulate. Does that make sense to you, Ben?
Ben: Yeah. It's very interesting. And this idea that I would need to, for example, prioritize taking care of my vascular function and prioritize mitigation of some elements of carbohydrate intake, and also, pay close attention to glutathione status. It's very interesting. There are some things on here that I already knew like the poor vitamin D availability. That's reflected on this report, the CC copy, or not the CC copy, the GG copy of the cypR gene associated with suboptimal activation of vitamin D and a few others.
But I know we're getting a little bit long in the tooth, so I wanted to quickly ask you also, because what you've been talking about is this genome pulse report. And obviously, there's a ton we could go into on this, but you guys also do the hormone pulse report. And I was wondering if you could just give me a quick overview of what that is and how it's different in any primary takeaways from that.
Mansoor: Indeed. Just before we leave that, Ben, because I do know that your work on the circadian rhythms of the body is so incredibly awesome, and the things that you advocate have just been under money, just make sure that, Ben, you recognize that both you and your boys are–you carry the heterozygote, and therefore, suboptimal predisposition for BDNF production, brain-derived neurotrophic factor, which is arguably one of the most important genes in the genome and one of the most important genes from a circadian rhythm, sleep quality, response to exercise and so on and so forth. So, just before we leave the genome pulse, do cast your eyes on that and all of the awesome things that you already know that you can do to improve your BDNF production, which of course we can all do with better production of BDNF. It's just FYI.
Ben: Right. Exercise, sauna, things like that.
Mansoor: Yes, yes, yes.
Ben: Learning new things, feeding my children plenty of psilocybin, things along those lines. Yeah.
Mansoor: Indeed. Keeping that neuroplasticity at a young age, learning languages, music, things like that, or all of these lifestyle things that we can bring in that are not pie-in-the-sky, they're not airy-fairy, they're real things that we could do. Okay. So, we come to the genome pulse. The genome pulse, particularly for men —
Ben: Wait, you mean the hormone pulse?
Mansoor: Sorry, the hormone pulse, my bad, my apologies. So, what I like to call the first part of the hormone pulse–what are we looking at, Ben, for both men and women? The first thing we need to know, Ben, is in both men and women, we're speaking of essentially the same molecular cascade. We're essentially speaking of how does the human body, male or female, convert progesterones into androgens, think testosterone but there are other androgens, as well as then from androgens into estrogens.
So, yes, ladies out there, if you're menstruating, that is if you're in your menstrual years, premenopause, you are making your estrogens, your estradiol largely from testosterone. In other words, you don't make estrogen unless you make first testosterone. And yes, men, we don't have a monopoly on testosterone. We also make estrogens. So, my first point here is human beings, we have essentially the same cascade of progesterones into androgens into estrogens. That's the first.
When we understand this, we have what we call the T-intersection, T, unsurprisingly for testosterone, and the E intersection for estrogens. What do I mean by the T-intersection? Very quickly, what we're able to see genetically, and that's why it's so awesome, had I not seen Ben Greenfield, I would have been predicting depending on age and a modicum of healthy diet and lifestyle. And I was not being facetious, so trying to be ingratiating to you. Ben Greenfield has literally the single one of two of the best possible hormonal cascade genetics when it comes to physique. How could I make such a, frankly, awesome statement or bold statement? It is as thus.
You see, when we look at how the body makes testosterone, and uses and metabolizes testosterone, I have what I call the T-intersection. Think of a lowercase T. In other words, a cross. What are the four points of the cross? The four points of the T are, number one, on the left, how efficiently are we converting progesterone into testosterone? Ben, you have this one gene. Imagine that. One gene, CYP17A1 that converts progesterone, specifically and more so pregnenolone into your androgens, DHEA, androstenedione, androstenediol, and testosterone. Let's just say testosterone for simplicity. You've got the version of that gene that is considered relative to the other version of the gene, the slow version of CYP17A1.
So, one might say, “Well, hold on. Does that mean that Ben isn't making enough testosterone?” No. It actually means that compared to how much faster Ben could have converted his progesterone into testosterone, Ben has the version that makes this testosterone just at the healthy level. Having an overly fast CYP17A1, Ben, not you, the other folks, is a predisposition for hormonal dysfunction downstream. So, Ben converts his pregnenolone. Ever since he hit puberty back whenever, he converts his pregnenolone into testosterone at what is, study after study pan-ethnically, just the right rate.
Now you've made your testosterone. You're at the juncture. You're at the middle of the T. When you make testosterone, Ben, three things happen to testosterone. Well, one, we're going to use it, obviously, and benefit from it. That's obvious. We are going to take some of that testosterone and convert it into DHT, dihydrotestosterone. I like to call it my Jason Statham testosterone, right? So, one molecule of DHT is worth five molecules of T.
Ben: Yeah. Also, it can make you go bald if you're not careful.
Mansoor: Indeed, indeed. So, you, Ben, have the medium speed version of the SRD5A2 stored, 5 alpha-reductase that converts testosterone into DHT. Now, when we take that into composition, you have the gist right slower CYP17A1, progesterone, pregnenolone into testosterone. You have the medium conversion of testosterone into DHT. You have the medium, of the other things that we do with testosterone, aromatase CYP19A1 converts testosterone into estrogen. And men, we need it as well. You've got the medium version of that.
The last thing that we do with the testosterone and the DHT, having made it, we metabolize it, we flush it out. How do we do that? Through glucuronidation, your UGT. Notice you have just about the medium Goldilocks version. You are neither too fast, nor are you too slow at getting rid of your testosterone DHT. Having made it, how does this all combine? It combines as thus. Ben Greenfield is the lucky son of a gun who makes testosterone at just about the right rate. He converts just about the right amount of testosterone into that more voracious anabolic DHT so that it creates good lean striated muscle without excessive hirsutism and going bald, without too much of a concern of BPH later in life because the men who had the fastest CYP17A1 converting pregnenolone to testosterone faster than you can shake a stick at, converting testosterone into DHT at the highest rates possible, these are those DHT bald men, much leaner, yes, much more wiry muscle type, but at a significantly increased risk of BPH into their early and mid-50s and 60s because they were too DHT dominant for their entire life.
Ben Greenfield has the perfect balance of the T-intersection. Quickly, quickly, Ben, the only difference between your little angels, your boys and you, they've got the identical perfect balance that you have, except they have a higher predisposed conversion of testosterone into estrogens. In other words, when they make their testosterone, and Ben had the nice medium conversion to DHT, they have that as well. And Ben has the nice medium clearance of the testosterone DHT, they essentially have that as well. But River and Terran have a greater predisposition of converting testosterone into estrogen. How was this going to play out, Ben? You will find that when River and Terran mature from a pubescent perspective, you may find that their puberty is slightly delayed versus yours, for example, slightly, and you will find that their body type in response to exercise and diet and lifestyle is that they will have a tad more resilience to creating lean muscle mass as you might have been able to get, because that increased estrogenization, which is going to have nothing to do with their malehood or anything of the sort. But from a physiologic perspective, that tad more estrogenization in them versus you tend to confer a little bit more difficulty, we might say, in gaining that leaner cut, if you will. Do you get that, Ben?
Ben: It makes a lot of sense. Interesting. So, they may have gotten that part from mom, not from me, huh.
Mansoor: Indeed. And look what would have happened. Even in you, Ben, even in you, you had the medium aromatase, right? You were heterozygote. So, you're converting testosterone into estrogens at all things equal, mano a mano, male to male, at a medium in the range of how much you convert. Will you, exactly you, Ben, in an alternate universe, everything was the same genetically, but if you simply had the slowest version of aromatase, CYP19A1, such that when you made that testosterone, everything else was the same. You're making it at the same rate. You're making good amounts of DHT, not too much, not too little, and so on and so forth.
But if the only difference in you, Ben, was that you had the slowest CYP19A1, right off the bat, innately, you would have had a predisposition to having a little bit more of a cut physique. Your ability to get that lean striated cut would have come easier if you had the slower CYP19A1. That's the awesome nature when you're able to start looking at this cascade and being able to read the interpretation of how it manifests itself.
Ben: One thing I was going to ask you too was this ACTN3 gene that's associated with muscle twitch fiber type because there's a lot of talk out there about how certain people are more predisposed to power type exercise versus endurance type exercise response. What's your opinion on that gene?
Mansoor: Well, now you've hit a sore point. The ACTN3 gene, which yes, absolutely, it defines, as you well noted, the muscle fiber type, some being more associated with a faster twitch or not. When you take this gene, Ben, and there are actual reports out there, loads of reports out there in what we call performance genetic reports, you will see this gene. Now first and foremost, this gene has two SNPs. In other words, genes can have multiple SNPs in it. And this gene has two SNPs within the same gene that people report.
Number one, before we get into even the SNPs, Ben, as a trainer, okay, the difference in muscle twitch between someone that, let's call it, has the lower functioning ACTN3, the less optimal, although that's a wrong word, the one version of the ACTN3 versus the next, the difference in muscle twitch capacity, Ben, for the 99.9% of individuals that will come to you looking to be healthier due to some exercise regimen that you'll describe and design for them, Ben, this gene is going to have zero implication. That innates slight difference. It might mean they can shave off 0.5 seconds on their 50-meter dash.
In other words, as a world-class trainer, you're not going to look at that gene result and say, “Well, Mrs. Jones, I'm going to give you a more endurance-based exercise motif than a more resistance-based or power training exercise motif, which ironically, and really, it's just pure hubris, that's exactly what these reports, and I'm not calling anyone out, I'm just saying from a genetics perspective, this is an example of a gene that–reported on. Yes, there are some nominal cellular differences, but when it comes to bonafide physiologic outcome, I'm going to ask you, Ben, and not to put you on the spot, to put myself on the spot. If you got this gene result in a report and that gene in that report says to you, Ben, your patient is better suited for power type exercises, would you really use that information and somehow drastically change the training potential of that person?
Ben: No. I'd certainly consider it. I mean, I'd certainly consider shifting things more towards lower rep, higher weight, more explosive activities targeted towards fast-twitch muscle fiber type.
Mansoor: Good. Perfect. And now what if I ask you–remember, I said that gene has two different SNPs in it, two different SNPs, same gene, two different SNPs. But what if I told you very often, one of the places in which the gene varies comes back with the result, you are better suited to power training, but the other variation in the same gene for the same person gives the diametrically opposite interpretation? Now, how would you use that genetic result?
Ben: Well, if both SNPs were tested and they came up with completely different results, I'd just probably throw them out and roll with what that person was responding best to from a qualitative standpoint.
Mansoor: Badda bing. And in many, and we're not talking 5% or 10%, in many, many times, because these two SNPs are independent of each other, they're inherited in an independent manner, many times, these two SNPs within this gene come back as directly opposite informative outcome. And so, these are some of–we go right back to the beginning, Ben, and I know that we're going to wind down. It goes right back to what are the genes that give intelligent–that are meaningful.
Ben: Wow. Well, we just went through, like for me to get this hormone pulse and the genome pulse, that's called the functional genomics test package, right? That's the title of this?
Mansoor: Yes, it is.
Ben: So, the hormone pulse is the one that tells you, like issue with any hormone-related cancers, weight gain, weight loss, potential metabolic syndrome, some information on physical exercise performance, hair loss, hormones, fertility, a lot of the stuff that we were just going over. And then the genome one is basically, if I understand correctly, kind of like six different paths; your carbon, your metabolism, your vitamin and micronutrient requirements, your cellular methylation, your detox and antioxidant capacity, cardiovascular health, and then mood behavior and neurotransmitters.
And basically, what you guys do is you do the genome pulse and then the hormone pulse, and then you also have the option for people who want to get like some kind of a customized supplement package sent to them that kind of addresses some potential deficiencies. That's something that they can follow up with after they've done something like the functional genomics analysis that you have.
Mansoor: And the reason we separate the hormone pulse is not for any other reason other than we wanted to have people be able to say, “You know what, I want the hormone pulse without the genome pulse. I want the genome pulse.” Or you want both. In order for us to make an intelligent interpretation of the type of micronutrients that you might need, we're going to flip those reports because of course, they're also logistic. Obviously, the hormone pathway, the general pathway is not existing independent of all of these others. That TCF7L2 gene, Ben, that influences insulin resistance. Insulin resistance is absolutely parallel, or informs, and is informed by the estrogen pathway of the body. So, all of these things are interconnected.
In conclusion, what you would have observed here, Ben, is trying to interpret, intelligently interpret genetic information is something that is often beyond the capacity of a simple report. You see, a report is two-dimensional. It's serial; one gene after the next after–by its nature. But what I've hoped, if at all, if there's one thing that I've conveyed to your incredible audience is this. Genetic pathways are not serial; they are multiplex, they are intertwined. And so, what we advocate, Ben, more so than who does your test, it's about making sure that the interpretation of the results is as robust, is as non-superficial as possible. That's really where the substance and meat is at.
Ben: And I know that for people who don't want to like hop on the phone with a doctor. You guys, basically, along with the reports that people get, these two PDFs very similar to what I got, you include like a webinar series that just walks people through how to interpret all these different markers that they get after they test with you, correct?
Mansoor: Yes, sir. And we're doing that because of–like you just said, to ease having to figure–you go to sit with someone. Also, Ben, we are creating the largest curated library of videos that illustrate these pathways, talk about these pathways. So, in other words, in the comforts of your own home, you can determine this. What pathway am I going to study or listen today? What pathway am I really going to try to own and personalize with? So, yes, those webinars, those educational videos are really what we're putting our emphasis and attention.
Ben: Yeah. I've seen some in there. They're super-duper useful. And what I'll do is–first of all, everything we talked about, including some of my own results, if people want to download those and kind of peruse them to see what the results actually look like, you just go to BenGreenfieldFitness.com/dnapodcast. That's BenGreenfieldFitness.com/dnapodcast. And I'll link to those.
I'll also link over to Mansoor's company, The DNA Company. They are offering everybody who's listening something special. Basically, this whole functional genomics test package, it's normally about 450. They're giving it to everybody for 399. That includes all the webinar videos. That includes the hormone pulse test, the genome pulse test, and these 80 plus page PDF reports that are super insightful. And then from there, you can basically watch the webinars, get a chance to kind of see how to interpret some of your results, and even look into getting some customizing ingredients sent your way to address specific issues that you might need to address. So, I'll put links to all of that as well over at BenGreenfieldFitness.com/dnapodcast. And you'll need a discount code or anything, just click through from that URL and you can try out this testing for yourself.
Mansoor, I feel like we almost barely scratched the surface of all the different SNPs we could have talked about, but we covered a lot of big ones, and I'm hoping this has been helpful for people. And if this has been helpful for you and you're listening in, you can also leave comments, questions for Mansoor, for myself, and we'll try and jump in and answer some of your big genetic testing questions. But in the meantime, Mansoor, thanks for coming on the show and walking me through all of this and taking this deep dive into genetics with me.
Mansoor: Ben, it's been an absolute honor. So, if you ever need any further feedback, you know where to find me. And for your audience, I will look out, as you said, to any of these questions and we'll coordinate getting answers back to anyone. It's been an honor, Ben. Thank you.
Ben: Cool. Thanks, man. I'm going to have a beer and get some glutathione injections and I guess learn something new to increase my BDNF, as if I haven't learned a whole bunch of new things in the past hour and a half anyways. But all right, folks. Show notes again at BenGreenfieldFitness.com/dnapodcast. Long that special offer from the DNA Company. I'm Ben Greenfield along with Dr. Mansoor Mohammed signing out from BenGreenfieldFitness.com. Have an amazing week.
Well, thanks for listening to today's show. You can grab all the shownotes, the resources, pretty much everything that I mentioned over at BenGreenfieldFitness.com, along with plenty of other goodies from me, including the highly helpful “Ben Recommends” page, which is a list of pretty much everything that I've ever recommended for hormone, sleep, digestion, fat loss, performance, and plenty more. Please, also, know that all the links, all the promo codes, that I mentioned during this and every episode, helped to make this podcast happen and to generate income that enables me to keep bringing you this content every single week. When you listen in, be sure to use the links in the shownotes, use the promo codes that I generate, because that helps to float this thing and keep it coming to you each and every week.
I'm constantly blown away by the amount of genetic data and actionable information one can garner from a simple bit of saliva.
In today's episode, you're going to get an insider glimpse into how to go way beyond something as simple as 23AndMe or Ancestry and instead learn how to get truly useful health information that you can use to enhance health, performance, sleep, gut function, neurotransmitters and cognition, and much more.
My guest on this podcast, Dr. Mansoor Mohammed, has an extremely impressive background in the field of genetics. His credentials include:
- Specialized Honours in Molecular Genetics | University of Guelph | Guelph
- Doctor of Philosophy with Distinction in Molecular Genetics & Immunology | University of Guelph | Guelph
- Postdoctoral Clinical Cytogenetics Fellowship | University of California | Los Angeles
- Postdoctoral Clinical Cytogenetics Fellowship | Baylor College of Medicine | Houston
Dr. Mansoor is now the President and CSO of The DNA Company, a leading and innovative provider of comprehensive functional genomics testing and consulting and first in the industry to bring you individually customized supplements based on your genetics.
He is widely regarded as a pioneer in medical genomics and has been the recipient of multiple academic and industry awards. He is the holder of several patents in the general fields of molecular diagnostics and genomics research and is one of the most sought-after national and international conference speakers in the genre of personalized medicine.
Prior to his role at The DNA Company, Dr. Mansoor was:
- Founder and President of ManaGene (2010-2018)
- CEO of Combimatrix (Nasdaq traded leader in diagnostic genomic microarrays) (2006-2010)
- Director of Genomics at Quest Diagnostics (The world’s largest reference laboratory with a market capitalization of over $10 billion US) (2003-2006)
- Director of Research and Development at Spectral Genomics (one of the industry’s first commercial genomic microarray developers spun out of Baylor College of Medicine under Dr. Mansoor’s scientific leadership)
Dr. Mansoor maintains an active clinical practice as a genomics consultant to some of the leading executive health clinics in Canada and abroad.
During our discussion, you'll discover:
-What makes each DNA test different and how to choose what's right for you…9:30
- Consider the various elements of genetic testing:
- SNPs (pronounce “snips”; single nucleotide polymorphisms)
- Copy number variation (CNV)
- INDEL (insertion/deletion polymorphism)
- Understand how the various labs go about testing the elements
- Humans have two identical copies of the DNA code (from each parent)
- When testing for SNPs, the genetic paragraph is “read” and looks for variations between the two
- The more paragraphs you try to query simultaneously, the greater risk of error (false negatives/positives)
- Characteristics of a proper DNA test:
- Concern is for the physical manifestation of the genes, not the genes themselves
- Cellular function is key indicator
- Identify the genes that influence the desired outcome
- Pinpoint the specific DNA to test vs. “shotgun” approach
- Avoid drawing data for data's sake
-A review of my DNA test and how it compares to my two sons…25:00
- Two different reports: Genome Pulse Report and Hormone Pulse Report (looking at the GPR)
- Vascular function
- Cells that line the vascular system receive the most wear and tear
- 9P21 markers (not genes) are correlated with the lining of the blood vessels; “the heart of the human genome”
- A alleles and G alleles
- The more G alleles you have, the less resilientis the endothelial lining
- Increase good quality vegetable matter
- People with multiple G alleles benefit less from vegetable matter (like red wine) than those with none
- Smokers are more likely to die of vascular disease than lung disease
- GlutathioneS-Transferase (GST) pathway is one of the key pathways in the body
- Glutathionylation: the cellular process that neutralizes toxins in the body
- What happens when someone doesn't have 2 copies of a gene…
- You sometimes have genes you didn't inherit from either parent
- Talking about SNPs in the gene is irrelevant;
- As is epigenetics (alter the expressionof the genes, not the genes itself)
- 3 vitally important GST genes:
- Theta 1,
- Pai 1,
- Should a person only have 1 copy of a gene, they will produce 50% less than someone with 2 copies
- I have 1 copy of the GSTT1 gene (as does 60% of the population)
- Important to not exceed a healthy toxicity threshold
- I do not have the GSTM1 gene at all
- Useless to discuss SNPs for that gene
- The M1 gene is a backup: it can be lost with less consequence than other genes (such as the T1)
- What this means is that I have low to average glutathionedetox capacity
- Must be more cognizant of diet, environment, etc.
- My two boys are missing the GSTT1 gene completely
-Personalizing diet and/or supplements based on DNA test results…57:25
- Nothing compares to an optimal diet (eating whole foods)
- Customized based on dietary limitations (lactose intolerance)
- Ethnic and geographic factors, as well as the environment during weaning, affect how to interpret test results
- Elites of Victorian-era England adjusted their lifestyle (living in Scottish highlands in the autumn months)
- Reduce, not promote, supplementation, to where only necessary
- Our bodies are not designed to accommodate many of the supplements on the market
- “Is there a cellular function that is dysfunctional?” Then address thatthrough supplementation
- More is not always better when it comes to genetics
- 3 disparate aspects of cellular function:
- Endothelial quality
- Detox capacity
- Insulin productivity and function in response to diet
-Differences between the hormone pulse report and the genome pulse report…1:18:25
- BDNF(brain-derived neurotropic factor) is one of the most important genes in our body
- First thing looking at: How does the body (male or female) convert progesterones into androgens, into estrogens
- T-intersection (4 points):
- How efficiently converting progesterone into androgens
- 3 things happen when you make testosterone:
- Use it
- Convert some of it into DHT
- Metabolize (glucuronidation)
- I have the perfect balance of the t-intersection
- My boys are identical, except have a higher predisposed conversion of testosterone into estrogen
-About the ACTN3 gene and its relation to exercise types…1:28:50
-And much more…
Resources from this episode:
– Click here for testing with Youtrients through The DNA Company. Use my link to get their complete functional genomics test package for $399 USD (that’s a savings of $50 from retail price), and your test package includes both Hormone and Genome Pulse panel tests as well as a clinical report for each panel, along with full access to their webinar series, which introduces the science and interpretation of your genomic results with regards to key biological systems and processes. Click here for that special offer from YouTrients for Ben Greenfield listeners.
– My Hormone Pulse results from The DNA Company
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