So, here's the deal. There's a wonderful animal model for aging that involves a little worm called C. elegans. It only lives about three weeks, so you can do an intervention in it and kind of instantly know what's going to happen. So in this model, the influence of the bacteria, the microbiome, and the wall of this little creature's gut, the lining of the gut is only one cell thick, and they're all kind of held together with what are called tight junctions, locked arm and arm like a game we played Red Rover, Red Rover, that kids don't play anymore. So the bacteria are foreign, if you will, and there is an interaction with the bacteria in the gut. And what this model shows is that as those bacteria begin to break holes in the gut, break down the gut, then you can show that that is when aging starts. And the more the wall breaks down, the faster you age. So let's break down. What is aging exactly? So I think most people would sort of go to mobility, aesthetics, and maybe accumulation of disease. How would you define aging specifically? So aging to me is the either quick or slow breakdown of the gut wall. How do we know that? We can take a look at 105-year-old people around the world. You can look at their microbiome, the collection of bugs in their gut. They will have a very diverse set of bugs. They'll have, you know, it takes a village, this really incredible tropical rainforest. And those microbiomes, that collection will be identical to a healthy 30-year-old. So what that says is that these healthy 105-year-olds are healthy because they have the microbiome of a 30-year-old. And it's this microbiome that is not attacking the wall of their gut that's actually existing with the wall of the gut. And I talk a lot about this crazy bug that may be the key to longevity. And it's got a great name, Ackermonsia musinophilia, say that three times. Say that once. So this bug lives in a mucus layer that aligns our gut. And if we're lucky and the way we're designed, we're supposed to have a layer of mucus lining our gut before we get to the cells. And that mucus is there to, number one, trap my favorite subject, lectins, which are plant proteins that are looking for sugar molecules. And number two, it's to protect the wall of the gut from bacteria that might do us harm. So Ackermonsia lives in the mucus layer. And it actually eats the mucus. And here's the best part. The more mucus it eats, the more our gut cells produce mucus. And it actually increases the mucus layer. And the book is actually lots of tricks on how to make this guy happy. Because the thicker our mucus, the younger we are. In fact, fun fact, metformin, we now know works by increasing the amount of Ackermonsia in our gut, not by some magical, mystical thing happening in our body. In fact, interestingly, about 25% of people, when they start metformin, get diarrhea. And it's actually because the gut microbiome changes dramatically on metformin. And one of the reasons is that Ackermonsia becomes predominant. Interesting. So at a cellular level, what's happening with metformin, something that simply triggers the body to produce mucus in general? Is it changing the microbiome, you called it a rainforest earlier? Is it changing the makeup of that rainforest? Or is it just actually compelling the body to create more mucus? No, I think it's actually changing, it's selecting out for Ackermonsia. Now, how does it do that? Because there's actually kind of a shag carpeting on the lining of our gut. So plants have roots going into the ground. We know the roots actually absorb nutrients because of the soil microbiome. All the bacteria, all the fungi actually deliver the nutrients into the roots of the plant. Well, we have a root system. And that root system is this shag carpet that makes the lining of our gut a tennis court. So the reason it's so big in surface area is it loops around itself with little one-cell thick protrusions called microvilli. These are our roots. They literally are our roots. At the bottom of these microvilli, or what are called crips, at the bottom of the crips, there is a pocket of bacteria that are essential. And they're down there in storage. In fact, fun fact, we now know the appendix is not useless, it's one of these storage systems to repopulate our gut.  But down at the bottom of these crips are these little collection of bacteria. And at the bottom of these crips are our stem cells that actually repopulate these microvilli.  It's really good stuff.  All right, really fast because I think this is important. And for some reason, even though I've had you on the show before, I read you read the book, like the way that you've started talking about some of the places that you're going to find, also known as glyphosate, in the system that basically they're part of why they're doing it. They're originally created as a, or patented as a antibiotic, which that was already shocking. And then you said they use it as a way to be able to dry the crops out so they can harvest them on a specific day. Very good. But then you said they don't, no one wipes them off. And so it ends up in Cheerios and other things. And I was like, what? Like I thought if I was washing my vegetables, I was going to be fine. So this was a little bit startling to me. Yeah, you know, a little off subject, but they've looked at recently a study of 35 oat products in the United States, and all of them had glyphosate in them. Some of them at very high levels, some of our breakfast cereals, most of our granolas, most of our granola bars. Most California wines, including a couple of organic wines, have glyphosate in them because the fields are sprayed, the weeds are sprayed with glyphosate between the vines to kill the weeds. Research at MIT has shown that not only does glyphosate kill bacteria, because bacteria use the same reproductive pathway that plants use, it's the chikamate pathway. Humans don't use the chikamate pathway. And so Monsanto, when they invented it, said, hey, this kills plants, but don't worry, it doesn't kill humans because we don't use the same pathway for life. And everybody said, oh, that's great. This is a miracle. What they didn't tell anybody is the bacteria use the same chikamate pathway. And again, they patent this as an antibiotic. They didn't patent it as an herbicide. What else are people doing that is breaking the bonds or killing the bacteria? The antibiotics in their food or that they're taking themselves. In fact, a study just out this morning shows that women who take antibiotics just because of urinary tract infection, sore throat, have a much higher incidence of heart disease than women who don't. That's scary. This gets into something in your book that was super freaky. I've never heard somebody say, and I'm not saying that no one has ever said it, I had never heard anybody say until reading this that heart disease is an autoimmune disease. So because it ties into this point, how is heart disease, autoimmune disease, how does that start in the gut? What is that whole chain reaction? So Michael DeBakey, one of the premier originators of heart surgery from Houston, Texas, would always say that cholesterol has nothing to do with causing heart disease, that it's an innocent bystander that literally gets sucked into inflammation at the wall of the blood vessel. I use the example of, let's say I'm an alien and I'm circling above LA and I report back that I'm pretty sure that ambulances cause car accidents because every time I see a car accident there's an ambulance there and the ambulance must have caused it. Well, association is not causation. So the fact that we see cholesterol in deposits, and I see it every day in the operating room, there's cholesterol in these plaques doesn't mean that the cholesterol caused the plaque. So I learned this as an infant heart transplant surgeon. What we found was we thought naively that if we got these hearts in as a newborn, that the immune system of the newborn would not be mature enough and would say, oh yeah, that's my heart. I don't know any better and it wouldn't attack it. Well, we were partially right, but as the years went and we studied these kids, they started to get coronary artery disease. Their blood vessels got thicker and thicker. That is super interesting. And we're going, what the heck? Did they look just like somebody who we would have associated with too much cholesterol in their diet? It looks just like diabetic coronary artery disease. Interesting. Just like it. And so when you actually look at the blood vessels, the kids, the lining of the blood vessel is from the donor, from a foreigner. The blood going through is from the kid. And the blood says, wait a minute. These are foreign cells and they're, I'm going to attack them. Just think of a splinter under your finger.  So that's inflammation. And what was happening was then cholesterol was basically coming as a patch, an ambulance. And it was getting caught up in this inflammation. So then we look at these adults who obviously don't have heart transplants. And you go, well, that's funny.  And there's an attack on the blood vessels that looks identical as if it was a foreign object. So that got me going, you know, this is an immunologic reaction. And in just few weeks, and I can't tell you the paper because it's embargoed, I'm giving a paper at the American Heart Association Vascular Biology Meeting that makes a pretty good case that lectins, which are a foreign protein that can stick to sugar molecules on the surface of blood vessels are the cause of atherosclerosis in humans and that removing the lectins reduces the markers for that. All right, really fast. And we talked about this in our first issue or first episode, but I think it bears repeating like what's the real quick breakdown of lectins and the rhetoric you started using around kidney beans? I found really interesting. Yeah. So lectins are the plant defense system. One of the plant defense system. I'm pretty dogged on a good one. Plants do not want to be eaten. They don't want their babies eaten, and they have evolutionary pressures to keep being eaten, and have their babies not being eaten, and lectins are one of the ways to do this. They are sticky proteins that look for specific sugar molecules to stick to. And that incites an inflammatory response wherever they stick. We talked about joints wearing out. Joints do not come with a cell by date or used by date. There is no evidence that the wear and tear theory has anything to do with a human body. We can constantly rebuild cartilage, but like I talk about in the book, cartilage is broken down by certain cells and rebuilt by other cells.  You could actually find bacterial particles in your joint fluid. Wow. Okay, so really fast because I know where you're going with that, but now connect those dots. How did those parts get into the joint? Lectins broke down the wall of your gut. And on the other side of your gut is 65% of all your white blood cells. 65% of your immune system is lining your gut. What are they doing there? Because the gut is where the outside world gets through and they're there to sound the high alert and attack them when they get through. One of the reasons we store fat in our gut, one of the reasons we have a beer belly or a wheat belly is we are actually putting fat down where the action is. It's to supply the troops. That's why we put it there.   This is in humans, published studies. This is not conjecture and I reference this in all my books. Wow. Okay. So here's my understanding of fat 45 seconds ago, which may now be changing. One that fat is essentially an organ, but I think of it as an energy storage unit that we can certainly access and break down and turn it into energy, that the body is very efficient at burning ketones, certainly the brain. So what exactly is it doing at these areas of inflammation? So maybe 15 years ago, we thought the fat was actually causing the inflammation because wherever we found fat, there were lots of white blood cells. What I think recent information has proven is that the fat is not the evil guy that we thought it was, that the fat is there because of the inflammation and the inflammation is there because you have a leak in your gut. You have a leaky gut.  And so it's just like any army. You've got to have a supply line. You have to have food for the troops. All right. Now let me ask a really difficult question. I have no idea if this even makes sense, but it makes sense to my layman's mind. So many people have gotten to a metabolic point of dysfunction so extreme that they really never access their fat stores. So if they're existing in that state and they have metabolic syndrome and the body is like, yo, here's the fat. Take it. We have inflammation.  You're going to have all the energy that you could ever use, but the body doesn't know how to click over into that mechanism because insulin levels are elevated. Is the fat getting there and the white blood cells are unable to use it or that's a whole different thing and they're still able to use it? That's part of the problem. That's part of the problem. Let me use an example I used to use with my patients, the flu virus. So the virus has a barcode on it that our immune cells scan literally and say, oh, that's a nasty virus. That's the flu virus. We know this guy. We need to get ready to attack this and we need to get all of our immune system up and running and we need to make sure that immune system has enough power to do this. So what do we do? We actually make you, me hurt. Hurt to move because if we move the muscles are going to take all the energy. If you lay down, then all the energy is available for this battle to go after this virus. Our immune system literally reads barcodes to tell whether somebody is a friend or a foe. And lectins have fascinating barcodes that mimic other proteins in our body. And when this immune system is ramped up, the immune system goes around the body and looks for proteins that are lectins.  They're not quite the same, but it's close enough and we should shoot to kill and we'll ask questions later. Okay, so I'm going to walk through the process that we've just discussed because, wow, for me anyway and for anybody listening that's like me, once I can picture it, once I can understand it, then it's like I can begin to manipulate it and predict what I should do and not do. Okay, so you eat something. It could be lectins, which you'll find in the skin and seeds of nightshade vegetables is one example. Good choice. Or peanuts. Or peanuts. When you eat these things, they like glyphosate, like ibuprofen apparently. They will go in and they'll disrupt my microbiome. They break down the single, the bonds between the single cell lining of my gut. That allows either entire elements of proteins, in the case of lectins, or pieces of bacteria. I'm assuming dying pieces, dead pieces, a broken arm of- They're actually the salt wall of bacteria. It turns out when bacteria divide and they do all the time, I mean there's trillions and trillions and trillions of them, you make about anywhere from a half a pound to a pound of dead cell wall bacteria every day. And so those pieces are normally excreted with your poop. Most of your poop is actually bacteria. That's so weird. That's what it is. Now, our immune system is so afraid of bacteria. They're supposed to stay on their side of the wall. That if they see the signature of that bacterial cell wall, it doesn't know that it's not a whole bacteria, it doesn't know that it's dead. So we can take in human volunteers, LPSs, dead bacteria and inject them into your bloodstream and you will go into septic shock as if we put living bacteria in you. Whoa, because what's actually happening is my immune system is going crazy. Exactly. The immune system doesn't know any better and so holy cow, there's thousands and millions of bacteria all of a sudden in us and we've got to do something.  And so those particles, whether they're the lectins, which by the way on lectins really fast, the whole notion of thinking about plants, not as these inert things, which until starting to read you, I always did, I just thought of plants is completely inert. When you talk about them as being sort of the world's most sophisticated chemical warfareist, that's where it's like, whoa, then you begin to realize maybe what's really going on. Okay, so these lectins or particles of bacteria get into the bloodstream, immune system scans it, maybe they've ended up in the thyroid, maybe elsewhere, and it just fucking goes nuts, starts attacking, you get inflammation, which has a whole host of knock-on effects from could be cholesterol trying to patch, could be the fat wrapping around the blood vessels or the arteries or whatever the case may be. And we're now, most of us are now convinced that Alzheimer's and Parkinson's and dementia is neuro inflammation. And what people are picking up on, because they're all going to talk about the beta amyloid plaques, and you've talked about how some of the companies targeting that may actually be accelerating your onset of dementia, which is really terrifying, is that this is again the alien blaming the ambulance for a car accident. So most amyloid is actually produced by bacteria in the gut. And Dale Bradison keeps saying, he says it's not the amyloid in the brain that we should be looking at, and no wonder $40 billion of investment in anti-amyloid drugs has been a total and useless failure, $40 billion. He says because amyloid is produced in the gut by bacteria. And we know certain bacteria that make it and certain that don't, and why would we give the amyloid producing bacteria what they want to eat, which is simple sugars and saturated fats, the Western diet. Plus, the amyloid can't get out of the gut unless your gut is leaky. It's too big a protein to be absorbed. So Dale and I for years have been saying, hey guys, you're looking at the wrong spot to go after Alzheimer's. So really fast, let me ask, are you saying the beta amyloid plaques are not actually created in the brain and that they would never make their way to the brain? You won't make them unless they get to the brain and then stimulate more production. That's so weird. Why would the brain have the ability to produce something in the brain that would never be turned on unless it started from a problem in the gut? That seems way counter-intuitive. It's basically, so we now know we have a leaky brain. Okay. Meaning things are crossing the blood-bearing barrier that should not. That would have never done it. There's actually a beautiful new paper that probably explains why cholesterol and amyloid and dementia actually coexist in people with the apoE4 gene, the quote Alzheimer's gene. I got interested in apoE4, which 30% of people carry as a heart surgeon because it causes heart disease and Dale Bredesen got interested in it because it causes dementia, Alzheimer's. And lo and behold, we now know there's an intimate connection between carrying the apoE4 gene and how cholesterol can be mischievous to you and your brain and not necessarily somebody who doesn't carry that gene. What is the apoE gene, what is it doing? Great question. So it's a carrier molecule of, among other things, cholesterol. And if you carry a 4 mutation or a double 4 mutation, you do statistically have an increased risk of developing Alzheimer's. You also have an increased risk of developing heart disease. Because it changes the way cholesterol is transported. Interesting. It's more efficient? So it's getting more ambulances to the scene? It's actually worse. Let's suppose the apoE4 is a subway and it's carrying cholesterol and it stops at a subway stop and cholesterol gets off and it goes into the cell, does its thing. And the cell says, okay, I've got plenty, thanks a lot. You can take the rest of the cholesterol back and take it someplace else. So it gets back on the subway and the subway moves on. With the apoE4 gene what happens is it carries the cholesterol to the cell on the subway. But when the extra cholesterol tries to get back in, the subway doors are closed. Super clear. All right? That's the problem.


Yeah, good morning. Thanks, Nani, and the panel for this good opportunity. Yeah, I mean, it's very interesting to see some of this good number mainly coming from Africa. And now let's move a bit in the region where we are sitting here in Southeast Asia and in particular from Vietnam where International Lifestyle Research Institute, INRI, we are based and we are working in the country in the region. I would like just to add one point on the rule of livestock. You see, Africa context is very particular and when you move to Southeast Asia and Vietnam in particular, you have had very intensified livestock systems. For a country of 90 million people, we have basically 30 million pigs produced per year and the meat consumption is mainly from pork.  And the important point to make is in fact, most of this pork is produced by the small hounder basically 80% to 90% pork is produced by small hounders in Vietnam and that actually leading to some challenges in managing the topic we talked today about zoonosis and AMR. I actually visited a CP farm during the Mahidun conference this year and actually they show us very nice farm, highly, you know, high level of biosecurity. And you see, it's very nice and basically CP in Thailand, one to lead to zero antibiotics used in pig production. But when you look at the context of developing countries, it's not something that will happen very, very soon. You see, you know, 90, 80% of small farmers, they don't have this facility and mechanisms and facilities to do on this thing. So I think that, you know, it's very challenging to see how we manage zoonotic disease and AMR in developing countries. So, however, we compare to Africa, I don't know, in what context, but in Vietnam in particular from the policy point of view, we see a lot of potential and we can be optimistic in the sense that the government, they take up on this thing to develop on this, you know, national strategy and action plan to manage AMR and AMU in livestock and aquaculture sectors. So this is from the enabling environment. It's good, but the implementation, people always ask the question how we implement that at the ground level. So I think that, you know, in one of the other sessions on AMR, we discussed it and we tried to make the point so that, you know, we need to generate more evidences from the economic point of view to really convince policymakers to take action on zoonotic disease and AMR in developing countries. Because this is so crucial, this role of livestock play for the poor and for nutrition and food security and food safety in this country. You see, 10 million small households in Vietnam are involved in other countries' production and 4 million households basically are producing pigs. So this really is a huge asset from livelihood generation, so the government need to do something on that. But in another side, you cannot expect that the government do everything to control this thing. So from the research point of view, there's a lot of discussion now at the moment to go more in the implementation research. You know, generating evidences to advocate the policy is important at the same time. And in the other hand, I think that we are really having to move to a phase where we have to do research to propose some of this action measure to control zoonotic disease and AMR in the country. You see some of the data from research showing that, you know, to produce one kilogram of life with a pig, Vietnamese farmers use basically the range of 200 to 500 milligram antibiotics. It's a lot compared to our Danish colleagues, they use only 50 milligram antibiotics to produce one kilogram of life pigs. So I think that, you know, it's a really 10-time difference. And I think that the way forward is really to propose and give intervention on the incentive base, because you see the incentive is key for farmers. You see why they have to reduce antibiotics in growth promotion, et cetera, leading to the reduction of gateways, for example. And they cannot sell with this big, with higher price. So the incentive has to be considered on this intervention. A good news for you is, in fact, you know, our Ministry of Agriculture and Rural Development, and we have colleagues from DAH, from Vietnam here, and livestock development department. The regulation in Vietnam is, in fact, from 1st of January 2018. So, you know, one month ago, you are not allowed to add antibiotics in the feed at growth promotion measures. It's a very good thing. So we need to go more on the intervention from the incentive base approach. And finally, I want to make the point, this is my last point, so the one health is important. To do that, you know, you cannot do only from other countries. You need to involve other people from health and environment sectors. And to implement this one health approach in different countries, we need the capacity. And I'm glad to mention also that, you know, some of the initiatives happening for the last few years in Southeast Asia looks very promising. For example, from university point of view, you have the Southeast Asia One Health University Network. Si Hun actually is funded by USAID, where we teach students at medical, public health and VESCUN about one health. But we also go to the field to train professionals, people, from animal health level and preventive medicine level. We need to tackle at different levels, not only from university, but also from ground level, where the activity is really happening. And I think that, you know, we need to do more in terms of capacity from different levels, combining the training and also the research. I think that the research is something missing in the region. We need to do more, generating more evidences and coming up with solutions for small families. Thank you.


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And now, energy and environment ministers from the group of 20 rich nations were unable to agree on the wording of a key climate change commitment in their final communique, Italy's Ecological Transition Minister Roberto Cingolani said on Friday. Cingolani told reporters that ministers meeting in southern Italy had failed to resolve two disputed points and that these would have to be passed on to G20 heads of state and government to decide. He said negotiations with China, Russia and India had proved especially difficult, adding that one of the striking points was the wording surrounding 1.5 to 2 degrees Celsius levied on global temperature increases that was set by the Paris Agreement. The G20 meeting is seen as the decisive stage ahead of the United Nations climate talks known as COP26, which takes place in 100 days time in Glasgow in November.