Your Brain on Grains with David Perlmutter, MD

by Mike Mutzel


Mike Mutzel: Welcome back, everyone. If you can hear us, it would be great if you can make a chat just to make sure we sound okay and we sound great to you and all that. We’ll get going here in just a few minutes. Dr. Perlmutter does have a presentation lined up, but we want to make sure that we can answer all the questions that you do have. You can raise your hand, hit the hand-raising button, and we can unmute you towards the end. Alternatively, you can type in a question and I will do my best, and so is he, to address that personally. Questions that we don’t answer, hopefully, we can get that later – maybe answer them on Facebook or on Dr. David Perlmutter’s website. So are you pretty excited, Dr. Perlmutter, for the book release?

David Perlmutter: Very excited. It’s breathtaking what’s happened with Brain Grain. Here we are 13 days before launch and it’s getting as much attraction as it is. You know it’s very interesting. This is Alzheimer’s awareness week, and I’ve been watching the news, watching all the failed attempts to create a treatment for a disease that is preventable. So it really just makes you scratch your head and wonder about the misplaced priorities in healthcare. So, very interesting. I think what we’ll talk about in getting started here is really what are the fundamentals of brain degeneration, so we’ll start off with that.

Mike Mutzel: Well, I know we have a big football evening going on today, Broncos-Ravens. How do you feel about high-contact sports and the association with myocardial impairment and all that?

David Perlmutter: I think there’s no question that those issues are real and important and the brain is a very, very delicate organ, and you can’t accept things like stingers, and those types of events I think you’re going to get away with it, and those types of traumas are permanent and are cumulative. That’s non-acceptable to me – an occupational hazard. But let’s do an intro and then we’ll get everybody started. It looks like everybody’s signed in.

Mike Mutzel: Welcome back, everyone. This is Mike Mutzel and Bettina Newman. I’m very excited that you could join us tonight. We have an awesome presentation lined up. We are honoured to have Dr. David Perlmutter, Chairman of the Xymogen Board of Advisors, and board-certified and internationally recognized neurologist. He speaks for many prestigious organizations, domestic and internationally, IFM and A4M, and is a fellow of the American College of Nutrition. He earned his MD and residency in neurology from Miami School of Medicine, and he has authored many books in the field of neurology, including the “Better Brain” book, “Power Up Your Brain,” and “Grain Brain,” which we’re all excited for its release on Tuesday, September 17th. Dr. Perlmutter, welcome.

David Perlmutter: Thank you, Mike. Let me just move right ahead if we can because we are going to pave the way for an understanding right off the bat about the fundamentals of the science of brain health and brain disease. I think the first question that we really want to ask is, “What is it that actually leads to brain degeneration?” What causes brain degeneration? A very simple question on the outside, and ultimately, what you’re going to learn is that it’s actually very simple on the inside that these issues that are fundamental to brain degeneration are not very exotic and esoteric. Let’s take a look at that as we move forward. So the reason this is important is because in the New England Journal of Medicine in April of this year, the RAND corporation published this report in the New England Journal showing that we’ve got a big problems in our hands when it comes to dementia. We’re spending about $50,000 a year to care for patients with dementia, and this is about 15% of the population over the age of 70 years, and it’s 50% of the population of those who lived to be age 85 or older, and that’s the most rapidly growing segment of our population today. What do these numbers mean in comparison to other issues? Well, we’re spending about $200 billion each year in taking care of patients who have dementia. I want to contextualize that for just a moment because when you look at what we’re spending on heart disease and what we’re spending on cancer, dementia is costing us twice as much as the ever popular heart disease and triple what we’re spending on cancer care. So, we really have to put this into perspective – just from a monetary perspective, it’s a very, very big and underrated issue. Dr. Prichard published in the Public Health this year is a valuation of the top of the most populous 10 countries, and look at the cause of death between 1979 and 2010, and what he found was really quite amazing and that is that the most rapidly expanding cause of death in Western culture is neurological disease. Beyond that, deaths from brain disease increased 66% in men and 92% in women in the one country that leads the pack in terms of death from brain disease, and that is the United States. This is at a time when deaths from other causes are actually declining, and what Dr. Prichard said is this is in sharp contrast to the major reductions in death from all other causes. And what’s really alarming is it is starting earlier and affecting people under the age of 55 years. For all of you, that’s younger than I am, and that this stuff is happening. I’m seeing patients in my practice every single day, younger than I am, who are now experiencing brain disorders with cognitive decline for which there is no pharmaceutical fix. So it’s really very, very important that we try to get our arms around the notion of preventive medicine as it relates to brain health. Well, here is our continuum that we’ve developed of what the science currently is telling us what ends up leading to Alzheimer’s disease. Early on, there’s inflammation in the brain; this produces damaging chemicals that we call “free radicals” that ultimately kills brain cells; and specifically, in the Alzheimer’s patient early on, these are brain cells that produce a chemical called “acetylcholine.” So the pharmaceutical companies in the Western have created a drug that actually reduces the breakdown of acetylcholine in hopes that might give people an edge or exception from Alzheimer’s disease. These drugs called “anticholinesterase” actually lead to supposedly an increase in the amount of acetylcholine in the brain, but really, when you realize how important all the antecedent events are, treating the lack of acetylcholine is definitely focusing on the smoke and ignoring the fire. We have to pay strict attention to those things like inflammation, free radicals that lead to the death of brain cells because those are our leverage points if we are going to prepare a program to actually reduce the prevalence of these types of diseases, not worry about what we can do to fix it once the cow has gotten out of the barn. Because by the time that acetylcholine is decreasing, the cow has been out of the barn for a long time; it’s already probably moved to Los Angeles and is making cheap folic commercials. So, we need to look at these factors – inflammation and free radicals – that lead to the death of cells, and ask ourselves, “What are these factors then that lead to this event?” Because in Parkinson’s disease, it’s the same scenario – we have death of brain cells that ends up on the right side of the screen with decreased dopamine, and we give dopamine – we give drugs that are pure dopamine or dopamine-like drugs to treat the disease while we ignore its causes. Again, focusing on the smoke while we ignore the fire. So again, this is a preventive medicine approach, which has so much attraction in terms of being economical, and as well as very functional in terms of reducing a person’s risk for these devastating conditions. We have 5.4 million Americans now that have Alzheimer’s disease, a disease for which there is no meaningful treatment and certainly for which there is no cure. If you want to be reinforced in that contention, watch the evening news all week this weekend. Tomorrow night again on evening news, you’ll see reports about the latest, greatest attempts to treat the disease after it has begun, and I’m offering up tonight an understanding on what we can do, in the first place, to keep it from happening.

Well first, let’s focus our attention on free radicals. Now, we are all familiar with free radicals. If you’re not I’ll give you an example. Free radicals cause something that’s called “oxidative stress.” What oxidative stress is all about is basically – here’s an example – if you took a piece of iron and put it out in the weather, after several days, what happen to that piece of iron is it would oxidized, it would rust. That’s the exact same process that’s going on in our bodies because of the action of free radicals, and our bodies are loaded with free radicals. So, this is what damages are – fat are protein and even damages our DNA, our code of life; it violates the code of life.  Normally, our bodies produce a way of getting rid of free radicals, and those are what we call “antioxidants.” This is, of course, the reason that everyone is taking the latest and greatest antioxidant, whether it’s a berry that was discovered in some mountain of a newly discovered island in the South Pacific, or it is some great new vitamin that’s being marketed. This is the reason that we take antioxidants – to reduce the damaging effects of this process – oxidative stress caused by the production of free radicals. Oxidative stress is the action, the damaging effect of free radicals on our tissues. Now, the medical literature dating back 15 years (in this case, 13 years) looking, measuring the correlation of the damaging effect of free radicals in a disease like Alzheimer’s has demonstrated to us (in this case, from the Journal of Neurology, which is probably, arguably the most respected neurology journal in the world) showing that if you look at the brain of an Alzheimer’s patient and measure the damaging effects of free radicals, it is dramatically increased in comparison to those Control, a patient who had diet obviously, and they measure the damaging effect of free radicals in those individuals. So, this really points a very well-substantiated finger at the role of free radicals in terms of damaging brain tissue. In fact, in 2007 in the same journal, we learned that the damage to lipids and proteins, and even DNA and RNA are early events in the dementia process in a characteristic called “mild cognitive impairment,” meaning that you begin to be cognitively impaired; you don’t have full-blown Alzheimer’s, but you can be sure it’s coming, it’s down the street. So people talking about MCI or mild cognitive impairment, and that’s the type of thing that is experienced when people go into the room and forget why they went there, can’t follow a conversation, begin to really lose things more aggressively, can’t find your keys, begin to become forgetful of names, and this is what we call mild cognitive impairment. We kind of laugh it off by saying, “Well, these are just senior moments” and everything’s kind of funny, but in reality, mild cognitive impairment is a harbinger to very pernicious things to come.  What it’s telling us is that these free radicals play a pivotal role in the pathogens of Alzheimer’s, that this oxidative damage, the action of free radicals, the rusting if you will, is an early event in Alzheimer’s and can serve as a therapeutic target to slow down the progression or perhaps (if here’s best part) the onset of the disease. In a nutshell, what it is saying is if we could target free radicals and reduce oxidative damage that might keep the onset of the disease from happening. And here we are back in 2007, that’s pretty exiling that the well-respected journal in neurology is telling us we’ve got to pay strict attention to oxidative stress because this might be a powerful leverage point, so that we don’t have to hope that medical science is going to deliver us a cure for a disease that could have been prevented. The onset of disease prevention of Alzheimer’s. Again, this is why antioxidants are so darn important because they help to quench these damaging free radicals that are not only damaging fat protein, but also damaging our code of life – our DNA. That said, years ago (way back in – I think 1989 or 90. Oh, that’s actually 2002.), this report came to us from Dr. Schults in the general archives of neurology. So that you know, that is a journal put out by the American Medical Association, and what they did was they took two groups of Parkinson’s patients – half of them got a Placebo and the other half got an antioxidant to combat free radicals and that was called “coenzyme Q10.” Incredibly, after one year, they evaluated how did patients do, and this is a scale that determines disability. It’s called “Unified Parkinson’s Disease Rating Scale.” I don’t mean to be too technical, but the lower on the scale that you are, the more functional you are; the higher you are, the more difficult that you have with activities of daily living, dressing, cooking, walking, thermal rigidity, and all those types of things. And there was the dramatic reduction in the way the progression of those individuals who have the highest level of this simple, non-prescription antioxidant called “coenzyme Q10” on board during the one-year period – a 48% reduction in the ray of worsening in Parkinson’s patients just because they took an antioxidant. So, if any of you out there are dealing with Parkinson’s or there’s somebody in your family or healthcare provider treating Parkinson’s, it’s important to understand that, in general, when people go to the doctor and get a Parkinson’s medication. Again, think back – that’s treating the smoke, it’s not treating the fire; it’s treating the symptoms, but it’s ignoring the underlying disease process. I really think it’s important that patients get the opportunity to have both of those issues addressed. Here’s what they concluded: “In our study, coQ10 in the treatment of high dosages was safe, well-tolerated, and reduced the worsening of Parkinson’s, as reflected in this UPDRS scale.” Therefore, here’s a great conclusion – it would be premature to recommend its use – which I love. I think it’s important to know for you healthcare providers that many drugs that we commonly use actually desperately deplete coenzyme Q10. Now, almost everyone these days understands that the statin medications are a prime initiators of depleting the body of coenzyme Q10, to the extent that, I will say in our practice that everybody who’s on a statin drug (and I will tell you, that number is dwindling) is put on coenzyme Q10 because those drugs diminish the body’s production of coQ10, turns out that the production of cholesterol which, I happen to think is a wonderful, good thing for the body and specifically the brain, the enzyme that is a key player in the manufacturing of cholesterol happens to be the same enzyme that manufactures coQ10, and the drugs disrupt that enzyme. Yes, you get less cholesterol formation, which I don’t believe is a good thing either because it is actually damaging to the brain as we are now all seeing, but you also get a significant drop in coQ10. At the very least, if you’re going to use any of these drugs, beware that coQ10 levels, a desperately important brain antioxidant, are going to decline, so you need to keep that coenzyme Q10 level up to snuff.

Let’s look again at free radicals – what causes them – and generally, what we talked about and what we, I say, we parenthetically see these unknown factors out there. Even to this day, most medical literatures are saying, “We just don’t know what’s causing these increased free radicals.” But if you dig a little deeper, you’ll find it out that in fact, it’s very clear what some of these factors are, and there’s absolutely modifiable.

If we identified some of these factors that lead to increase free radicals, could that help us, for example, prevent Parkinson’s? Let’s take a look. It’s been known for a long time, at least the past decade (Actually, I lectured about this about 15 years ago and wrote a paper on it for the council of medical doctors and patients), that exposure to pesticides and solvents is a dramatic risk increaser for getting Parkinson’s. The notion that she was, “I don’t know why I got it,” “Now, I’m shaking, and I can barely walk,” “Why did this happen,” “No one knows,” is really not holding water anymore. Nonetheless, that is the party line. Well, we don’t know why you got to take these and hope for the best, because this was published by the American Academy of Neurology and was just published earlier this year. What did they find? They looked at a 104 case-control studies, more than 3,000 literature citations, and what did they find? That indeed, what we’re doing to ourselves, by exposing ourselves to things like pesticides, herbicides, insecticides and solvents dramatically increases our risk for this disease for which there is no cure. So the notion that Parkinson’s is what we call idiopathic, meaning we don’t know the cause, meaning I, the doctor, I’m an idio because I don’t know the pathy or pathology, is really not what the peer-reviewed literature is telling us. As a matter of fact, if you look at the bottom of this, mancozeb increases the risk of Parkinson’s by a 118%. Well, when I read this report, I have to admit to you that I wasn’t really sure what mancozeb was. Well, I kind of am sure, but just for the purposes of our discussion. Let’s take a closer look at mancozeb; I really did know. Where would you go these days to learn about something? Well, you’d go to the internet and you would go to Wikipedia. It turns out that mancozeb is something that’s used in the experimental laboratory to create Parkinson’s in the primate model. So they give this toxin to primates and then they induce Parkinson’s in these poor animals. And then what happens is they use these animals, of course, to test the drugs because this is a very, very dangerous chemical. I decided to look a little bit deeper on what is this mancozeb stuff, and I again, went to Wikipedia. I found that this is actually available on Amazon and in garden stores; it’s a fungicide that you’re supposed to put on your vegetables in your vegetable garden. This is, according to the Journal of Neurology, associated with the 118% increased risk for Parkinson’s disease, a disease for which there is no treatment. I guess you guys are getting where I’m going with this that there’s a lot of stuff going on out there that we’ve got to pay attention to. These “unknown factors” are actually in fact quite well-known. These ideologic factors, these causes of our most dreaded diseases are in fact well-known and well-described. Again, the two key players here, the leverage points that we’re going to develop this evening and the next four and half hours (just kidding) are inflammation and the downstream effect of inflammation on free radicals. Here is one of the unknown factors – glucose. Can you imagine? Blood sugar is a direct initiator of inflammation and increases the production of free radicals. A couple of others things that we may have a chance to talk about, Mike mentioned earlier a head trauma for those of you who have been a little bit early, and also, it turns out the gluten, in individuals who are sensitive, is a powerful upregulator, as you may expect, of inflammation, and it can affect the brain. Gluten sensitivity can cause inflammation to brain.

Let’s focus then on our next segment, which is going to be “What is the role of glucose in terms of increasing inflammation?” In fact, sugar representing a powerful brain toxin because indeed, the blood sugar that you measure when you go to the doctor is directly related to the sugar that you consume. There’s no surprise there. Carbohydrates that we consume dramatically increase blood sugar and as such play a pivotal role in increasing the inflammation and free radicals. Let’s jump into that with both feet. Last month, believe it or not (how up to speed our weight), in the prestigious New England of Medicine, a powerful article appeared that related glucose level to risk of becoming demented. A big study over 2,000 individuals, 76 years of baseline, followed these individuals for almost seven years. Here’s what they did – when they started the study, they measured their baseline glucose, “What is your blood sugar when you start this study? And then we’re going to follow you every two years for an average of 6.8 years, and every two years we’re going to test how swift is you are demented.” What they found is quite remarkable, that there was a significant increased risk of dementia in direct correlation with blood sugar. And what was really dramatic is this was happening in nondiabetics. You know we people understand that perhaps diabetes plays a role in dementia, knowing that in fact, if you are type 2 diabetic, you double your risk for Alzheimer’s, but that said, even our blood sugar is 105 and 110 that most doctors are going to tell you, “That’s totally fine. Don’t worry about it,” you are already increasing your risk for becoming demented.  Again, what we talked about or we are told that these are unknown factors that we just don’t understand; there’s no literature that describes what are these factors that lead to brain degeneration. With all due respect, that’s not true. This is the New England Journal of Medicine; it’s put up by Harvard, and this was published almost to the day, one month ago. This was what the literature is telling us – these are not high blood sugar levels. Here’s what they stated: “We found that increased risk was associated with higher glucose levels even at the lowest end of the glucose spectrum among people who had not received a diagnosis of diabetes. In conclusion, our data provides powerful evidence that higher glucose levels are associated with an increased risk of dementia.” Now, I could end this discussion here. That is a powerful, powerful take-home message. It is not only powerful, but it is empowering because it is actionable. It is actually actionable because your blood sugar is totally under your control; it is based upon the food choices and to a lesser extent, the exercise choices that a person makes. Higher blood sugar from eating higher carbohydrate food raises your risk of dementia; it raises your risk of brain degeneration. Now, what part of the brain degenerates? This study published in the Journal of Neurology just came out last year, and it shows again that the higher your level of fasting sugar, the more you will have atrophy or loss of tissue in the hippocampus, which is the brain’s memory center; that’s the first place that goes when you have Alzheimer’s, that’s where you focus your attention when you’re looking at an MRI scanner of a person with Alzheimer’s.  So, having a higher fasting glucose – again, not to any level where people are going to be saying that you are in trouble or have diabetes – is already associated with hippocampal atrophy or actually, your brain’s memory center. Here’s what they did – again, they took 266 cognitively healthy adults, and they measured their baseline blood sugar, they looked at their brain scan and measure the size of their memory center, and then they brought these same people back four years later. And low and behold, those individuals, who had the highest fasting blood sugar at the onset of the study, had dramatic shrinkage of their brain’s hippocampus. This is a very, very powerful curve, that even at low levels blood sugar, even at a 108, they’re already having issues. Look at this curve, I mean, you can have a blood sugar of a 108, 110, and you’re already are in trouble; your hippocampus, your brain memory center is shrinking. Glucose levels are found to be significantly associated with shrinkage of your hippocampus, your memory center. You can argue the point about “Size doesn’t matter,” but I can assure you, that when you’re dealing with the hippocampus, the size is everything; there is a direct correlation with the size of the memory center and the functionality of your memory. Why does this happen? What is so darn damaging about glucose? Glucose in your blood stream binds to proteins, and we call this process “glycation.” I really want you guys to stay with me on this, understanding that when I use the term “glycation,” I’m talking about your blood sugar binding to your proteins, and that includes one important protein called “DNA,” not just the proteins that hold things together like muscles. It turns out that when glycation occurs, this powerfully upregulates or enhances not only inflammation, but the damaging effects of free radicals or what we call “oxidative stress.” So here is the mechanism by which we ultimately kill off brain cells, and we begin to forget where our keys are. That said, foods we eat determine whether or not we’re going to lose our keys. I guess that sort of makes things easy to understand. So again, food choices are fundamentally important. Now, what is the evidence that glycation is related to inflammation and free radicals? That was published back in 1998, but this is really a cornerstone that when you glycate proteins, it has a huge effect in increasing inflammation and increasing free radicals – the cornerstone of things like Alzheimer’s disease. Glycated proteins increase inflammation and free radicals by as much as 50 fold as we learned in this study published in 1999. When you glycate a protein, when you bond it to sugar because your sugars are elevated, the production of these damaging free radicals increases 50 fold. Wow. So you really want to know what can you do to reduce this process. Well, how do we measure glycated proteins? You’re going to be surprised to learn that it’s actually very simple. You don’t need some sophisticated laboratory study. There is a test that anybody’s doctor can do, and if any of you on tonight are diabetic, you are totally familiar with the blood test called “hemoglobin A1c.” If you’re not diabetic, it’s a good test to get from your doctor because it’s a measurement, yes, of your average blood sugar. But beyond that, hemoglobin A1c is a glycated protein; it’s hemoglobin – that’s the protein within your red blood cells that carries oxygen, and the A1c part means it simply measures how much sugar is bonded to the hemoglobin and basically, it’s used as a test to measure your average blood sugar over a three- to four-month period of time. But now that you understand that this is a glycated protein that can increase free radical production, you begin to understand that hemoglobin A1c is a powerful marker of brain aging. Here’s a study published way back in May of 2005, and it correlated the degree of brain shrinkage based upon the hemoglobin A1c. Now, most doctors will tell you that, “Your hemoglobin A1c is 5.8-5.9 – no big deal. Don’t sweat it. We’ll check it again in a year or two,” but as you can see by this study – again, published by the Journal of Neurology, perhaps again the well-respected neurology journal – when your hemoglobin A1c is in 5.6, 5.8, 5.9, your brain is shrinking rapidly. Why? Because you’re glycating your proteins, your blood sugar is binding to proteins because you’re eating too much carbohydrate, and it’s leading to free-radical formation that ultimately kills brain cells, and your brain shrinks. Now, this is a graph showing the degree of brain shrinkage based upon carrying the so-called Alzheimer’s gene that you can’t control, and I will tell you that the degree of shrinkage of your brain from having elevated hemoglobin A1c far exceeds the rate of brain shrinkage from carrying the Alzheimer’s gene, and you can do something about this. So, if you happen to know that you carry the APOE-e4 gene, you say, “Oh my gosh, my brain is shrinking. What am I going to do?” Know this – know that the degree of brain shrinkage from having elevation of the A1c is far in excess of carrying the gene and, these things are additive. So if you’ve got the gene, by all means, you’re going to do everything you can to take all the straws off the camel’s back. If you look at the subtitle of my new book, it is a surprising truth about wheat, carbs and sugar. Carbs and sugar are your brain’s silent killers. It’s not just that Dr. Perlmutter’s doing this webinar with you tonight and he happens to think that’s the case. What I’m doing tonight, what we did in this new book is made these statements and backed it up with the most well-respected peer-reviewed science that is available today and 2013. Because we glycate our proteins based upon the foods that we are told are good for us; these foods are very, very high in sugars – and everything’s low-fat, and nothing could be worse for your brain; your brain needs fat, but these foods are high in sugar and truthfully, fructose, which means high fructose corn syrup, which you’re looking at right here, is a far more glycating sugar (monosaccharide) than glucose. And fructose, as a high fructose corn syrup, has become the No. 1 sweetener in America today, coming from corn, basically because it gets back to the Kennedy administration when we attacked Cuba and we no longer get sugar from sugar cane, we had to develop other ways of satisfying our sweet tooth, so we turned to corn. That’s not a political statement; this is a statement of historical about fat. Again, when we target ourselves with high-fructose containing foods and other carbohydrates like you’re looking at, we get into big trouble; our hemoglobin A1c goes up, we glycate our proteins, it increases free radical production, and that’s bad for the brain. Look at the size of the hippocampus in a patient rather in patients who are diabetic versus those who are not diabetic. That’s very graphic, because by enlarge, lows diabetic or type-2 diabetics, and those individuals by enlarge, have type-2 diabetes because of their lifestyle choices. So that’s what I’m talking about tonight, and it’s not about any necessarily any magic supplement, or any magic pharmaceutical or intervention, it’s about getting the word out that to prevent these malicious events from occurring in the human body and specifically in the brain, people have to start understanding that the cornerstone of total body degeneration, including the brain, heart, immune system, and even related to cancer, has to do with the overabundance of carbohydrates in our diets. So, we are told low-fat this and low-fat that; by default, the calories are filled in with carbohydrate. Should we take drugs to make sure we do not become diabetic? Well, this study was also published in the New England Journal of Medicine – the most, I would argue, one of the most prestigious medical journals on the planet – and this is already 11 years ago. They gave people the standard drug, who were non-diabetic, but have a slight elevation in their blood sugar; they gave them a drug called “Metformin,” or they said, “I’ll tell you what – we’re going to cut your calories, and we’re going to ask you to exercise 150 minutes every week.” That might sound like a lot, but in reality, that’s about 22 to 23 minutes a day; no big deal. They followed these people for up to three years or so, and they determined who got diabetes. And the reduction – both groups reduced the risk of diabetes – no question. If you took the drug, 31% decreased risk for becoming diabetic; but if you didn’t take the drug, your risk went down by 58% just by changing your food and getting a little bit of exercise, by not taking the drug. You know it seems easier – why don’t you just take the drug and be done with it? Well, who died? The deaths in the Metformin group were dramatic. If you just took the placebo, your death rate was 20% lower than Metformin, the drug group. If you did the lifestyle part where you changed your diet and exercise, your risk of dying was cut in half compared to those individuals who took the drug to reduce their risk for diabetes. So, above all, do no harm – and the above-all-do-no-harm part of this is – let’s tell people what they should be eating and, let’s encourage them to exercise. Primum non nocere – above all, do no harm. Well, you wouldn’t have a can of cola for breakfast, would you? Because that is a huge carbohydrate load; a can of cola has 39 grams of carbohydrate – that’s breathtaking. You know in Grain Brain, we’re trying to keep people’s total daily carbs limited to 60 to 80 daily, so you already hit half your carbs just by drinking the can of cola. So what would a better choice then for breakfast? What would people generally have in breakfast? And typically, what people have is a glass of orange juice; a glass of orange juice has 36 grams of carbohydrate – that’s 9 teaspoons of sugar. So what are you gaining then by drinking a glass of orange juice and not having a coke? Really nothing. You’re giving yourself 9 full teaspoons of table sugar just by drinking the can of orange juice. So, what should you drink? Maybe it would be better (You know where this is going.) if we all drink artificially sweetened beverages because that will help us lose weight. Well, this study was published in the journal called “Obesity” back in 2008. They followed 3600 adults for eight years and marked how much of these artificially beverages they consume, and then followed their instances of becoming overweight or frankly obese, and looked at their body mass index. Body mass index is various measurements that are compiled basically to tell you how much fat you are retaining. Here’s what they found that’s really quite interesting – if you plot the number of artificially sweetened beverages per week against the change in the body mass index, it is dramatic. Now, in the middle of this, you see this is showing you how much weight you’re gaining just by sucking down artificially flavored and artificially sweetened beverages. Let’s look at the middle curve here – 3 a 10 drinks; 3 a 10 diet drinks – that’s an awful lot. That’s about one a day. “I always have my diet coke at lunch,” people will say. This is what’s happening. It’s not just becoming obese. Look at this conclusion: “We observed a classic, positive dose-response relationship between consuming these beverages and long-term weight gain.” So, you’re not gaining anything by drinking diet drinks. Well definitely, you would expect that if you drink sugar-free beverages, artificially sweetened beverages. At the very least, it would reduce your risk of becoming diabetic, a disease which doubles your risk for Alzheimer’s. And here’s what they did: This is a 14-year study over 65,000 women and again, they measured their consumption of artificially sweetened beverages versus those who drink sugar-sweetened beverages, and tried to determine who got diabetes and who didn’t. The first thing they looked at were people who just drink standard cokes and things like that, and looked at the dramatic increased risk of becoming a diabetic. So, is it better then to consume artificially sweetened beverages? Here’s what the curve looks like. That’s sugar-sweetened beverages there, and this is the curve for artificially sweetened beverages – much more dramatic. You dramatically increase your risk of becoming diabetic by drinking sugar-free drinks. The reasons for this are a bit complicated, but what NutraSweet, aspartame does is it specifically damages the part of the brain in the hypothalamus that tells us we’ve eaten enough. So the more of these drinks that you consume, the less you are able to push away from the table. At least, that’s one of the reasons because that’s been studied.

What about blood sugar and cancer? I think it’s important to understand this. This is a study from Korea, looking at the males and females. They measured their blood sugars every two years, and a dramatic increased risk of dying from cancer directly correlated with your fasting blood sugar in males and here is in females. This is a big, big picture. It’s not just that you happened to have diabetes or you happened to have a slight elevation of your blood sugar, the implications of a higher carbohydrate diet and low-fat are profound. A dramatic increased risk of cancer in men, and 235% increased risk in women. And it’s modifiable – it’s modifiable based upon the lifestyle changes that we make, basically upon the foods that we eat.

Mike, how much time do we have left?

Mike Mutzel: I’d say about five more minutes, then we canstart getting into questions. How does that sound?

David Perlmutter: Oh, my gosh. Let me see where we’re supposed to go. What I’d like to do – let me go ahead and start with questions. I think this may be a great time for that.

Mike Mutzel: Sure. Just one second here. Alright. A lot of questions came in about vegetarians, and I know that this is very a low-carbohydrate diet, and that would may be imply more fats and meats, and such. What would you advice for vegetarian and/or vegan folks?

David Perlmutter: Absolutely, that’s a wonderful question. Vegan diet, vegetarian diet – these are excellent, wonderful, healthful diets. The only thing you have to be careful of – actually, there’s several. A high-fat diet is certainly consistent with being vegetarian – high fat, low carbs – because fats are things like olive oil, nuts, seeds, avocado, coconut oil. When you add those to your diet, you are adding in life-giving, immune-enhancing brain-protective, heart-protective wonderful fat. So, a vegetarian diet, a vegan diet – these are all things that you can eat that are wonderful. When I’m talking about a high-fat, low-carb diet, I’m not saying that we need to be sucking down the pork rinds from a local convenient store. There are absolutely bad fat choices that people can make. If you choose to eat beef, I really and strongly in favor of making the choice for grass-fed beef because frankly, commercial beef that people get, and one of the reasons that beef took such a hit in New England Journal, took such a hit in Dr. Crandall’s book, “The China Study,” is because most meat that people eat is very, very worrisome. When you create cattle that have been fed on soy, corn and other obviously genetically modified grains, very high in pro-inflammatory omega-6 fats, you are absolutely paving the way for our most devastating conditions including brain issues that we’ve talked about and cancer. So, he was absolutely correct. That said, understand that for 99.9% of our existence on this planet, we were hunter gatherers; we would kill things, and we would find things on the ground and eat those things. And those are the kinds of foods that have served an influences to select out our current geno, that our DNA that we have today that we carry has been given to us from a 2.5 million years of evolution based upon those foods being available. The other things I would let vegans and vegetarians know (They probably know this.) is to ensure that they’re going to get adequate amounts of B12. Now, most good diets don’t require a huge amount of supplementation, but without eating meat and eating vegetables that have been washed and don’t have dirt all over them, we’re really not going to get B12; it is something you might want to have checked with your doctor’s office, and if in fact it’s low or even mid-range, I would consider supplementing with B12, and also with vitamin D. Again, we make vitamin D out of a very strange chemical in human physiology. It’s not just you go to the sun, and the sun makes vitamin D; the precursor for vitamin D, the raw substance from which we make vitamin D is something called “cholesterol.” So again, we have to wonder about this bad rap that cholesterol is getting, but veganism and vegetarianism – wonderful approaches to being healthy.

Mike Mutzel: Fantastic. With regard to ages, I know another way that we can get advanced glycation in products is from cooking method, and I think that’s something that is under-recognized. Can you look into that a little bit? If someone were to cook these healthy, grass-fed beef and wild-cut salmon and stuff, how do you feel about heat and frying versus growing? What’s your favorite cooking method?

David Perlmutter: So again, to clarify, ages (A-G-E) means advanced glycation in products, and it’s an acronym that stands for, again, the binding of sugar to protein – the process of glycation that we talked about earlier – the browning of meat and fish, etc. that is caused by the glycation of the surface proteins in those foods. So, that’s why it’s really better to now reduce heat, and don’t go for medium-medium, well and well-done, you want to undercook foods – the higher heat, the more glycation happens. That’s actually a very, very good question. So generally, fish is baked. Actually, my wife cooks it, but my favorite of eating (That’s what I contribute.) is fish, for example, done in an egg wash, and then covered with almond flour, and then cooked in olive oil. Another thing to keep in mind is getting the habit of using a wok because a great way to cook your vegetables a little bit of oil in the bottom of the pan just to get things from sticking, but then the water that’s released from the vegetables once they start to cook really just ultimately helps to cook them, so you’re basically steaming in the wok. The notion of a layer of oil in frying the food is creating some damage to the delicate fat in the olive oil or whatever you use to cook, and that creates some set of problems. So, baking is a great idea.

Mike Mutzel: That’s great. I love to cook fish that way as well, interestingly. Let’s talk about carbohydrates. You recommend up to 60 at most 80 grams of carbohydrates was the notes that I took. Are we talking sweet potatoes CMs, and where are this carbs coming from?

David Perlmutter: Well, sweet potatoes CMs are certainly high-carbohydrate foods. In general, to make it easier to most people, we tend to favor vegetables that grow above the ground as opposed to the lower-ground vegetables like you mentioned, like white potato and beets, because those vegetables really, they’re survival depends upon them storing carbohydrates in the form of starch. So if you want to load up with carbs, those are what you’re going to want to eat. Even above-ground vegetables are going to have some carbohydrate, and you may include an apple a day or a handful of blueberries or something along those lines. So, you’re going to get carbs along the way. There’s going to be a little bit of lactose sugar and cream in your organic coffee, etc. You just have to be careful and obviously get a sense of the carbohydrate load in all of the foods that you’re eating and most importantly, not just the total number of grams of sugar and grams of carbohydrate, but I think it’s really important to get a sense not only how high blood sugar will rise from a particular food, but more importantly, how long it’s going to stay elevated. The longer it’s elevated, the more that glycation causes happens. And we measure the degree of this process by looking at what’s called the “glycemic index.” The glycemic index takes into account not just how high your blood sugar will go from eating a hundred grams of a particular food, but how long it will remain elevated. In the drperlmutter website (it’s drperlmutter.com), we actually have a wonderful glycemic index of a variety of foods. You can look at it and learn.

Mike Mutzel: Fantastic. We’ll make sure to email that out to everyone. A lot of people are asking about the recording. We will definitely get this recording out to you tomorrow. Quite a few questions, Dr. Perlmutter, came in about the ideal postprandial or fasting blood glucose, and also hemoglobin A1c. Where are we really shooting for for prevention of these devastating neurological disorders?

David Perlmutter: It’s time to rewrite the books. When you look at the data that was just published that I showed you from last month from the New England Journal of Medicine in August 8th, it is a wakeup call that we’ve been led to believe is normal is actually way too high. Lab values for normal are derived from what is ultimately what was average after they took a large group of people, checked this and that, whether it’s sodium or glucose or whatever they are measuring, and then they would determine what is the average, and then two standard abbreviations in either side of the bell curve would be considered the normal range. That has nothing to do with what is ideal, what is best for health. What we’re leaning now is that we’ve been way off in terms of blood sugar. And really, once the blood sugar is over, even 95, that starts to be an issue according to our latest science, so I’d like to keep blood sugars mid-90s or lower and hemoglobin A1c 4.8 to 5.2 is the range. I make that statement based upon the curves that I showed you about the degree of brain shrinkage that dramatically increases as we increase glycation of proteins, and that’s why that is such a valuable marker.

Mike Mutzel: Fantastic. We do have quite a few live questions, and only a few more minutes here. But before we get into live questions, I just want to make sure that everyone’s aware that you can essentially get a free copy of the book purchased from any one of these vendors – Powell’s books, Barnes & Noble, Amazon, etc. – and then get that receipt emailed over to grainbrain {at } xymogen.com. If you’re a wholesale customer, you will get the dollar equivalent and then some aback. Such a great way to start with the book and for those of you….

David Perlmutter: People are making money buying the book – that’s pretty interesting.

Mike Mutzel: Right. It’s amazing. I’m really excited to get that two weeks from Tuesday. Just in case people, Dr. Perlmutter, we made it on a little bit late. You talked about that prior to this release, it’s already the top 3 selling right on Amazon today.

David Perlmutter: Yeah. It is breathtaking that Brain Grain is the No. 1 book on Amazon right now in dementia, in neurology, and even in Alzheimer’s. I think it’s very, very exciting because I think it’s going to be a paradigm changer because it’s telling people that they can be empowered – to do things, to reduce their risks for these diseases that are so devastating and for which, there is no treatment. In a sense, it’s pretty breaking new territory. I really believe the mission of writing that book was, “Okay. Make these statements, but you darn well better be able to back the mob with the science,” which was what we did. When you write a book, actually, one of the most disenchanting aspects of it is that after the fact and all these articles coming that are published that are saying exactly what you said, but you couldn’t include it in the book like that last New England Journal of Medicine article was over the top. It’s non-confirmatory in terms of our thesis that carbohydrates are damaging. I would have loved to have included that, but such is a nature of hard print.

Mike Mutzel: Well, I guess that’s a good thing your Facebook is very active. I know you post amazing articles and updates, so that’s such a great way for you guys to stay in tuned with that. I will email you the archive tomorrow a link to Dr. Perlmutter’s website and Facebook, so you can follow the conversation there.

David Perlmutter: I’m dialled in. Let’s do it.

Mike Mutzel: Alright. Hey Ann Klein, you are unmuted. Please do have a question. Some people get stagefright here. We’ll just go nonetheless. Anthea Noonan – okay, no.

David Perlmutter: These are tough questions. I have to tell you. I’m speechless.

Mike Mutzel: Hey Carla Moosa, you are live. Carla, you might need to speak up a little bit; it’s hard to hear you. Carla – you are not speaking in the microphone from what we can tell. Okay – that sounds great.

David Perlmutter: I got you.Yes, go ahead.

Carla Moosa: Is there a difference between taking the ubiquinol or the coQ10 because the study showed coQ10 at 1,200 mg, which might be higher than what is necessary because the ubiquinol is the more active form?

David Perlmutter: You make a very good point. I would say that the study that I demonstrated is certainly in extreme. I mean, I think I’m getting feedback, but recommending 1,200 mg of coenzyme Q10 is a lot. It’s not only a lot of coQ10, but it’s also very expensive. So what I like to do is – we generally don’t use that level of coQ10, but we use other balancing antioxidants along with it that can help salvage the coQ10 and can augment its activity – all the things like n-acetylcysteine, acetyl-l-carnitine, and alpha lipoic acid. That’s the big 4 in terms of brain health. That’s actually a very good question. Thank you.

Mike Mutzel: Thank you so much, Carla. We have a lot of questions, so I’m trying to get to you as fast as I can. Cindy Fusco – we can hear you loud and clear.

David Perlmutter: Go ahead.

Cindy Fusco: Okay. So now, I’ve actually experienced personally, but also by watching other people when they try to change the way they eat. The carbohydrates – what they’re used to. Can you make any recommendations besides using nuts? Fruits – you have to watch the glycemic index on it. What can you recommend for people?

David Perlmutter: That’s a very good question. I will say that it’s most of the time fairly challenging for individuals to suddenly go very low carb and higher fat. There is a process that we go to called “keto-adaptation,” where the body takes some time to begin to understand that it needs to start burning fat and not carbohydrate because it’s been bombarded with carbohydrates since day 1. And so, it takes some time. People just have to be encouraged to hang in there and after two to three weeks, it gets a lot easier. What people will find really early on when they first make the shift is that suddenly, when they’ve had for breakfast was some scrambled eggs, with spinach, a slice of avocado covered in olive oil – my goodness, suddenly at 10:00 in the morning, “I’m not hungry.” In fact, comes lunch time and, “I’m not really that hungry either,” because you start to burn fat as a fill source; it’s like a candle basically, or an oil lamp providing a constant source of energy as opposed to throwing gasoline on the flames that burns very, very quickly and shoots the insulin level up, blood sugar plummets, then by 10 a.m., people are hitting the vending machines. So, it is a challenge; it is absolutely very much pun-intended against the brain that we’re talking about, but it’s worth it. It is so worth it to reduce this damaging process in human physiology, and there’s no other way. There’s no other way to make this happen; you just tough it out and it gets easier, and then suddenly – you know what patients after a couple of weeks tell me – they just feel so much better, they’re sleeping better, they’re much more energetic, and they are clearer of mind. Mostly, the healthcare providers issue in just being as encouraging as you possibly can and you know, you’re having to undo a lifelong of an individual’s habit, so it takes a lot of work.

Mike Mutzel: Fantastic. Tom Mounteer.

Tom Mounteer: Dr. Perlmutter – hey, this is Tom. A pleasure. Thank you so much about your information. It’s been a joy following you over the years.

David Perlmutter: Thanks Tom.

Tom Malterre MS, CN: I have a question for you. I’ve been doing a lot of analysis on animal fats, and looking at the persistent organic gluten stocks, brominated flame retardants and I’ve been seeing a tight correlation between the consumption of animal fats and the level of this persistent organic glutens. I also see in the studies if you look at both animals and humans, when you give them high fat diets, they’ll end up with more LPS migration, inflammation, obesity, and insulin resistance over time. It doesn’t necessarily happen immediately. So, what is our solution then? Are we looking at more coconut oils? Are we looking at more vegetable-based fats? How do we counteract these fats? Are we also recommending no consumption of farm salmons, so we don’t have the persistent organic glutens coming from the farm salmon?

David Perlmutter: I think, Tom, you absolutely answered your question, and so, when you’re eating high in the food chain, you are at risk for bioaccumulation of the various things that you talked about. I am dead set against any recommendation that there is a good farm salmon and go for it. It just doesn’t compute. I have to say that we’ve been hugely advocating wild salmon. I’m going to go off-topic here a little bit. It becomes very worrisome when 500 tons of radioactive water are being dumped into the Japanese current on a daily basis right now as we speak, and that radioactive cesium is being brought up the coast of Asia across through Alaska and down to Pacific Coast. So, what’s going to be left? It’s a scary proposition. If Japan cannot deal with what’s going on, they’re going to freeze the mud wall and hope that that contains the water. I’m going to make a political statement here; I probably shouldn’t, but I will. I’m thinking that the hundreds of millions of dollars that we’re going to expend over the next couple of weeks in going into other countries and doing things with our worse ships. I just think money could be better spent giving the Japanese a hand at keeping the entire world from becoming polluted with radioactivity. It is happening; it’s at the center of the front page New York Times, and it’s a scary, scary stuff. I’ve been way off topic for persistent organic glutens, which is the argument in favor of grass fruits, no pun intended. No. 1 – telling people let’s support organic foods because that’s where it starts. I did discuss that a little bit today, that gosh, we’re telling people to put this mancozeb on their food, on their vegetable gardens; that is a powerful mitochondrial inhibitor and fungicide. So, it starts with that level that we’ve got to stop polluting our nest. Gregory Bateson, an anthropologists from Harvard, said that man is the only animal who will defile his own nest, a sure sign of madness. Tom, you are downtown right on on this one. Again, the sources of fats should be really good fats – organic, extra virgin olive oil; organic coconut oil; organic nuts and seeds, by enlarge. If you’re going to choose animal products, it should absolutely be organic and free-range; that’s not ideal these days, when even free-range is still breathing a polluted atmosphere in a notion of bioaccumulation, so your points are very, very good and very well. Thank you.

Tom Malterre MS, CN: I appreciate your work. Thank you.

Mike Mutzel: Thanks Tom.Alright. We have time for about two more here. Michelle Makari? Michelle, are you live? Let’s see… Michael Bell? Kent Toland? Kent, you used to have a question. I guess not. Okay, I’ll try a few more here. Jul Berger? Jul, are you live? Alright, maybe let’s try two more here. Holly Rantala?

Holly Rantala: Right.

Mike Mutzel: Hey Holly, do you still have a qeustion the question?

David Perlmutter: Hey, you’re live in front of 2,000 people. Go ahead.

Holly Rantala: Okay….

Mike Mutzel: Well, I guess she’s on the cell phone or doing something. Okay, we have a couple more here. Sorry about that.

David Perlmutter: Mike, why don’t you just go ahead? Do you have any questions that you can read? Maybe we can do one or two.

Mike Mutzel: Yeah, that’s a good idea.Bonny, are you live?

Bonny: Yes, I am.

David Perlmutter: Okay. Great. Great connection.

Bonny: Yes, sounds great. Perfect. I actually have a question about, I guess you didn’t talk about glial cells and all, and how they help heal the brain and affect the brain. You’re saying that there’s a lot of permanent damage and stuff without reading on about how glial cells restore brain damage.

David Perlmutter: Are you talking about microglial cells? Are you definitely talking about microglial cells?

Bonny: Yes.

David Perlmutter: Would you turn down your volume? And I will answer your question. The microglial cells are what are called the “macrofunctions,” and they are just microglial, but not small glial cells; they’re a totally different variety of cell. These are cells that go around the brain and pick up the garbage, help kill the neurons, but in addition, the microglial cells are the initiators of the inflammatory process. So, you could imagine that in the original flow diagram that I demonstrated to you, what I normally use when I speak to professionals is the very first thing on the left side before we get to the inflammation and then succeed to free radical production, we have what’s we called the “microglial activation,” turning on those microglial cells. That is certainly a focus of leading engineering science. What is it that’s activating the microglial cells and therefore leading to upregulation or turning on these very powerful inflammatory mediators? So, what the microglial cells do is they help to keep the brain clean, they help to scavenge things that don’t belong there. But in the process of their activation in doing what they do, it does turn on the production of these inflammatory mediators, so we have to keep the brain in a situation where we don’t activate microglial cells. One of the really interesting leading theories right now from England looking at one possible initiator of the activation of these microglial cells actually, oddly enough, focuses on herpes simplex virus type 1 with research done here in the States in Vanderbilt looking at chlamydia and pneumonia as an organism that is actually activating these microglial cells. So, they play a very, very critical role. You can actually image these microglial cells in vivo showing them turned on as a graphic example of the brain on fire. I think moving forward, we’ve got to do everything we can to keep from that activation, but that was actually a very good question. Thank you.

Mike Mutzel: So, we have one more cool question, and we’re going to hang it up here. Tony Brown, you are live.

Tony Brown: Hi. This is Tony Brown.

Mike Mutzel: Hey Tony, sorry to interrupt. Could you speak into your microphone or cell phone? You’re a little far away.

Tony Brown: I’m sorry. Yes.

David Perlmutter: I got it. We’re good.

Tony Brown: You okay?

David Perlmutter: Sure. You’re good.

Tony Brown: Thank you. Great presentation loaded with information. I noticed you took the belt in those with APOE full combination of a high risk of Alzheimer’s, but they also have a higher risk of stroke. How is that? How do you suggest that they manage their diets because it sounds like that it is balancing act?

David Perlmutter: That is actually a very intriguing question because there is some literature that would suggest that carrying both APOE-e4 alleles would impart in an individual some detriment with reference to fat metabolism, and it does make it kind of challenging. That said, in those individuals oddly enough, we are even more aggressive in creating what’s called the “ketogenic diet.” In other words, even the higher levels of carbohydrate restriction to the extent that we actually put those patients who carry the APOE444 allele set, which may increase the Alzheimer’s 12 fold. We actually put them on a diet that puts them virtually in a situation called “ketosis,” where they’re burning fat all the time. The reason we do that is because the main problem that these people experience is early failure of mitochondrial function. It may be a little bit much for some of the listeners, but ultimately, the mitochondria, which is the energy producer parts of the neuron, beyond just producing energy, the mitochondria dictate whether the cell will live or die. They control the process called “adaptosis,” which is cellular suicide basically. So, we need to do anything we can to nurture the mitochondria, and we can do that by creating a very high-fat availability type of diet, so that their very few carbs used in higher fat allows the mitochondria to be healthy, it enhances their replication and dramatically reduces free-radical formation, and therefore reduces pre-programmed cell death, to the extent that there is actually a medical food that people can buy that does nothing more than increases chelated alpha-ketobutyrate or fat availability for brain cells, but you can accomplish that by cutting back on your carbs and increasing your consumption of things like coconut oil or medium-chain triglyceride oil. I’m not sure if that’s where you’re going with that question, but that is where the current science is. I’m glad you took us to that place. Thank you.

Mike Mutzel: Alright, everyone. Do you have anything else, Dr. Perlmutter?

David Perlmutter: No. Mike, I want to thank you. I want to thank Xymogen for tonight’s opportunity and I’m grateful that people thought this as important and took time to listen. I hope that, you know the message was kind of fundamental and straightforward, but I’m doing my best, I think, at this point of my life, to bring these statements to awareness, but based it on what is the current science is telling us. So again, I sure appreciate that opportunity. Thanks.

Mike Mutzel: Great, and we are sure to appreciate you. Thank you so much and have a great evening.

David Perlmutter: Great. Good night, everybody.

Mike Mutzel: Good night.


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