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#153 Dayan Goodenowe on Dementia

by Kira Dineen
August 6th 2021

Did you know genetic changes account for an estimated 10-15% of all Parkinson’s disease? And these genetic changes can be passed down to family members. T... More

Are you a genetic counselor, genetic counseling student or someone that wants to learn more about genetics. Then I recommend this workshop next week on August 11 for over four hours. You will hear from genetic professionals from around the world about different areas of genetic counseling. I'm excited to be one of the presenters covering prenatal genetic counseling. Other colleagues are sharing their expertise on precision medicine, ethical issues, adult Genetic counseling, cancer, genetic counseling and laboratory technologies. You can join us in this collaborative worldwide workshop next week on August 11. Here's how to register, you can use the link in the show notes which is available. If you listen to this in a podcast player, just swipe and you can also access it via our website DNA podcast dot com. Just look out for the blog post for this episode and the link will be in there for this webinar again, it's on august 11th. Looking forward to connecting with you all there. How is it that we find ourselves surrounded by such complexity, such elegance, the genes of you and me jeans.

Are you all made of DNA were all made of the same DNA. Hello, you're listening or watching DNA today. We are genetics podcast and radio show. I'm your host here, Deneen and I'm also a prenatal genetic counselor on this show. We explore genetics impact on our health through conversations with leaders in genetics. These are genetic counselors, researchers, doctors, patient advocates, researchers and many, many more people. My guest today is dr day and good now. He is the founder and ceo of pro drum sciences and this episode we're gonna be talking about dementia. Alzheimer's disease. Parkinson's disease and what we know about biomarkers and the genetic predispositions for these conditions. So we're diving into all this today. So Dr Goodman, thank you so much for coming on the show. Your book just came out for Breaking Alzheimer's is the name of it. Um So thank you so much for coming on and exploring all of these topics with us today. Well thank you kira.

It's really a pleasure to be here. So I thought we could start out with making sure everybody understands the relationship with dementia and Alzheimer's disease because it's not necessarily the same thing. So I wanted to make sure that everybody understands this background information before we get into all the biomarkers in the genetic predisposition. So how are these two related? How are they different? Well that's a really good question. Now Alzheimer's, as we currently understand it was discovered by a Dr. Alois Alzheimer. Alzheimer by in the early 1910 or 15 in that range and it was really related to pre senile dementia. He had a patient who had dementia and she was young and after she died he did no pathological analysis and he discovered that there was these amyloid plaques in between the neurons and there were Nurofen bya larry tangles within the neurons. So this became called Alzheimer's disease and Alzheimer's was considered a type of pre senile dementia at the time People thought senile dementia which was more common, obviously was more related to cardiovascular disease, atherosclerosis and then you fast forward around 50 years or so.

Then in the 19 sixties people were looking at people that were dying postmortem analysis of with alzheimer's with dementia and they're recognizing, hey, these older people have similar pathological um formations in their brain as classical alzheimer's. And so then they created a subclass of dementia called dementia of the Alzheimer's type or later on stage on stage dementia. And then as time goes on. But we have there's really four types of dementia. There's the alzheimer's type, there's the basket of dementia, frontal temporal lobe dementia, Lewy body dementia. So dementia is a reduction in cognitive functioning. And then when you subclass if I it's kind of saying, okay, what type of dementia? How do I how do I characterize this particular patient? And most the time that's been done postmortem. So we don't necessarily know um what the actual um characterization of that dementia patient is until post mortem we're getting better and better.

Now with symptomology with better technology, we can we can diagnose the type of dementia. Pre death much more accurately than we ever used to be able to. But that's still most of a classification scheme, it's not really a causation scheme. Now we've known what causes dementia since the seventies and it's Colin ergic neuron dysfunction That's absolutely. And the very first drug ever approved for alzheimer's was a drug that improved Colin ergic function in the brain. So, dementia at the biochemical perspective is reduced transmission of Colin ergic neurons, whereas Parkinson's is the reduced transmission of dopamine neurons and then people have anxiety and depression are typically certain energetic or nora ephron ergic systems. Epilepsy will have different neurotransmitter systems of the brain that get fundamentally impaired. But that's the approximate dementia is a is a is a physiological dysfunction of the colonic neuron system. Then we can ask the question uh Okay, well where is this coming from?

And that is where you get into much more of a heated debate as to what is causing these Colin ergic neurons to lose their function and they shrink. They don't actually die right away. Can the main cell body for these colonies neurons called the nucleus marsellus? And they project the cell bodies are in the deep brain and then they project their axons up into the cortical regions in the hippocampus and so on. And that's it's their acts on terminals where we see the dysfunction. But quite often the neurons actually shrink, they don't actually die. And so they're still there, they're just kind of inactivated and that's kind of where there's a lot of actually hope in terms of the Alzheimer's or dementia part of this world. So that's what's kind of gone on over time. People have in the late 19 nineties or early 19 nineties, they discovered this amyloid plaque and they actually able to sequence of protein a beta one peptide one through 42 that changed the whole world. And it kind of coincided with the whole um genomics revolution of gene sequencing.

Gene ship formation and it was the whole world was really a buzz. A lot of things are changing. Right then we're doing large scale biology where we sequence all the genes or we look at all the gene transcripts simultaneously and we'd say okay what's going on here? And then that kind of created this whole focus on jeans and then the gene products which are the transcript that gene ships and then those transcripts get converted to proteins. So the proteomics part and all of that comes directly from your genome. Curious about your own genetic risk for Parkinson's disease. Picture genetics newest DNA testing kit. Picture pd aware is designed for you. There's a 4-9% higher risk of developing the disease if you have a family history of it. So Picture Pd aware is for anyone who wants to assess the genetic risk for developing Parkinson's disease. Picture genetics is working in collaboration with the Parkinson's Foundation and the P. D. Generation study to make it easier for you to find out your risk for Parkinson's disease. This is by providing you with knowledge and tools you need now to plan for the years ahead.

This includes genetic counseling with your picture pd aware kit. So you're fully supported and educated about what the results mean for you and your family visit. Picture genetics dot com and use code DNA today for 25% off and free shipping again. That's picture genetics dot com with code DNA today for your picture pd aware kit. Get actionable genetic insights today to benefit your family of tomorrow. So a pretty four. Okay. We've known about this protein since the 19 sixties as well. And then in the 19 seventies we found out that there was a mutation in it and it was mostly related to cardiovascular disease back then. And so it wasn't until in the early nineties that they discovered, wow people with this E for mutation or sniff basically. So single nucleotide polymorphisms had a higher incidence of Alzheimer's disease. So the genotype has essentially two snips basically to two protein changes or two amino acid changes, changes from assisting to an ar jeanie. And what that does is it prevents so an E two carrier. So for all of you who don't follow E for april the genotyping in great detail.

There's three Jenna types. There's E two L E L E three Eliel and there's E four L and of course you get one from each of your parents. So there becomes six combinations. Most of us have the E three which is the most common. So E three. E three is about 60 65% of the population. And then people have the E two. E three is about 10 15 and but the E four's are about 2025% of the population. So when they found this out and they said wow wow there's a whole bunch of alzheimer's patients that have this E. Four genotype versus the others and then associate what what's going on with this thing. And it turns out that the E force they don't have systems so those proteins can't form these little disqualify bridges and that affects their ability to f lux cholesterol of the cells. So the fundamental difference between the three different gina types is their ability to e flux cholesterol. Then the story is even more interesting because E four. So the april e lipoprotein cholesterol transport protein also is kind of cool. It's interesting because your LDL in your body is called april b.

So you have these lipid proteins that transport cholesterol and lipids around your blood supply and that's the one that sends cholesterol to all your cells on your LDL proteins and then yourselves actually suck that in. They tag on the LDL protein and actually internalize it and then digest the cholesterol for your memories. Then you have your HDL system with people say well I want you know we said we want good HDL because that's your reverse cholesterol transport system. Now that's apolipoprotein A. S the A's and B's and most of them. The the HDL is do not go into yourselves when you're in your cell is happy. He's got lots of cholesterol. You want to get rid of extra cholesterol gets sent to cholesterol out the the HDL system and then that truck sit back to your liver for clearance. So those two things balance your cellular cholesterol needs. The E. Type of liver protein is ambidextrous. It can be either LDL like or HDL like so people that are born with a mutation in april the group routine be like they don't make any LDL they all of a sudden create a whole bunch of april e.

And it acts like LDL inappropriate. That's what keeps them alive. Now. What makes E so unique is that it's the only able to put protein in the brain 100% of the brain protein. It gets a little bit of a from your blood supply. So it is the brain has all April E. The periphery has like 5%. It's a minor player in the periphery but in the brain it's the whole thing but it's different in the brain. It works it does both LDL and HDL functions. So people think that the brain has a different circulatory system. So in the periphery you have your liver that's making a lot of cholesterol and its shipping cholesterols using an interstate highway system called your arteries basically all around the body and it's sending it back and forth. So we shipped cholesterol on big semi trucks in the periphery. But in the brain everything is local. Like it's like a it's like a year in chinatown. It's like all these little streets behind each other. You can't you can't even get a semi trailer in there if you wanted to. So it's got a whole different purpose of transporting cholesterol from where it's produced. Which is an astra sites.

So in the body most of our livers in the liver most of our cholesterol and liver. And the brain is the astrocytes. And so the brain has to figure out a way how do I do both LDL and HDL functions because cells need to be fed cholesterol and they also need to be able to get rid of extra cholesterol. So april e because april we can do both. L LDL and HDL functions. The brain uses it for both purposes and it does it all locally. So what happens then is that the people with the april gina types? Now that's why this has a big effect. And brain. So if your E two carrier your cells are really good at e flux in cholesterol they can't really hold cholesterol. They make it they can they can spit cholesterol the cells very very efficiently. And e three carriers are. It's like the three bears basically it's fine and the force can't get rid of cholesterol very well. So they're there cholesterol savers if you will. And so when they make cholesterol themselves they don't get rid of it. And so now that's not a big deal when you're young because HBO is not the only system of your body relies on to distribute cholesterol.

The other one is your membrane lipids like plasma logins and these plasma logins deal with cholesterol certification. HDL cholesterol transport and so they work like a yin and yang in your cell membranes and when you're young you have lots of plasma logins. Your proximal function is great and in fact when you're young the E four genotype is actually a protective genotype it's good for you. That's surprising because we hear this E four genotype is being like oh you have the bad one or like you have the worst one. It's elevating your risk for Alzheimer's so that's interesting that there's another side to that. It gives a protection so you're for bacterial and viral infections. E four carriers are somewhat protected from that because their cells are more resilient. Now when you get older what happens is your paroxysm a function decreases and your plasma levels start going down so the counter balance to the A P E H D. L. E flux starts becoming imbalanced. So you're running a three legged race and your partner is just starting to get weaker and weaker and what happens as you get older with the plasma levels decrease then the balance is thrown off and cholesterol accumulates.

And this is where the amyloid story comes in. So amyloid which is normal and natural. Okay Which is one of the main hallmarks of Alzheimer's pathology is processed like the precursors and protein called amyloid precursor protein A PP. So everyone's getting really big biochemistry lesson here today but if your need for carry this kind of fun because what happens then is it? But we think about, we get focused on the car accident and we don't think about all the other cars that are driving by just super happy. So About 95% of this amyloid precursor protein normally gets processed by an enzyme called alpha secretase and that doesn't create any amyloid plaques, totally healthy. Normal girl lucky enzyme. It's only when the last little 5% gets processed by the enzyme called beta secretase that we get this amyloid plaque formation. Well it turns out that beta secretase likes to be in the cholesterol rich part of your membranes and alpha secret taste likes to be in the loose region. So it's kinda like ones in the ghetto and one's in the suburbs and so when we as you get older the cholesterol levels of our membranes can get elevated and so the region the lipid raft region starts to expand and as it expands the number of beta secretase enzymes expands with it.

So all of a sudden your body starts creating more of this amyloid plaque. So E four carriers have higher levels of amyloid in their brain versus non E four carriers that's that's the biochemical correlate and then that that amyloid formation in the brain is actually really good bye marker because it actually tells us that this membrane dysfunction, it is very very poor association with cognition fundamentally. Like if you if you correct fertile or other factors in the brain, colonists, neuron density, amyloid no longer has statistical significance with cognition, but if you don't know those other variables and will it still becomes significant. So E four carriers on average have higher levels of amyloid, but once you know the brain amyloid level you do not need to know the genotype. So an E three carrier with high amyloid is the same as any for carrier. So you can bypass that part if you have the second part of that information because the first part is really giving us a sense in and giving us a landmark kind of like, okay, where are we in terms of these risk levels?

And you've been talking about these plasma logins If for people that have that E four variant or maybe two E four variants, can we elevate their plasma login levels so that we're giving them the same risk level as someone that genetically has a lower risk, you can reduce the risk, you can completely neutralize the E four genotype. So E four carriers with high plasma logins have the same same risk as any three carrier. Even more exciting is the E three carrier, if you have high plasma logins you have the same risk as an E. Two carrier. And in our studying over 1200 subjects. E two carriers that had high plasma logins, we found no cases of dementia and the entire population. That is a that is a big statistic you have there. Right. And so it's a big number. And so it means is that you can you can modify your genetic risk by changing the biochemistry. So if you if you're ready for carrier, as long as you're membrane structure is maintained the way you were when you're younger, you have no increased risk of alzheimer's disease.

And that's the kind of cool thing about biochemistry is once we understand the biochemical mechanisms of it, we can interact because like I said, jeans aren't magic and biochemistry isn't magic either, things are logical. I tell people, no matter how fancy we get, we still can't get past the first law of thermodynamics, which is energy, can't be created or destroyed. So I tell people that your books are always going to balance. You may not like what you see at the end, but they will always balance. So we have a lot of control over over that. So now we can restore plasma widgets and we're gonna listen to laboratory. So if we do postmortem brain analysis of patients, okay, we look at the plasma levels in the brain, people that have high plasma lesions in the brain have low levels of amyloid regardless of the genotype. And then obviously the blood work does the same way so we can measure that blood levels in the blood levels correlate with people's brain levels. You know, get a leg because you have reserved capacity and it takes a while to deplete them. So plasma, which is one of those weird molecules.

So it's one of those things where like I'm my background is in the biochemical mechanisms of disease. Okay. And I studied it for years and years I went to school for And I not after school, I studied it even more 15 years And so this technology, this biochemistry profiling technology that I invented in 1999 when we applied this to Alzheimer's, we saw all these molecules decreased in the blood of people with Alzheimer's disease. And they were weird. They had these seven oxygen's whatever and turned out their plasma colleges are going, what the hell are these things? I had no idea what they were And I should know because they're not trace level molecules. We're talking 20% of your brain, high levels of your heart, your lungs, your kidney, the reading of your eye, high levels of plasma levels. So it's not some trace level molecule that is just some real interesting sidebar to life and Children that are born with mutations in plasma logins, they don't live, They're lucky to get to age 10, okay, with great caring parents, but it's a very, very challenging situation and it turns out.

So you think, wow, you know what? These plasma widgets, what's the big deal? They're high levels. We should really get them in our food supply. Well, the very last step in their manufacturer creates this bond called a vinyl ether bond and that is designed to be sensitive to acids because it has mountains have three purposes in your world. One is it chemically neutralizes peroxide. So you have oxidative stress and you have your cells start creating super oxidase, mutated, super oxide peroxide so on. And that's where you get your oxidized LDL and c reactive proteins and so on. So proxy. So plasma logins that finally through bond actually reacts with peroxide and neutralizes them. So we'll be presenting data on this at the Alzheimer's conference next month in july on how the relationship of blood plasma lipid levels after we supplement and elevate plasma levels the effect it has on your antioxidant system. So one part of plasma logins is physical, it actually physically neutralizes Reactive auction species, which is very different than vitamin E or co Q 10.

Like those are kind of hot potato holding the molecules like you get an electron that's free and these these uh free radical scavengers, they'll kind of they'll pick it up and they'll hold it for a little while. But sooner or later they burn their fingers and they got to get rid of it because they don't actually neutralize the retractable plasma, which is actually blow up, they actually get consumed and sacrifice when they neutralize reactive auction species. So you make a lot of them but you can consume a lot of them. So one part is actually at a chemical level it does that then it has to other functions that are really important. One is membrane structure and relationship like HDL transport april april the amyloid precursor protein and all that kind of stuff which you can talk about. But the biggest thing is membrane fusion and release of neurotransmitters and the most basic part of our brain and our neuromuscular junctions like the human body lives in a lipid matrix. Right? We're not a bowl of soup or that of beer brewing were separated by lipid membranes that defines us and sell molecules go in and out of these membranes.

But these memories have to fuse with each other. And neurotransmitter release is you've got to basically you gotta you gotta ball of neurotransmitters in a encased in a lipid vesicles. And when you want those neural transmitters to be released in the synaptic cleft, they have to translate that into physically fuse it's an actual biophysical process of its physical and that process requires plasma logins because this vinyl ether bond. You know the physics of it says it's like a all the inverse hexagonal phase, whatever these membranes refused to let their transmitters released if you have low levels of plasma logins. You can't release neurotransmitters. So it reduces neurological transmission and that's why we're seeing such powerful cognitive effects independent of anything else in people that are on the supplements. So that's one of those, those are three main functions. And so the weird thing about them is that it's finally to bond if you eat a nice juicy steak or an animal product that has plasma login is um as soon as it hits a hydrochloric acid of your stomach that bond bursts.

So you must make your own plasma logins. So we need a lot of them and we consume a lot of them. And so you have this mass balance equation. So at some point in time when we're young we build up a reserve capacity and it's stored in our membranes in our brain. And then if we get into a situation where we're not making enough of them, um then the mass balance equation goes into the negative and you start losing them. And so the lower your plasma logins, the faster your rate of decline is. And that's why when we look at blood levels, the lower of the lower the plasma emission level, the faster the rate of cognitive decline is in people. Because the plasma login bleeding out of the brain basically occurs faster and faster based on the net balance. So you can improve them. And then, you know, in the historical way, resistance training that exercise improves paroxysm a function. So there's a lot of a lot of the things we talk about cardiovascular and metabolic health and how that's linked to Alzheimer's disease. That's all real.

Um because your body is integrated. So anyway, so those are the big issues on plasma logins. And it's a pretty cool story because it's so you is one of those where you basically you can't unsee it, like once you see it, it makes sense. And it makes sense of the mechanistic level and also at the pathological level of where Um, you know, we're seeing things happen in the brain. And so that's what we do one step at a time. We've been able to look at the postmortem brain analysis. Even mortality is even more crazy. Um like we have this longitudinal study we did in Chicago was 1,262 people. We tracked them over six years And their elderly. So the average age was in the 80s. So obviously during that period time, a certain number of people will die. And we have all that information and statistics. And so were originally looking at the longitudinal effect of plasma leptin levels on the future occurrence of dementia. Can we predict who will get dementia based upon their blood levels? Okay.

And then serendipitously after as well. You know, we have this mortality data. Well, we should be looking at what is the effect of blood plasma militants on, you know, all cause mortality. And it turned out pretty severe. So a 30 year difference severe, like the worst graph I've ever written in my life. So it's basically a 65 year old with low plasma legions had the same five year mortality as a 95 year old with high plasma weapons. That's like shocking when you hear that statistic that's after correcting for dementia. So dementia itself is high mortality. People think, oh, I'm going to get dementia and I'm going to live for 10, 15 years with it. No, the average time to death after a diagnosis of dementia about five years, people can stay at home for a couple of years. Once they get into long term care, it's usually a couple of years. Um you'll live longer with a stage three colon cancer diagnosis than you will with the diagnosis of dementia because it's it's serious, it's your brain health. And it's not because it's not random right?

By the time you have cognitive impairment, you reserve capacity of your brain has decreased. So you've been sick for a while, but just not knowing it because your body has a lot of resilience. And so that's that's kind of where um being quite shocking. How do you keep research articles organized? I've struggled with this as a student for years and now as a genetic counselor, I have so many papers saved on my Mac. But it's often hard to find one and even harder to sight when I'm writing. I finally found a solution though it's simple and easy. It's called paper pile. The goal of paper pile is to radically simplify the workflow of collecting, managing and writing papers. This app allows you to highlight an antarctic papers, manage, references, share and collaborate and get this even site directly in google docs. I wish I had discovered this when I was doing my thesis would have saved me hours of time and frustrations at every step. Paper pile aims to provide a just work solution that eliminates any unnecessary complexity, especially the paper piles, new mobile apps. You can sink your library to all your devices so you can read an an A. T. On your ipad, iphone or android devices.

So if you're a student researcher, writer really anyone who's downloading and reading papers, you got to check out paper pile for a streamlined approach. You can start your 30 day trial at paper pile dot com with code DNA. Today Paper pile costs only $36 per year but with code DNA. Today you save 20%. Again that's paper pile dot com for all your papers in one place. Nice and tidy, intrigued about genetics. Of course you are. That's why you're listening to this podcast which is why I think you'll be interested in an upcoming webinar on august 11th in this three hour virtual workshop. A wide variety of genetic counseling topics will be explored including prenatal genetic counseling presented by myself, precision medicine overview of common genetic conditions and more Join us in this collaborative worldwide workshop next week on August 11. You can register via the link in the show notes of this episode which is also available on our website DNA Podcast.com. It's also the biochemistry. People think on genetics that your genes give you this mortality risk but what they do is they give you a disease risk and then the disease is what kills you, not the genes.

So ap for genotype have no increased mortality. So the only risk of death of an E. Four carrier is those four carries that become demented but if you're an E. Four carrier and you can avoid dementia, there's no mortality association with that E. Four genotype anymore so it's powerful to be able to take the supplement that you've developed because you can bring up those plasma login levels so that you're decreasing the risk of all of these downstream effects of what you're saying of decreasing of developing dementia from this. Exactly. And then there's two types like they evolved into I say program neuro which has the D. H. A. Plasma and I say you take neuro for performance, okay athletes what cognitive impairment when you're older Parkinson's but there's another aspect of plasma which is they also if you have a different fatty acid on it, it doesn't have the long chain omega three D. H. A. On it. It has say the Oleic acid or omega nine molecule then it's part of your mile and sheath the protective coating of your neurons, both in the brain with your white matter, all the good in her sights, but also in the periphery on your Schwann cells for ALS type diseases.

And so Glia is a product that we have that has the omega nine plasma login and we say take glia for protection. So for concussion recovery, autism reducing neural inflammation. So autism is a mitochondrial disease that's caused by white matter, hyper inflate hyper inflammatory disease. Same thing with multiple sclerosis. Multiple sclerosis is a neuro inflammatory disease. And women will recognize their symptoms go away when they're in protesters for instance. So an M. S. Woman who gets pregnant, her symptoms will go away for most cases and then later on when they go into menopause that's usually when they transition from relapsing, remitting into secondary progressives once they start losing the protective effects of estrogen which is a very powerful neural protected. So anyway, so those are the kind of things that look at in terms of neurological health and understanding really at the basic fundamental building blocks and kind of working from the inside out inflammation is just a good example.

People think that you need to suppress the T cells are the activated microglia but they're there for a reason there's a chemo attractant signal that says hey there's a six cell here, I'd better come over to it, give it the final metal ball death punch if you will and then clean up the mess and that is typically oxide ization of the membrane. And that that's that's what activates this chemo attractant inflammatory signal. So if you can get into those cells the beginning and prevent them from becoming oxidative damaged resolution goes away. And so we have this, you know, brain health is never just one thing. Okay. You know, we always, there's always gonna be one priority. There's always going to the main shiny object in any given situation if it's a stroke or if it's Alzheimer's with Parkinson's And but once you get into it, all of these diseases have overlaps because and then it becomes what is your personal canary? Your coal mine, right?

So if you apply a common stress to 100 people, you're going to get 100 different results, but you're going to get multiple different outcomes because each person now has their genetic predisposition. So your predisposition chooses your disease doesn't really cause your disease is the most part. So that's kind of a and that's powerful because you can, if you can understand the biochemistry of your personal genotype, then you can build an environment that your genotype is happy to live in. And then that way you keep it silent. Um so that's kind of what I do. We basically do human biochemical engineering and the plasma logins are one part of that puzzle because you just don't want low plasma which is just not worth the risk. If your network carrier it's just like it's a no brainer. You need high levels of dhe plasma logins just because you know you need to be ahead of the curve. And that's the whole concept of biochemical reserve capacity. And people think this is some strange concept but it's not right. The reason why you go jogging or you work out is to create reserve capacity.

Like if you lift weights and the goal is not to is when you're not lifting weights. Okay so the day that I'm not lifting weights and I'm just using my keyboard and my mouse. Okay I'm not I've created reserve strength so that I am operating on my days off. Under my capacity. So I've created reserve capacity and say if you run or jog or whatever it is you say okay now I can on my days off I have created reserve capacity and that reserve capacity allows me to operate in the regular world at a very under under capacity is like having a big savings account. Like I have a heart savings account if I run or if I have I have a muscular savings account. If I work out well biochemistry is the same way if you can create like your metal transfer system or your oxidative stress system, your cholesterol regulation system. These are biochemical systems and we have reams of data, lots of awesome large epidemiological clinical data sets that we know what your optimal cholesterol levels and blood are supposed to be.

We know what your uric acid should be like. This is not this is no longer ambiguous. Like all cause mortality for all of these biomarkers are well established and very, very large numbers. And so our biochemistry is telling us what it wants to look like. Yeah, they're screaming much that you outlined in the book to of just with all the data you've gone through and everything. And I think we could keep talking about this for hours. Honestly, we just geek out over it, right? But it starts making sense. And that's the other thing. People like your body is designed to work. Like if you can make it past your first year, you basically have a sufficient genotype, okay, if you have something so bad in your genotype that you've mutated, okay, you're going to know it, okay, You're not going to have to wait till you're 50 to find out. Okay. Like you're going to know it very, very quickly and now that takes more serious intervention. But a lot of those can be dealt with as well. But bottom line is like it's um We think that, you know there's not this big 80 year ticking clock going on um is an accumulated, you know, factors.

But we can go into that in a subsequent conversation. But uh bottom line, those people should, people should embrace their genotype, whatever jeans you have there, you there personally. You they're born when you're born. They don't know if you're going to be born in the United States or Somalia or brazil. And so they have no choice in the matter. They have to live with whatever they're born with and they learn to adapt to the environment just like you do. And so your genes are you and the earlier people realized that don't fight your genes work with them and find the happy space for them. Certainly better, Better everybody will be and people can learn more in the book. We've been referencing that just came out this summer. Breaking Alzheimer's, we're doing a giveaway for 10 copies, so make sure to head over to our social media, just search DNA today on twitter, instagram, facebook, youtube, all of the places so that you can enter to win and you can learn more DNA podcast dot com. And also pro drone sciences dot com. And we're gonna include links to everything in the show notes for this episode, which you can also access at DNA podcast dot com.

And if there are any questions, feel free d to email into info at DNA podcast dot com. Thank you so much. Doctor Good now for coming on the show and just sharing all your expertise. That's so interesting to dive into how genetics plays a role in the dementia and all of the different aspects we talked about. So thank you so much. Oh, you're very welcome. Thanks for having me. Did you know genetic changes count for an estimated 10-15% of all Parkinson's disease and these genetic changes can be passed down to family members. That's why picture genetics just released their picture PDF aware and at home DNA. Kit that tests for changes in the seven genes associated with Parkinson's disease. Picture PD aware is easy to order and understand with good looking reports. Plus you're fully supported through live chats, emails and genetic counseling. To order your picture. PD aware kit, use Codina today for 25% off and free shipping. Get actual genetic insights today to benefit your family of tomorrow. Thanks for listening. Everyone join us. Next time to learn, discover new advances in the world of genetics.

#153 Dayan Goodenowe on Dementia
#153 Dayan Goodenowe on Dementia
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