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Speaker 1 (00:00:00):
Welcome to The Dr. Gundry Podcast. The weekly podcast where Dr. G gives you the tools you need to boost your health and live your healthiest life.

Dr. Gundry (00:00:14):
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So welcome to The Dr. Gundry Podcast. Now here’s a shocking statistic. A new case of dementia is diagnosed every three seconds. Whoops, there goes another case right now. So it’s estimated that over 50 million people worldwide are struggling with some form of dementia; a number that’s expected to rise to 82 million people by 2030, and quite frankly, that’s right around the corner. In fact, I bet you know someone who has struggled with dementia themselves, either who has already passed or is currently struggling with dementia. Now it hasn’t received much press, but there is something that might be a major breakthrough in our understanding the causes and prevention of dementia. And today I’ll be chatting with one of the researchers behind this breakthrough, Dr. Dan Goodenowe. Dr. Goodenowe is the founder and CEO of Prodrome Sciences and has spent the past 30 years researching the biochemical signs of aging and disease and what can lead and prevent dementia.
On today’s episode, he and I are going to discuss his exciting new research into the causes of dementia, what your blood can tell you about your risk for dementia and Alzheimer’s and why we might just unlock the secrets of how the brain ages sooner than you think. Dr. Goodenowe, welcome to The Dr. Gundry Podcast. It’s great to have you here.

Dr. Goodenowe (00:03:17):
Well, thank you, Dr. Gundry. It’s a pleasure to be here with you today.

Dr. Gundry (00:03:21):
I’m really excited to have you on this show, because what you’ve been researching has been a pet project of mine for the last couple of years when I first was introduced to these compounds. But I must say that ever since I learned about plasmalogens, I just can’t say enough about how important they are and how little anybody talks about them. So why don’t we start. Give us a little behind the scenes. Look, you’ve been doing this for 30 years, how’d you get to Prodrome Sciences and where are we going?

Dr. Goodenowe (00:04:05):
Well, thank you for that introduction. Yeah, the story about plasmalogens is actually really an interesting one on many levels. It’s an interesting one in terms of just the medical community, but also how science works from beginning to end. It’s a really nice story. It’s like a detective story where you’re following one clue after another, trying to find the culprit in the crime here of dementia. And the plasmalogens are one of those interesting molecules where they’re phospholipids; they are part of all the membranes of the body. They’re not new. We discovered them about a hundred years ago and we’ve known about them for a long time. We know about their importance. So children who are born with genetic mutations that impair their ability to make plasmalogens have extremely high mortality. They don’t even live to age 10 and depending upon the severity of the plasmalogen deficiency, it effects their lifespan. So we know that it’s an obligate molecule for the human body, and we know that infants that are born prematurely, some of those infants will have what’s called bronchial dysplasia, which is basically driven by low levels of plasmalogens.
And so the importance of plasmalogens have been known for a long time and where they’re made have also been known for a long time in a special organelle called the peroxisome. But we just really ignore them because the most of our life we make enough of them. And it’s not a small amount in your blood. 20% of your entire brain living volume are plasmalogens; 35% of your heart, your lungs, your kidney, your eye function. So we’re not dealing with some very allosteric micro molecule that’s just found from someone’s super high microscope in the human body. We’re dealing with something that’s quite all of it to human life. And it kind of-

Dr. Gundry (00:06:01):
Let me stop you right there for a second. And let me go back for a second because some of our listeners will say, “Well, now wait a minute, what the heck is a phospholipid? And okay, a plasmalogen is a phospholipid, but that, that doesn’t mean anything to me.” So why don’t we start there?

Dr. Goodenowe (00:06:27):
So the best way to think about phospholipids is the thing called the human body, the human body has worth a trillion cells. That’s a lot of little individual three-dimensional spheres. And you can think of human body as a very large, massive apartment building. And every one of the individual apartments are separated from other apartments by the walls in an apartment building. And well, those are usually the heavy structural walls that separate one apartment from another apartment. But then there’s rooms within the apartment; how we compartmentalize, how we do things in the kitchen and bedroom and the bathroom and we keep things separate. Your body compartmentalizes its activities that way. And what the body uses to make all these walls are called phospholipids. And that’s the biological material that basically gives the human body its physical structure.
So a phospholipid is like a soap that you use for dish soap. So it has a polar head group that likes water. So it uses all the water. Then there is a non-polar or lipid like molecule that goes into the oil side. It’s like having oil and vinegar and you can get them blended. And what happens is phospholipids create what’s called the phospholipid bi-layer; non-polar group of one attaches to the non-polar group of another and the polar head groups stay on the outside. And so that’s how the body creates what’s basically a biological wall. And then that is that biological walls is how the body compartmentalizes all its activities. And so of course, things have to go in and out of this walls, just like in your house. You have doors and windows and you have electrical outlets that connect one cell to another cell. And you can imagine if your walls of your house just started to shrink, all of a sudden your doors wouldn’t be open properly where they closed, they wouldn’t close properly they open a little bit, maybe with weak air. And so that’s where the physical structure and human body comes in.
And a lot of these of phospholipids, all the building blocks of these phospholipids, you can get in your diet, like [inaudible 00:08:29] and our essential fatty acids that we get from our oils. Plasmalogens are unique in that virtually a hundred percent of the plasmalogens in your body; your body must make itself. And that what gives it a really … It’s kind of the most interesting plan and also lessons. It’s like building a wonderful washing machine and it is intentionally putting a weak belt in there, knowing that it’ll work for 20 years, but sooner or later that belt going to bend and that’s kind of the process of making the body. The nice thing about plasmalogens is it requires no dietary plan. You can make plasmalogens from the simplest fat molecules on the planet. So you don’t need Omega 3, you don’t need Omega 6 or Omega 9. So your body plasmalogens are so important to the body that it doesn’t require any dietary range. But that is also its Achilles’ heel because since it doesn’t require any dietary routines, you actually can’t get it from your diet. You have to make it. So as we get older and as the population gets older, we start seeing proximal failure from liver damage. And it’s very well revised in very many studies.
And so our ability to make plasmalogens starts to decrease with time. And of course it doesn’t decrease gradually. Some people have great proximal functioning, until they are 100 years old and some people start failing in their fifties and thirties. And so we have those types of discrepancies. When you talk about science, people think this, show these nice, beautiful graphs of how this molecule decreases with age. But that’s not how it happens for individuals that you meet. Most people will have normal levels for quite some time and then something will happen and then it’ll drop off. And then they will have low levels. Then we average all the people together, it gives a nice, beautiful looking graph on a piece of paper, but that’s not really what happens to individuals that you meet.
So what happens to make those graphs go down, it’s the number of people who become deficient increases. So say when you’re fifties, maybe only five or 10% of people have low levels, then you’re 16, 15 to 20, 30%. So the people with good normal levels have the same levels in their nineties that they have when they were 30. So they have no change. But the number of people who have low levels start to increase, and that brings the whole average down. And then when geeky scientists like us make graphs; it makes it look like everybody’s plasmalogen levels decrease a little bit every year. And that’s really not how it happens. That’s kind of interesting. That’s what plasmalogens are.
And what’s really interesting what these and their special powers is a special bond called vinyl-ether bond. And that’s what gives it its antioxidant capabilities, like its massive free, radical scavenger in the body. But it’s also that vinyl-ether bond is what gives membrane fusion. So the release of neurotransmitters in the brain was wired or highly correlated to cognitive function. And it affects protein function in the membranes. So it changes its solidity of your membranes, so that proteins do the involving work. That’s the thing. So then that special bond, that vinyl-ether bond unfortunately is very sensitive to acids. Since our body has lots of plasmalogens, you think if we eat a nice juicy steak or eat animal products, that you should be eating plasmalogens. But that vinyl-bond is sensitive to acids. And so when it hits your stomach acids, which is basically concentrated hydrochloric acid in your stomach, it breaks that bond. So dietary sources of plasmalogens are minimally bioavailable. That’s the phospholipid part of the story.

Dr. Gundry (00:12:27):
Okay. So we make them, if we’re lucky enough, we make them all our lives. So what does this have to do with dementia? Because obviously plasmalogens are needed in our brain, so keep with this detective story.

Dr. Goodenowe (00:12:47):
Yeah. So this is where it gets really exciting. So back in the nineties, we had this whole genomics revolution, right, the whole scientific method was changing. People were starting to say, “You know what, if the normal scientific method was, you have a hypothesis and you said, you know what, I want to test this hypothesis and I’m going to design an experiment to improve or disprove my idea …” right, and so you presuppose a question to answer. But in the genomics revolution, when we started sequencing human genome, people said, “Well, we don’t know what all these genes do. Let’s just stick with all of them, right, and let’s do large scale or big data type research, measure everything. And then you can call hypothesis creating and that who generate the data first. And then from that data, try to understand what’s going on.” And that changed the scientific method for the first time, well, in a millennium. And so that happened for the genetic system; biochemistry. So my background is a synthetic organic chemist and my PhD is in psychiatric medicine, looking at the biochemical mechanisms of psychiatric disease. So neurochemistry; how neurons and how certain systems in the brain interact with each other.
And so at the biochemical level, we didn’t have that kind of technology. We couldn’t measure all the small molecules, all your neurotransmitters and all the stuff we get from our environment. And so I had to stop a little bit from my research and become a toolmaker. So I invented this technology called non-targeted metabolomics, which allowed us to measure thousands and thousands of small molecules in any kind of biological metric, human blood, for example. And that allowed us the first time to measure thousands and thousands of things without any knowledge beforehand. So I didn’t go looking for plasmalogens. Plasmalogens came looking for me.
That’s where the story got interesting. So when we did this study on humans with different levels of cognitive impairment, and we measured it using this technology and measured thousands of molecules in the blood, a whole bunch of these molecules that had this very strange molecular formula were decreased in individuals with dementia and the level of their decrease correlated with the severity of the cognitive impairment. And I didn’t even know what these molecules were at the time. I hadn’t even seen these things. And so literally I googled this back in early two thousands and this plasmalogen molecule popped up. Because like I said, we’ve known about them for a hundred years and I’m going, “What the heck is this going on?” right, and so then there’s like 30 years old in your blood. There’s not just one. And so then that’s step one. So, okay. So we see this association.
Now the question from an association is, is that association causative or is it just a bystander watching an accident on the freeway? I guess is it part of the accident or is it just a coincidence? And so you go, “Wow, that’s interesting.” And so then you have to start studying more research and then we find out that not only is it decreasing the blood, it’s also decreasing the brain of individuals with Alzheimer’s. And originally people thought that was because as we get older, we get oxidative stress and it was breaking down these molecules. But what my main contribution was the discovery of this association in the blood, not in the brain suggesting that actually we’re dealing with the liver disease here more than a brain disease. Low levels of plasmalogens in the blood precede low levels of plasmalogens in the brain. And so that, of course required much more research.
And so we looked at people … How far before dementia symptoms, can we detect this in blood? Now on average seven years, the decrease occurred about seven years before we see cognitive symptoms in humans and we’ve done large clinical trials to reproduce this. And then you go one step further and say, ‘Well, okay, that’s interesting.” So mechanistically how? It’s like, so now you’ve got this true association of [inaudible 00:16:49] before genotype. We know it’s real. We know there’s an association, but we have to ask the question. So how is it acting, how is it that this observation is actually creating this phenotype that we can visually see that it’s not mysterious, that we see cognitive abilities decreasing?
And so then we started looking at more detail and that’s the correlation with membrane fusion, the releasing neurotransmitters and how they specifically relate to the cholinergic neuron system. So people that have Alzheimer’s, anyone who has a family member, he gets familiar with the drugs, the Aricept; that’s an acetyl cholinesterase inhibitor, is designed to increase acetylcholine. So we know for fact, and we’ve known this since the late seventies that the acetylcholine neurons are the neurons that get impaired and their impairment is what causes dementia. So the cause of cognitive impairment has been known unambiguously for well over 30, 40 years. That’s not in question. The question comes, how and why? What are the reasons for those cholinergic neurons to lose their functionality? And that’s where the amyloid hypothesis comes in and so on. But amylin again is a great biomarker, but it’s not doing anything. It shouldn’t be there. So the observation that increased amyloid levels in the brain, the protein [inaudible 00:18:23] is clearly shouldn’t be there.The question is why is it there?
And so we studied the role of membranes and we found that we could … If we increase the level of plasmalogen in the membranes, we’ve reduced amyloid levels. We could actually turn amyloid formation on and off based upon the level of plasmalogens in the brain. And when we looked at human brains samples post-mortem and we correlate, found that people that had high plasmalogens in their brain had low levels of amyloid in their brain, and then the high levels of cognitive functioning. So they’re in their cholinergic neuron system was in better shape. So we have this one step at a time getting closer and closer to, okay, this is not just smoke. This is fire. This is actually causative.
And then the next step was when bent molecules that could, since I’m a chemist, I could design biochemical precursors. So we could then study selectively increase different plasmalogens. Because the human brain has two main systems; is your white matter system, which is the installation part. It protects all your neurons. And so people with multiple sclerosis or autism or the white matter disease, and Alzheimer’s, and Parkinson’s is it gray matters. That’s the copper wire inside the-

Dr. Gundry (00:19:44):
Insulation, yeah.

Dr. Goodenowe (00:19:45):
Right. So those are your plasmalogens. And when people say, I want to Omega 3s in my diet, those Omega 3s are for the gray matter for the buyer and the inside, but your Omega 9s, your oleic acid, it protects the white matter. So they’re very different. So the different plasmalogen in the white matter than in the gray matter. So we could selectively increase different plasmalogen levels and ask the question, what happens if I increase DHA or the long chain Omega three.
And when we do that, we improve neurotransmission, we prevent Parkinson’s. So if we treat animals with the plasmalogen precursor that has the Omega 3 in it, we completely prevent Parkinson’s that we can’t actually cause neurodegeneration. So animals that have a biochemical reserve of plasmalogens are protected against neurotoxins. And we do the same thing with multiple sclerosis studies. Animals that have a biochemical reserve or Omega 9 plus options are protected against demyelination like multiple sclerosis. So now we can get really into that cause and effect because we can say, “Okay, what happens if I create a situation where an animal has this biochemical reserve, are they or are they not protected against neurodegeneration?” And the answer is unambiguously yes.
So we can prove then, that yes, biochemical reserves of plasmalogens are neuroprotective. And so now that’s how the story goes from association with the disease to actually being able to mechanistically identify the cause of the mechanisms. That’s pretty exciting. So we’re now at a point where we can look at … And since this is the membrane structure issue, the Alzheimer’s is really the canary in a coal mine. So we’re seeing this generalized neurodegenerative stress on human brain. And the question is what is the weakest link in the brain, what part of the human brain is the most sensitive in the most people with distress? And that turns out to be dementia.
So when you see there’s plasmalogen reduction in humans, the most probable observation clinically, well, first be decreased cognition, that’s also associated with increased risk of Parkinson’s or stroke as well, that those happen in smaller percentages. So Alzheimer’s is that canary in a coal mine. Obviously there is some variants in human populations, but not all the same, but we’ll get large numbers of people. The first thing that we observed is reduced cholinergic function. So sorry for being a bit wonky there. Hope to explain some of that hemisphere.

Dr. Gundry (00:22:54):
No, yeah. This is good nerdy wonky stuff. So let’s maybe pull it back to where the rubber meets the road. You mentioned before that we make plasmalogens, we make them all the time. And I think I heard you say that they’re primarily made in our liver. And okay, so what’s your hypothesis about why they stopped being made in some people and other people there a hundred years old and they’re still making them?

Dr. Goodenowe (00:23:31):
So I think it’s a combination of luck and environment. And probably there’s some level of genetics that give a little bit more resistance to it. So we know the liver toxicity issues with age. If you take a look at liver cancer rates over the last 20 years, it doubled or more. So we have some serious environmental influences occurring in our human populations. That’s one thing, so clearly environmental. And people, as you get older, your mobility starts to decrease. So they start walking and exercising less. And your musculature like your crossed zones are stimulated by physical activity, specifically resistance training.
So when you see clinical trials where resistance training has such powerful cognitive benefits, that’s one of the reasons we see that, is that if you resistance training … Basically what resistance training does is take all your peripheral muscles and turns them into mini livers, wakes them up and they start doing biochemical functions. Because your body is fundamentally lazy. Like your body is designed to do the least amount of work possible, right, so if I drop you in the middle of the desert, we want you to be able to walk across the desert, expanding the least amount of energy. So well balanced arm swing or feet walk. So we’re going to use our heart, we’re going to use our lung for 95% of our treatments. And so are our biceps and our legs and different things; we can only use them intermittently. And so, as you get older, all of this real estate of the human body to take advantage of. You can wake them up because they really haven’t been overused in our lifetime. And so that’s one aspect of getting it. So I think mobility, I think our diet of how people eat less well as they get older. And so there’s a combination of factors, oxidative stress, outbalance of mitochondrial function.
So those are the things like that’s my … I have a personal pet peeve in the aging community and that’s because I don’t really believe that aging. We have reduced functionality. Aging is really an association. So there’s many things like this … The human body survives about 60 years and they’re major old proof. Now from age one to 60, you pretty much have to step in front of a bus to die, statistically. So the systems are really quite robust and self-regulating. And then you start losing certain functionalities. And so the loss of function is associated with age, it’s not caused by age. And so I think you have these different things, oxidative stress that they have. That’s the kind of thing that plasmalogens … I mean I think people that have healthy lifestyle, limited drug pharmaceutical use, and then we have a higher odds of being good.
But what we have noticed though is that, so when the big university study in Rush, so the Rush University of Chicago, their memory aging or religious order study been going on for well over 20 years [inaudible 00:26:51] They had this huge longitudinal data set. And we looked at over a thousand individuals, 1200 and some subjects. And they isolated people the top 10%. And it was just a top 10% that had 80% reduced likelihood of the potential over six year period. So I think we’re almost getting to the vitamin D situation with plasmalogens in that normal levels for most of your life are fine, but just like vitamin D, even though it’s theoretically possible to get enough vitamin D, if you go out and you get inside and if you’re a construction worker, but for most of us, it’s almost impossible for us environmentally to get appropriate vitamin D levels. And I think we’re going to deal with the same situation for plasmalogens, where roughly only 10% of the population have naturally high protective levels. So the rest of the supplement-

Speaker 4 (00:27:49):
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Dr. Gundry (00:28:25):
Okay so that brings up two questions. Number one, early on you mentioned that you can certainly measure plasmalogen levels in the blood. Number one, can our listeners walk into their doctors’ office or their healthcare provider and say, “Hi, I’d like my plasmalogen level measured.” And of course they’re going to most likely be greeted with a blank stare. Answer that, but then, okay, let’s find out about my plasmalogen levels. And they’re low. What can I do about it?

Speaker 4 (00:29:02):
So good question. So first of all, yes, the plasmalogen testing is available in anyone in the United States around the world, basically. And so if your doctor isn’t aware of it, they can get in contact with our laboratory and blood samples can be shipped and your plasmalogen levels can be measured. And we don’t measure just your plasmalogen levels; we measure your other phospholipids. If your phosphocholine levels, we look at your 0mega 3, Omega 6 ratios [inaudible 00:29:28]. So we look at it more of a holistic approach. Plasmalogens are a critical component of it, but we want to know if your proximates are working or why your plasmalogens levels are low so we can fix them. So that’s number one. So yes, plasmalogen testing is available in a very simple and easy to understand way. So people either prodrome.com or dr.goodenowe.com, those will be linked out to people that can find that.
And then in the supplement, being able to restore plasmalogens, that’s been another big area of mine scientifically to understand that. So in our animal studies, we need around 10 milligrams per kilogram is roughly the dose maybe the last long-term. Like I mentioned, you have a lot of plasmalogens in your blood. So the average human has about a gallon of blood, that’s quite a bit of luck, right, and the concentration of plasmalogens is roughly about … The total amount of plasmalogens in your blood supply, maybe about a gram. Remember your blood is just a circulatory system and all your membranes will have like a hundred times higher. So really that’s what significant about plasmalogens. And so 10 milligram per kilogram is like half a gram to a gram is what you need for a therapeutic dose.
So important is that you can’t be driving a big semi-truck on the freeway and filling it up with a thimble full of gas, right, so you need to put enough gas in the tank to effect the plasmalogen levels. So the supplementation has to be sufficient enough at a dose that can actually effectively raise plasmalogens in the body. And so for that, you’re going to need over 400 milligrams of plasmalogens per day. And you need to get that properly in a proper, pure plasmalogen bioavailable form, that’s where my expertise in chemistry and design work comes in. And that’s what we’ve done over the last several years. So we have a really nice, a hundred percent natural bio-identical plasmalogen precursor, same concept is L-DOPA for Parkinson’s.
So in order to bypass this stomach digestion issue, we designed a molecule that is two steps up in the biochemical pathway. Because this is the very last step that your that makes it unavailable in your diet. So we make a molecule, it’s a human molecule, it is your natural biochemical intermediate that’s just two steps up. So then you can eat it, it gets absorbed and actually goes, not just your liver, it goes in all the cells of your body, your brain, everything so we can directly supplement every cell of the body. So that’s kind of where you’re at.
And the next thing with testing is that you don’t have to take anyone’s word for it, right, like even if you start feeling the physiological effects, which many people do very quickly, when you get re-tested, it’s not not black magic that you can want, here’s your blood levels before, and here’s your blood levels after, and you can target the level that we want to stay at, leave it there, and then go on and live the rest of your life, knowing that you have a reserve capacity of plasmalogens.

Dr. Gundry (00:32:49):
So you talk about biochemical reserve, can you literally build up a reserve of plasma allergens?

Dr. Goodenowe (00:33:00):
Yeah. That’s the exciting part. And so this is the stuck on stupid part of my scientific career. As scientists, we get so focused on the negative. So if you have all these clinical trials, you then have this cool technology that can measure thousands of molecules, right, a bunch of patterns in the space, and then we studied cancers and neurodegenerative diseases, and we focused on the disease. Okay, what’s wrong with the disease? Here’s someone with the disease and everything is disease, disease, disease, disease, for us. Probably 30 different diseases I’ve studied and develop biochemical markers for those diseases and biochemical programs, which means how the body changes before the disease occurs. But you just don’t walk down the street, get hit by lightning and we got the next morning with stage four colon cancer, but that doesn’t happen, right? There’s something that happens beforehand that sets you up for that. And that’s true. Measure that.
But what I was missing over the 30 years of research was the other half of that coin is that, I’m using normal people or healthy people as my other score, the football game versus the losing side, which is the disease side. And I’m focusing on what’s causing the disease side to be disease. And missing the most obvious is what’s good about the winning side? Like why are these people not getting diseases? And that’s where the biochemical reserve concept comes in. So this concept of saying, “Let’s look for disease, stop a disease,” that only gets you back to zero. That only gets me back to baseline. And so we can now move from baseline to biochemical reserve, to protective levels and to levels of … And the real fun part of this, is how far can we push human longevity and vitality?
No, one’s really thought about it, biochemical reserve past the perspective and say, “You know what, we have these systems, we can project them on their downward trend, just move them upward to a biochemical reserve capacity.” It’s why we take vitamin D for instance. So biochemical reserve isn’t a new thing. People don’t take vitamin C to prevent scurvy anymore. You don’t take your vitamin D cause you don’t want to get rickets. No one’s getting those diseases. So all of these vitamins, if you take N-Acetyl Cystine or if you take any kind of other supplements for maintaining glutathione or your [inaudible 00:35:28] so all of those concepts or biochemical reserve concepts, it’s saying, “You know what? I don’t want to wait to become deficient. I want to make sure I have sufficient levels now. And I don’t need to wait for a negative symptom to come in and fix the problem. I already know enough. I don’t, I don’t need to wait for my car engine to run out of oil or gas before I fill it up. I have enough knowledge beforehand.”
That is a concept of biochemical reserve. And can we do that in a systematic scientific way and more important, can you do it in a distributable way? This is the UPS FedEx problem is how do you deliver that type of medicine to large groups of people? Because you mentioned Alzheimer’s, you’re talking 30% of the population here and people don’t realize that most people don’t calculate in the survival bias in that equation. So when you talk 30% of 90 year olds that have Alzheimer’s disease or dementia, that’s 30% of the healthiest of the healthiest of us who actually made it to .90 That doesn’t calculate all the people who had dementia before them. So the cumulative incidents rate of the 95 year old is about 80%. So if you make it to age 95, you’ve already been without dementia. You’re only in that 20% of the population that didn’t get dementia.
So we’re not dealing with the disease. In fact, the people who don’t get dementia are the minority cumulatively. And so that’s I think what we’re excited about. I think dementia is going to one of those diseases of humans that really allow us to think of medicine in different ways, think of prevention in different way, optimization in a different way. And hopefully we can start eliminating age bias, where people as they get older, they don’t put up with getting older anymore. So I think we’ve got a good population with that as well.

Dr. Gundry (00:37:35):
A couple of things I think I’m hearing you say, number one, depending on the supplement, that supplementation doesn’t necessarily make expensive urine.

Dr. Goodenowe (00:37:49):

Dr. Gundry (00:37:50):
Okay. And I certainly thought that early in my career, and I certainly don’t think that now, because I can measure the effects of supplements in people like you can, and you can document what happens. The second thing is, okay, so I need plasma allergens, and you say it’s pretty hard to eat them because my stomach acid is going to do it, but there are tons of phospholipids. You mentioned choline and many of my colleagues in neurology, like Dr. Bredesen and Dr. Pearl Meyer, certainly think there ought to be a lot od choline in our diet. Maybe we should be eating egg yolks, right and left. And my colleagues in cardiology go, “Oh my gosh, choline is the worst thing that you can eat because your gut bacteria are going make TMAO out of it, which is one of the most lethal compounds for your blood vessels. So you got to stay away from phospholipids because bacteria eat them and make horrible stuff.” So what say you? Help us out here.

Dr. Goodenowe (00:38:58):
Well, phospholipids are critical. Choline is absolutely critical. It’s one of the most undiagnosed or underdiagnosed deficiencies. Virtually all liver cancers, pancreatic cancer, liver diseases are associated with choline deficiencies. So I’ll be presenting a bunch of work over a large, over a thousand person study in Chiba, prefecture, Japan on pancreatic and colon cancer in two weeks in Japan. And phosphocholine deficiencies are a major association with those cancers. And the level of choline in your blood correlates with your tumor group in pancreatic cancer, for example. Choline is absolutely critically important and it’s important because we at least didn’t consider choline a nonessential nutrient because technically your body can make it, it’s from ethanol. But the energy required to make it is quite demanding. And so, listen, it’s a major driver of blood homocysteine levels.
So I’m a big believer in choline. Now you can argue which is the best bioavailable source, whether you get this [inaudible 00:40:00] glycerophosphocholine, and those are really good questions and arguments because they are metabolized differently. When you take egg yolks, for instance, those molecules get metabolized by the pancreatic [inaudible 00:40:14]. And quadruple is another really critical molecule because it’s what you got your liver uses to make LDL cholesterol. If you can’t get cholesterol circulation. And [inaudible 00:40:28] then shows so amazing results in cardiovascular disease for a reduction in natural for our plaques, improvement of cholesterol transport mechanisms. So yeah, phosphocholine is absolutely something you don’t want to be deficient.
And [inaudible 00:40:44] is another one. So your active system is something that, well, everyone knows homocysteine elevation is a bad thing for cardiovascular disease and for Alzheimer’s, but most people don’t realize why. And reason why homocysteine is such a good marker is it’s usually biomarker cooling deficiencies. Because if you are choline efficient, your body is trying to make lots of choline, and that happens in the brain as well as in the liver and all the system by far. So long answer to your question, I’m a big believer in choline. You can have an argument over which is the best type of supplement, the pure choline or the alpha GPCs, those get absorbed without any blood digestion, but the phospholipid pathogens, they some level of digestion for volumes also.

Dr. Gundry (00:41:34):
All right, good. I’m glad I asked. All right. Follow up with that. So, how can I, or how can my listeners, what foods can my listeners eat to get their plasmalogen levels up, is there any way?

Dr. Goodenowe (00:41:52):
Not really, the only other sources have negative … There’s supplements out there, there’s biological sources of them, biological extracts and usually they have very, very small levels like a milligram or a few milligrams. And like I mentioned, your blood supply is like a thousand milligrams. So you can just imagine you’re adding a thimble full of plasmalogens to doing swimming pool size pool. And so you’re not really making a big impact. The natural sources are like certain liver oils will have some, but they have the negative consequences like sweating, and depending on the saturated size. This is where the scientifically designed side group is important. So we manufacture two types of plasmalogen precursors. One is the Omega-3 DHA. It’s a hundred percent Omega-3 and is pre-packaged with Omega 3 on the phospholipid [inaudible 00:42:46] position. It’s the only bioavailable source of plasmalogen precursors that way. And that goes directly into your neuron cells remembering function. And then we have a [inaudible 00:42:59] which is an Omega 9 plasmogen precursor. And it has a hundred percent [inaudible 00:43:04] is designed specifically for the white matter in the body. And it’s very potent antiinflammatory mechanism, especially in autism and multiple sclerosis.
And the unfortunate thing is that there in the natural world, that’s why these are natural supplements. Okay. So what we basically take as very what’s naturally found that very small percentages in [inaudible 00:43:27] oil that we create pure high bills molecule that is designed for specific purposes. So people can get confidence that they know what they’re taking and that’s where we’re at. Plasmalogen story is one of those it’s hard to get enough of them.

Dr. Gundry (00:43:53):
I’m aware, and I don’t think our readers or listeners are aware, Japanese study use plasmalogens derived from scallops in treating mild cognitive impairment. And that study was successful. Are those the plasmalogens that you’re talking about, or is that a totally different animal?

Dr. Goodenowe (00:44:22):
Totally different. Well, that’s the fully intact plasmalogen phospholipid. And that’s what gets metabolized by an enzyme called phospholipase, in the upper GI tract. So you get your phospolipid. And the important thing about plasmalogen supplementation is being able to deliver the right plasmalogen for the right purpose. And so yes, if you take plasmalogen from any source, you’re going to take enough of them, over time, they’ll have an effect. Absolutely. And so that’s great news.
The challenge we have to do for the scientific community is do larger studies. We have a problem going on in Santa Monica right now. We just did a trial in Minnesota that I’ll be talking about. But ultimately what’s nice about the program that we have now is that large numbers of people can take these products. They can measure their own blood, they can measure their own phenotypic observations, and collectively we’re going to start generating large amounts of actionable health information. And that’s what I’m excited about.
So yeah, so the plasmalogens can to be from other sources and eventually the obviously, if you can get enough from another source, it works, but the animal extract process is never a hundred percent accurate and our system doesn’t have any environmental contaminants because we use [inaudible 00:45:53] and vegan process. So we get our Omega 3s from an algae source and get her Omega 9S from a plant source. And those are source oF essential fatty acids. And we purify that first from the natural source, and then we can connect it to the plasmalogen vacuum. So what you get is a hundred percent vegan, fully purified product that has no risk of environmental contaminants or plant based products or animal based product, because it’s not actually extracted from an animal source. That’s the process that we’ve got. And that’s what we’ve used to testing all our preclinical structure, activity, relationships, and all of the certain sciences that’s behind us.

Dr. Gundry (00:46:47):
Alright. One last question, my medical practice has a lot of Medicare, a lot of insurance-based practice and the supplements are expensive. Why are they so expensive? Obviously I want you and other people to make a living, but is it the extraction process, is it the formation process?

Dr. Goodenowe (00:47:16):
It’s a lot of everything. It’s labor, the volume of manufacturing process. I feel exactly the same way you do. One of my collaborators, Dr. Bennett from Russia University says the best preventative has be as safe as water and just as cheap.
And that’s kind of where we’re at to ultimately try to get towards to this ability. So we’ve been able to systematically improve our manufacturing and improve our volumes. And my number one priority is to get this down into a price point that can be largely distributed because this is something everybody should have access to, period. And I think as we handle this both from the private pay perspective, so people can just pay for it and we’ll bring the cost down as quickly as we can in our manufacturing, but also from the bottom up perspective, in the sense that as we run more and more clinical trials, and we establish scientifically credible evidence of outcomes, but not from a drug perspective, from an actual supplement perspective.
And this is what our universities and our government funded research should be doing. They shouldn’t be in the business of pharmaceutical drugs. They should be in the business of looking at off patent molecules or natural based medicine, even the aspirin studies, and so on and so forth, right, so that the population at a whole, the public should benefit from all of this patented research that’s been done because once those patents expire, they’re supposed to be available for public use. And for public use, that should be our academic resources should be studying these things and making them … Like getting aspirin at Walmart. You don’t need a prescription for that stuff. It’s cheap enough. And so as we get better and better at things, these really targeted supplements should be able to get to that point. And then industries really generate sustainable revenues through the service side, servicing customers, helping them with their blood test, explaining what to do so you can pay for your time, you can charge for your services. You can charge for this, but have some common interest in the underlying science of these supplements.
So I think we’ll eventually get there. I think we’re seeing this, if you will, democratization of medicine and the people are starting to take things into their own hands and the power of the people is pretty big. So when you get large vine blocks of individuals and as we get better information tracking, I think you’re going to start seeing those shifts occur. Because, people get a little upset sometimes, but our current medical community is really good at acute care. If you get in a car accident, you’re going to get fixed because if I get cancer and I need two more surgical removal.
Our ability to handle acute medical needs is really, really good. And our system has worked really well to get there, but it’s not really designed for this type of work. It’s not really designed for preventative or this pilot chemical reserve concept, because, so we’re asking a square peg if they need a round hole. And I don’t know if it’s entirely appropriate for us to be forcing that on. So I think we need kind of a parallel, I think you’re seeing … Anyways, that’s why you and I are talking right now, because people need this information and they need to be able to act on it.

Dr. Gundry (00:50:53):
Correct. Yeah. That’s, that’s why I wanted you on the show to highlight an area that I’ve been fascinated with that, like I say, 99.9% of practicing physicians have never heard of a plasmalogen and wouldn’t know what to do with it if they saw it, I think.

Dr. Goodenowe (00:51:19):
But once I get it, it’s an interesting story because once people hear about it, they get a little annoyed, because how long have you not known about this thing? It’s really annoying that like, even myself, I’m an expert neurochemistry and pathomedical mechanisms, this wasn’t even on my radar 20 years ago. And so it should’ve been. And so I think once you get past that initial shock value and you say, “Okay, this is something that should be looking at.” And then interpretation, isn’t that hard. If people can operate an iPhone, they can understand these blood results.

Dr. Gundry (00:51:52):
So the blood results, so how do people find you find out about you? The blood tests and the supplements have to be done through a physician order if I understand it correctly.

Dr. Goodenowe (00:52:07):
That’s correct. And so drgoodenowe.com has much more, broad-based the [inaudible 00:52:16] work that we do in cancer, cardiovascular disease and neurodegeneration. And part of that is this plasmalogen, which is a really, really important part. And then from there, prodrome sciences does all the clinical research part. So any doctor who wants to be part of the program, wants to order supplements once it we’re a blood testing, can all be done through the laboratory testing infrastructure there. Any doctor who’s on full scripts can get ourselves through the formulary on full scripts. So the accessibility is pretty good. And if any person needs help finding a practitioner to provide them with blood testing resources or supplement resources, we can certainly direct them to individuals for that. And so we’ll do everything in our power to help people get the information that they need.

Dr. Gundry (00:53:03):
All right. Well, thanks for coming on. Let me conclude with, we both talked over the APOE4 gene, and I think one of the fascinating recent findings about why this gene is so mischievous is as you know, you have to have phospholipids to carry DHA into the brain. And because APOE4 won’t make the proper carriers to get DHA into your brain, I’ve been-

Dr. Goodenowe (00:53:46):
I know it was on my radar to talk to you about it the side. The APOE4 story is really an amazing story. Amazing, interesting story because there’s three main genome types, there’s the E2 and E3 and E4. And these three different genotypes have three very different epidemiological outcomes. Then number thing about APOE4 of things before it’s all related to cholesterol regulation and transport. And it’s when you’re younger, APOE4’s a very protective gene. It creates thicker, stronger membranes. So you’re resistant to parasites and bacteria and infections more than the rest. That’s why it’s genetically preserved in our population. It only becomes a problem when you get older. And part of it is plasmalogen deficiency. So we just published a huge paper on APOE4 showing that APOE4 carriers that have high plasmalogens in the blood have no increased risk of Alzheimer’s disease or dementia.
And we did a big all-cause mortality study and show that if you collect APOE4 plasmalogen level of blood, and whether someone had dementia, there was no increased risk of mortality if you had any fortune. Okay. So we can get this mechanistically down. So plasmalogens have a big role in cholesterol export in your DHA system, which is the only thing your brain has. So that’s where the equally, so we can have a whole podcast on APOE4 and-

Dr. Gundry (00:55:15):
Yeah, we may be back with that.

Dr. Goodenowe (00:55:17):
But I love to back for that one, but yeah.

Dr. Gundry (00:55:20):
All right.

Dr. Goodenowe (00:55:20):
I love that-

Dr. Gundry (00:55:21):
I’m sorry I brought it up. But no, I think this is actually really exciting because a huge part of my population are APOE4s and we’ve been trying to figure this out and it’s work like yours and you’re right, plasmalogens seem to be protective against this genes effect. So that’s exciting. All right. Well, we’ll try to have you back, but thanks for coming on the program and good luck with your endeavors.

Dr. Goodenowe (00:55:49):
Thank you very much for having me. I hope I’ve answered some questions and look forward to talking again in the future.

Dr. Gundry (00:55:55):
All right. Very good. Bye.
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All right. It’s time for our audience question. This week’s question comes from one’s Kiko on YouTube. I hope I said that right. Who asks, “I wanted to ask if you care at all about phytic acid. Oh, I care so much about phytic acid. No, I’m just being humorous. I have blood iron problems and it seems that phytic acid may be to blame as anti nutrient impairing iron absorption and other minerals. Flax seeds are on the yes list while they contain a lot of phytic acid. On the other hand, it seems important to include in the diet because of good Omega 3 to 6 ratio. But flaxseed oil is neither on the yes or the no list. Do you have an opinion about this oil? Thanks again.”
Well, I’m actually for most people, a fan of phytic acid and why is that? Well it’s because that in small amounts and the right amounts phytic acid can prevent iron absorption. And if you like the iron theory of aging, one of the theories of aging that I like, then higher iron levels associate with basically us rusting faster and lower iron levels within normal ranges, there is some very impressive research that correlates with slowing the aging process.
So one of the things that we can do in our diet to reduce iron absorption, which most of us get too much of in our diet is to have phytic acid containing foods. Like for instance, flax seeds. On the other hand, if you are a actively menstruating female, quite frankly, you’re going to lose a lot of iron every month. And that can be actually very problematic for a number of my patients. So in those cases really, you don’t want any help you in reducing your iron absorption. You actually want to increase your iron absorption. So that’s why you’ll see flax seed oil is neither good or bad in that. I take care of a large number of menstruating females.
And so the other thing about flaxseed oil, since you brought it up, flaxseed oil is a rich source of a short chain Omega-3 fat. And I have a lot of vegan patients who believe incorrectly that they can take short chain Omega-3 fats from flaxseed oil and make long chain omega-3 fats, which are DHA, DPA and EPA. And sadly, our enzyme system is horribly designed for that. So you could take all the shorts chain Omega-3 fats, and you will really only get about a one, maybe 2% conversion of those short chain fats into long chain fatty acids, which as we were just talking about today is what your brain has to use. So there are so many better choices for oils to consume than flaxseed oil.
I hope that answers your question. So yeah, if you’re trying to get your iron up, flax seed oil is way down the list as well as flax seeds. Okay. It’s time for the review of the week. This week’s review comes from Robodude69 on iTunes who writes the most logical educated and constantly updated health and nutrition advice. I love that Dr. Gundry updates his thinking when he gets new research. Well, thank you, Robodude69.
You’re right. I am not afraid to tell you that I’ve learned something new that goes against what I had learned before, or I had said before, and thank you for trusting me that when I find something that even contradicts what I said 10 years ago, or maybe last year, I’m going to let you know. And it’s based on my reading of the research and often it’s based on my patient population and what I’ve found that they’ve helped me out with. And one of these days we’ll talk about a recent paper that I presented that appends my whole idea of gluten intolerance and you’ll see more about in the coming week. So great question and thank you for that great comment. So that’s all for today. We will see you next week on The Dr. Gundry Podcast.
Disclaimer, On The Dr. Gundry Podcast, we provide a venue for discussion and the views expressed by my guests do not necessarily reflect my own.
Thanks for joining me on this episode of The Dr. Gundry Podcast. Before you go, I just wanted to remind you that you can find the show on iTunes, Google Play, Stitcher, or wherever you get your podcasts. And if you want to watch each episode of The Dr. Gundry Podcast, you can always find me on YouTube at youtube.com/Dr. Gundry, because I’m Dr. Gundry, and I’m always looking out for you.