Revitalize Your Brain With Plasmalogens

Dayan Goodenowe, PhD

Thank you, Dr. Sandison. I am very happy to be here.

Heather Sandison, ND

Let’s dive into it first. Personally, what made you interested in neurodegeneration?

Dayan Goodenowe, PhD

From the very beginning, just as a young boy, I was very interested in how the brain works. So as one thing leads to another, you can think of biology as the interaction of groups of organisms with each other. Then you go through school and you think of physics and you think of subatomic particles. But it was the chemistry that grabbed my attention because we kind of live in a chemistry world. The lowest common denominator is the atom, and according to the classical laws of thermodynamics, matter can’t be created or destroyed. It is the transformation of these molecules. Either we have chemical transformations that we do in chemistry, like burning fuel in your home, or we have biochemical transformations that the human body does. As you go on, as you go deeper into this thing, the most fascinating mystery of all is how the brain works and how the brain somehow creates a quantum mechanical power that it can use for choice-making in consciousness, which is a quantum mechanical thing, and understanding how that works. As I went through school, my PhD was in psychiatric medicine, looking at the biochemical mechanisms of disease. You just grab a piece of the yarn. You keep on pulling until the whole sweater comes apart, so to speak. 

One thing leads to another. So as you ask each question, it raises a list of other questions. Since my background is in synthetic chemistry and technology, not only do I have the opportunity to investigate these questions, but I also have the opportunity to build technology for them, and that’s where this whole Alzheimer’s and plasma halogens came in. It came from advanced mass spectrometry. It’s still the technology we use in the programs that can be tested today. Then, as you learn more, you start changing your preconceived or your plot options. We’re taught certain things, and we assume those assumptions are correct and are based on centuries of research. Some of them are, but some of them aren’t. A lot of science falls into this category of causation problems.  Associations are valuable because we use them for diagnostics. A huge part of medicine is about diagnosing a disease. 

Then it’s only kind of an afterthought. We think about the cause. Anyway, that’s how, for me, neuroscience works. Then, as we looked into molecules, this is where the story of plasma cells came in because they were identified using this high-field mass spectrometry to be associated with reduced cognition and the incidence of dementia, all of which cause mortality. I’ve seen some of this research work because of the plasma alone story, and we’ll get into it in a minute. We were invented back in the day, but we’re not invented. They were discovered back in the 1920s. Then we’ve known since the seventies that children with a deficiency in plasmalogen from genetic inborn errors of metabolism are very damaging. They die within a few years of birth. We know how important plasmalogens are.

Heather Sandison, ND

Isn’t this kind of plasmalogen, and what is that? What are we talking about? 

Dayan Goodenowe, PhD

As we start talking in the middle of the story. Exactly. What are plasmalogen? And why have you never heard of these damn things? This is where you almost like it as you like. I’m a neuroscientist. My piece is looking at the biochemical mechanisms of psychiatric disease. I had never heard of plasmalogen, never thought of plasmalogen; it was never in any of my textbooks, and I was never in any of my lectures. Then I use this mass spectrometry technology to find out about plasmalogen. Then, of course, you start doing the research as to what the hell these things are. I had the same question, and there are phospholipids, and they’re not trivial phospholipids; they’re a lot. You’re talking about 30% of your brain’s phospholipid volume being these plasmalogens, and so phospholipids are these molecules that are like soaps. We have a polar head group, we have a non-polar tail, and your body uses this phospholipid for many things.

Heather Sandison, ND

One would dissolve in oil, and the other one would dissolve in water. One molecule with a polar head on each side, one that would dissolve in water, one that would dissolve in oil. Everybody can kind of imagine that like if you put soap and water in the same container, you see how they separate. This is the bridge between those separated liquids.

Dayan Goodenowe, PhD

If you take, say, oil and vinegar. They have two layers, and you shake them, and then eventually they settle out. But if you put some egg yolk powder in there and shake it, all of a sudden it stays all together. the phospholipids and egg yolk, or what creates this emulsification. When you combine phospholipids, they create what’s called a phospholipid bilayer, and that’s a biological wall. Two of them combine, and the fatty acid non-polar chains combine in the middle, pulling polar head groups on the outside. You create this impervious lipid wall, and your body has 30 trillion cells like a massive apartment complex. Every single one of these cells is defined by this membrane, and this membrane is made of phospholipids and plasmalogen makes up a huge amount of it. In the brain, 30%. And 50% of the phospholipids in your heart. Plasmalogen is an incredibly large number. What’s so interesting about these molecules is that they’re so important to early childhood development. 

We talk about neurological perspectives, these phospholipids, and their different types. There’s the synaptic version. We talk about the omega three; we’ll get into that and the omega nine, which is myelin. These membranes that you have in your body have different purposes and different functions. From the neurological perspective, you have two main classes. One is the myelin sheath. It’s a protective coating on your axons that enables a signal to go from point A to point B, and you want that signal to pass through the axon and not leak out at all. So the plasmalogen there provides this protective coating. It’s called myelin. It’s a key ingredient in human breast milk for the myelination of children because the plasmalogen is in it. And we’re born with these raw bare wires. So this myelination process, which is about 60% of the brain, is white matter, which is all myelination. then the other part is gray matter. That’s usually the cell bodies, but also the synaptic function, where the wires end and they get bared if you will. Then they have to communicate with one another. 

That communication process happens at what’s called the synapse. That synapse is where neurotransmitters get emitted from one neuron to the next. But of course, it’s human biology, so they use biological materials to do this, and biological materials that involve the vesicular fusion process are dependent upon plasmalogen. If you have no plasmalogen in your synapse, neurotransmitters can be released. So that’s where plasmalogen is a critical component. From a neurological perspective, it’s those two components. Then, for cardiovascular health, it’s because you’re involved in inverse cholesterol transport. They’re critical to lung function. Children who are born prematurely will often develop bronchial dysplasia. They have a plasmalogen deficiency and are asthmatic plasmalogen deficiency. So there’s a few other core components of human physiology, all this stuff, all these stories with myocarditis. When you have heart inflammation, that causes a severe depletion of plasmalogen.

Heather Sandison, ND

These molecules are used all over the body in every single cell. Specifically, tell us again: how does this relate to dementia, and how was this relationship between low plasmalogen levels and dementia originally discovered?

Dayan Goodenowe, PhD

That’s what was my claim to fame: my original patent portfolio was related to this causation of plasmalogen depletion because plasmalogen is also your most important antioxidant in the body. They fall into one of the three classes of molecules that are so important to human physiology that the human body does not depend upon any nutritional source. Cholesterol, for example, is 75–80% of all the cholesterol in your body that you make yourself get very little from. You could eat a completely cholesterol-free diet and still have enough cholesterol in your body. The same thing with possible choline is another molecule that your body fundamentally makes from scratch, and the third one on that huge list of these plasmalogens. So since you make a lot of them, they also have this vinyl ether bond that makes them very sensitive to acid, which is what your body uses to fight inflammation. 

If you have oxidative stress, plasmalogens get depleted in oxidative stress. Studies back in the nineties have seen plasmalogen decrease in the brains of people still with Parkinson’s or Alzheimer’s. It was assumed that this was due to oxidative stress. The Alzheimer’s brain has oxidative stress, which is very well documented. Microglial activation—that kind of stuff. So this low plasmalogen level was assumed to be a symptom, not a cause. Then, when I looked at the temporal relationship between the predictability of the future and the association in the blood, it became very clear that this was not happening after the disease. It was happening before the disease. Then, when you start digging into it, you start understanding why. So the canary in the coal mine for dementia is the cholinergic system. We know that very accurately from the seventies. Things that improve choline transmissions, like choline inhibitors, for example, will improve cognition.

Heather Sandison, ND

Not for very long.

Dayan Goodenowe, PhD

But they still do. The clinical trials back in the early nineties, we’re pretty clear that it works, but it doesn’t work very long. It’s not disease-modifying, but if you give someone scopolamine, like a choline antagonist, you can treat dementia immediately. That’s a drug people use for abusing people called the Devil’s Breath. We know very clearly that, from a cognition perspective, the cholinergic system is critically involved.

Heather Sandison, ND

It plays a role, but it’s not the only thing that can cause dementia.

Dayan Goodenowe, PhD

That’s the core component. The nucleus basalis and its projections, the cholinergic projections throughout the brain, and act acetylcholine release from the presynaptic neuron activation of the muscarinic receptor and the postsynaptic neuron. Even those are pretty robust, and if you take a look at nucleus basalis shrinkage for our terminal fields if you look at functional connectivity of the brain, and you look at the cholinergic endpoints, those things all correlate very strongly with cognitive function. So if you look at historical data from that perspective, the question now becomes: what are the different mechanisms that can lead to the dysfunction of the cholinergic system? There are many ways to get there. There’s not just one way to get there. That’s why we have these multiple causations. You can have an inflammatory disease, you can have vascular dementia, and you can have Alzheimer’s dementia. You have these different types of dementia. You can get a concussion and lose dementia. You can have liver surgery and have dementia. You can have surgery for breast cancer and have post-breast cancer dementia.

Dementia is something that is a behavioral-psychological process. It’s a functional measure. It’s how someone can perform in their work around the world. It’s no different than how fast I can run 100 meters. Cognition is a performance value, not a biochemical value. The question is, what are the biochemical contributors to that? When you unravel that onion, you end up with this cholinergic system, which is why things that affect it, like the homocysteine levels, Homocysteine levels are elevated and increase the risk because that’s the methyltransferase system. The weak link in this field is easy to call in nerve transmission, and where the plasma has come in is that it’s involved in the circular release of neurotransmitters very clearly. The postmortem data is extremely robust, and you have a powerful linear correlation with the level of plasmalogens in the brain, especially gray matter plasmalogens and omega three plasmalogens, and cognitive function. We did very large studies with Rush University in Chicago. This has been reproduced in the ADI data sets. It’s been reproduced over and over again. It’s very robust information on this. The question is: how is this translating into the behavioral observation that we see in the person in front of us? That comes down to the fact that the CD choline neuron is very different from all the other neurons in the brain. 

When you have dopamine, serotonin, or adrenergic synaptic transmission, the presynaptic neuron releases a neurotransmitter. Dopamine, for example, for a movement like Parkinson’s, when the dopamine performs its function on the postsynaptic receptor, the neurotransmitter gets taken back up into the pre-synaptic neuron and gets recycled, ready for the next nerve transmission. Acetylcholine doesn’t do that. You release acetylcholine. Acetylcholine acts on the postsynaptic receptor. But then it gets metabolized down to choline and acetate, and the choline gets taken back up. This is where it becomes a very different scenario. This is way back when Wortmann and a bunch of people were trying to find a way to improve cholinergic systems. They tried massive doses of choline supplementation and a whole bunch of other things. People would smell like fish. It would be coming out of their pores. It was very difficult because, back then, we had a history of L-dopa for Parkinson’s, a miraculous drug. Like, you can give people L-dopa, and it’s the awakenings, and it’s incredible. So they thought, if this works for dopamine and Parkinson’s if we could find a precursor for choline, then we should be able to get the same observation in Alzheimer’s or dementia as we get in Parkinson’s. The problem is, that dopamine is a very selective molecule. It’s only involved in certain cell types. So the neurons that take up dopamine are very selective. Choline is part of every single cell of the human body. It’s one of the most important core nutrients in all human physiology. 

So the question is, you can’t just give it to people choline and expect it to hit the cholinergic neuron system. So that’s where the problem came in. Then it wasn’t until the late nineties, early 2000, that people discovered that there was a very specific optic protein called the choline high-affinity transporter that brought choline up into acetylcholine neurons. That transporter is only on the vesicle. What was happening in Alzheimer’s disease and what we see as the shrinkage, like Alzheimer’s causes or dementia, causes, neuronal shrinkage doesn’t cause apoptosis until the very late stage of the disease. But anyway, the point is that if you impair vesicular fusion, not only do you stop the transmission of acetylcholine, but you also stop the reuptake of choline into those neurons. So the plasmalogen deficiency causes choline starvation in the neurons. It’s blocking choline uptake because the uptake mechanism is on the vesicles. It’s not sitting on the presynaptic button. 

This was, this changed. This is where the causation comes in. This is why homocysteine these are not in Phos choline because if your brain has to make acetylcholine from scratch, it makes it from a method called pulsatile ethanol and methyltransferase is the metal-transfer system. When that gets turned on, homocysteine goes up. So this is why we have these markers: we have good markers, they’re accurate, and they’re good to measure for a reason because they tell us things. So that’s how the causation pathway came why these low plasmalogens were selectively or why we saw a strong association with dementia. And they’re social with Parkinson’s. They’re also socially affected by ALS or other neurological diseases. But, very clearly, of all neurological diseases, dementia has the strongest association because the acetylcholine neuron has a selective sensitivity to this, the vesicular fusion process in the brain. That’s a long story, but that’s how. That’s where I wrote the paperback in 2007 about peripheral ethanol in plasmalogen as a causative factor. I went through all of these details and extensive research in the past and kind of combined it all. But then that leads us to the next problem: What are you going to do about it? Why has this plasmalogen problem been plaguing us since the 1970s? We have these kids with Rhizomelic Chondrodysplasia. We got Zellweger syndrome; we’ve got leukodystrophy. We have neurodevelopmental disorders all associated with these little plasmalogens. There doesn’t seem to be any way of getting them in. So that’s kind of where I’ve put my medicinal chemistry hat on and synthetic organic chemistry. Still, we started looking at how we get precursors that can restore plasmalogen. So now we can do that.

Heather Sandison, ND

They are good for the environment. 

Dayan Goodenowe, PhD

Then you have the worry of what’s squealing and some other things that go in, and it’s all saturated, so you can’t target. You want to have specific Plasmodium-specific purposes. What I also discovered was that the structure of the precursor was important. You had to put the fatty acid that you wanted in the center position. If I want to restore myelin, I have to put omega-9 oleic acid in the center position, but I also want to increase neurotransmission, neuromuscular function, or reverse cholesterol transport for cardiovascular disease. Then I need to put Omega-3 DHEA, and that will be delivered into your cells and allow your cells to make the final product. That’s where the very pure individual precursors are required to deliver very specific outcomes, which is why we have dramatic results.

Heather Sandison, ND

Tell us about the results. What have you seen, and what kind of trials have you done on this? If someone were to take this, what could they expect?

Dayan Goodenowe, PhD

We had some pretty crazy results. We have a clinic in Canada now. It’s up and running, and it’s a restorative clinic, and we use higher doses and things. But in the general population, we have them, when we look at advanced MRI, I have more multiple sclerosis patients where you can measure the change in their neurovascular coupling. They find their functional conductivity, and people who have not lost vision for 25 years are getting vision in their eyes for the very first time in 25 years. I’ve ALS patients who are now walking. I have dementia patients who were under conservatorship and are taking their businesses back.

Heather Sandison, ND

How could it help dementia patients, and Alzheimer’s specifically?

Dayan Goodenowe, PhD

When it comes to dementia and Alzheimer’s. Alzheimer’s is a disease; it’s a pathological diagnosis. You have two types. Alzheimer’s disease is a challenge because we have Alzheimer’s dementia and Alzheimer’s disease. They both have the same acronym, A.D. and they’re very different things. If I take a postmortem brain and measure the pathology of the brain, I can diagnose Alzheimer’s disease. Whether or not that person had functional dementia is separate. Alzheimer’s disease is determined by the accumulation of amyloid plaques in the internal neuronal space and neurofibrillary tangles in the dendritic tissue inside the neurons; these dendrites are attached to the cell bodies. They occur in different places of the brain at different times. People think that they’re together, but they’re not. They’re very different. The neurofibrillary tangles are entirely driven by methyltransferase deficiencies. When you have homocysteine and those, and so you have tauopathy, they’re very highly dependent upon this elevated homocysteine or DNA. Also, almost every DHA is highly driven. All of the nerves have tangle-type pathologies, and these affect axonal function. Then you have the amyloid plaques, which are fundamentally driven by cholesterol transport through the membranes. so the APOE genotypes, for example, people that are APOE-e4 positive for one or two APEO, they’ll have higher levels of amyloid. The elevation of amyloid in APOE-e4 carriers contributes to the risk of dementia. If you’re an APOE-e4 carrier but do not have elevated amyloid, your genotype has no association with cognition or dementia. APOE-e4 will put you at higher risk of amyloid, which in turn is a biomarker of a fossil of cholesterol transport. So plasmalogens play the yin and the yang to the APOE. APOE is your HDL particle in the human brain. That’s Alzheimer’s disease. in Alzheimer’s, the Plasminogen precursors, because we’ve shown this in all this work. If you increase DHA plasmalogens, we can reduce amyloid formation, and postmortem brain studies, people who have high DHA plasmalogens in the brain have low amyloid in their brain.

We have very clearly seen in the laboratory and in humans the association with DHA, plasmalogen, and amyloid function. The mechanism is very drawn out, so people think of amyloid, and they think of the beta-secretase pathway. Beta-secretase is relatively small, contrary to the amyloid precursor protein. We’re getting into the weeds on this thing, but the mechanisms of this whole thing are extremely detailed. Alpha-secretase is the predominant enzyme that breaks down the amyloid precursor protein, and alpha-secretase is highly dependent on plasmalogen levels. We can turn alpha-secretase up and down just by changing plasmalogen levels in the membrane. People who have high levels of DHA plasmalogen in their brains have high levels of alpha-secretase, and when the alpha-secretase levels are high, APP is processed through that process. It also creates these secretory APPS, APP Alpha, and that’s hugely neurogenic. It’s what we use for neurogenesis. People look at this Alzheimer’s disease. They try to develop animal models that don’t make any amyloid. Like, for example, they try to block APP, and you can’t get a viable rat pup with no APP. APP is obligated for human survival, mainly survival. Anyway, so back to Alzheimer’s and Plasmalogen precursors, I don’t have a single situation. We don’t have any cognitive improvement with plasmalogen. Not one. I don’t have a single situation with people that I work with.

Heather Sandison, ND

How long does someone need to take them and what dose?

Dayan Goodenowe, PhD

Now that’s where we learn. We first reviewed our publication with Dr. Jordan’s group in Santa Monica. We didn’t escalate the dose; we started at one gram, 900 milligrams, and then we just did a pharmacokinetic study to say dose escalation and see if you could reproduce in humans what we had done in animal studies in the past. So we went from 900 milligrams to 1800 milligrams to 3600 milligrams. We just did dose escalation, and we saw a dose-dependent increase in plasmalogens. We saw in 22 people a statistically significant improvement in cognition in four months. We now see that with higher doses, the mobility improvements, like the neuromuscular junction improvements, were greater than the cognitive improvements. These are clinical dementia-rated subjects. We had 75% of the people with mild to moderate dementia improve an entire score on the clinical dementia rating in less than four months, and that’s just in a dose escalation study. Now, when we deal with it, we do a little more in higher doses. We have children who are on ten ml per day. They’re for leukodystrophy, and we’ve found that they’re no longer terminal. For example, these children are growing, and their brains are developing again. 

Heather Sandison, ND

So for dementia patients, I just want to pivot.

Dayan Goodenowe, PhD

We’re on dementia. 

Heather Sandison, ND

This is the Alzheimer’s Summit and so I want people to understand, so they can get the practical application of this and get the benefits of it. What would they need to be taking in for how long before they could expect to see a change?

Dayan Goodenowe, PhD

If we go to higher doses, if we go up to about five, even five to 10 mils for dementia, where people have an actual clinical representation of dementia, and if we go to a relatively high dose between five and ten ml per day, you will see improvements within a couple of weeks. I tell people to invest in one month of high-dose therapy, and then they can scale back from there.

Heather Sandison, ND

You can recover, please, and then you can go into maintenance mode.

Dayan Goodenowe, PhD

This is a reversal of how we started this. We thought we started saying, Let’s do dose escalation. Let’s start small and go up; we go carefully with people and make sure they don’t have any, because it can be quite stimulatory, like for an 88.

Heather Sandison, ND

Tell us about the side effects. We do have to worry about it?

Dayan Goodenowe, PhD

Know these might effects we have in people with bipolar or ADHD. Those individuals we typically treat with the omega nine plus mountains for myelination. because you’re quite stimulatory like the omega three, or people wake up and you start seeing them; they’re engaged; they’re moving. So if you have anxiety, or if you have any kind of ADHD tendencies, go a little slower.

Heather Sandison, ND

It can be stimulating.

Dayan Goodenowe, PhD

It’s very stimulating. Then that’s kind of typically told to people: take it in the morning or early afternoon, and by lunchtime-ish, we switch from the new way to three to the omega nine for nighttime. Make it nine, which we use for brain inflammation, concussion, stroke, and all autism-type programs. But for dementia, we’ve learned now that if we ramp up quickly, you start seeing, and you and we can see it on MRI quite robustly, like that the neurovascular coupling improves, the functional MRI like the board like we use a blood oxygenation level-dependent scanning to look at the connectivity of the nucleus basalis, and other cortical regions that very reproducibly improve. 

It does work. then we use plasmalogens as a kind of, now that I got your attention, let’s fix a few more things while we’re at it. Like, it’s not the only thing in the world; it’s a pretty big hammer. It is something that I have to say. As a scientist, I’m pretty shocked myself. Like, you don’t program them to see these effects. You’re not programmed to see people just wake up like we have people who haven’t walked for four years in six weeks, they’re dancing with their parents, with their little ones. This is kind of crazy stuff like that, and it’s crazy when it happens once. Then it happens twice, and then it starts happening quite reproducibly. Then the phosphocholine system we use in egg yolk oil will enable us to find the Omega nine. Getting phosphocholine in the brain is critical,  we now have a phosphocholine blend that helps that part of the brain. I’m a big fan of other core precursors, like N-acetyl-cysteine, L-carnitine, and CoQ10. When we start this process, the plasmalogen gets people hopeful that things are happening. then we say, Let’s not stop there. Let’s fix a few other things while we’re at it. You have your lifestyle and other health issues and try to remove things from your environment as much as possible. But at least we can get them. They get enough of a signal that they say, “What? Th is serious, and we can go. 

Then you can have a blood test that can measure these things. They show the change in plasmalogens. You can also look at other core components like your HDL levels, and you’re getting your triglycerides in the proper space, getting your homocysteine methyltransferase system properly, reducing the C-reactive protein, and the oxidative stress markers. One of the things that we found in the clinical trial that we published with Dr. Jordan’s group was that we had a dose-dependent decrease in monoaldehydes. Oxidative stress markers went down, and catalase went up. So we know that biochemically, we have a very logical, systematic, mathematical, if you will, approach to this. The only difference is that now personal individuals will have their own, like it’s food, like we’re not talking, and plasmalogen because we’re dealing with bulk like it’s not a trace level. You need actual full material, and if you take them in a fasting state to get past the blood-brain barrier, We like the whole concept of how we move things on kind of microns through the blood supply. the supply, your muscles, and your brain. Different systematic ways can improve it. But for most people, I say just take it in the morning on an empty stomach, if you can, with a little bit of protein, oil, or fat, kind of a semi-keto breakfast, and then you’re going to get your best results in those situations.

Heather Sandison, ND

Amazing. This is so informative, so hopeful, and so straightforward. I just want to kind of recap that. If someone is going to take this plasmalogen and start trying it,  of course, if you hear you’re listening to this, you’ve already heard a bunch of other talks about the Dr. Bredesen approach. So what you’re doing is exactly what Dr. Goodenowe is suggesting. You incorporate knowing or considering incorporating the program sciences supplementation into an overall comprehensive, lifestyle-based intervention for optimizing cognition at whatever stage you’re at. So, as you have said, you would take a big cup of five to 10 milliliters in the morning because it can be a bit stimulating. That’s part of what we want. We want to wake the brain back up. Then you do that for about a month or so. Try that for about a month, see how it goes, and then move into more of a maintenance dose. What would a maintenance dose look like? You would also be taking it on an empty stomach so that it can be absorbed and then shuttled to the right places to get it.

Dayan Goodenowe, PhD

That’s ideal. Like if you can’t, for GI, you can tell them the science. But everyone has to work in your life. You have to be able to because nothing is worse than compliance, which will eliminate almost any good effect. People have to be able to put it into their lifestyle. So that’s kind of where it is: go slow, start with a ml, go to two or three things.

Heather Sandison, ND

Our patients experience diarrhea. I know with it some of the fat-soluble things. MCT oils and coconut oils—we see that as people try to add those, they can run off to the bathroom, and that can be frustrating for caregivers and people suffering from dementia. It’s just a whole other level of complexity and mess. 

Dayan Goodenowe, PhD

We don’t see that at all. We don’t. It’s interesting. We have a lot of work in the gut world, and I use some peptides for the gut, so we also use humanoids, but the plasmalogens have improved gut function in people with colitis. So if anything there, it’s only constipated, but it’s certainly not diarrhea.

Heather Sandison, ND

I have to worry more about the activity and the alertness. That’s fantastic. Then, if you were to go down to maintenance mode, what does that typically look like? 

Dayan Goodenowe, PhD

For people in the early morning, like you and all of us in our over-50 crowd, if you will, in that three ml range, it is typically six capsules in the morning of neuro. Six couples at night of glia are typically the best long-term. when I showed my brain, I was able to reverse 15 years of brain aging with my brain using high-dose plasmalogen, and we can look at volumetric white matter microstructure. So there is the ability to restore function. Then if we want to kind of keep pushing the envelope a little bit, we need to; it’s just a matter of getting materials above a certain pharmacokinetic threshold. Then,  we have about 2000 doctors in our network. We have lots of experience. Our roundtables like the stories among the physicians and the different situations. I’m like, it’s not just like dementia is a huge deal. That’s our it’s the most obvious improvement. 

Even normal people like you come back and say, I just remember numbers better, and they remember trivia better, and they  know.” It is an interesting thing. People with long COVID that are getting just can’t get the brain fog that people are experiencing. Those are things, so it’s quite a big, diverse group. That’s why dementia itself—you have Alzheimer’s, vascular dementia, Lewy body dementia, or even post-concussion dementia-type things. These all have different pathways, but in the end, they still affect this synaptic system. That’s why that system can be affected by acute inflammation. It can be affected by nutritional deprivation. It can be affected by a failure to have the right methyltransferase system, like B12 deficiencies. There’s more than one way for that neurological system to become impaired. But restoring that system with the core components means we finally have tools that are logical like we’re not guessing. It’s not a shotgun approach anymore, and it’s a very reproducible work.

Heather Sandison, ND

You have written a book called Breaking Alzheimer’s. So for anyone interested in learning more from Dr. Goodenowe, who goes into much more detail in this book, it’s a great read. So tell everyone where they can find out more about you. The book and pro-drug sciences.

Dayan Goodenowe, PhD

At prodrome.com, you can find supplements, blood testing, roundtable access, and all that kind of stuff. Then, at drgoodenowe.com, we have the perpetual health clinics, where more of our research programs involve advanced MRI technologies. Those things are more at the Dr. Goodenowe: we have a charity for rare diseases in children, leukodystrophy, and we treat all these children around the world free of charge. So that’s all found at drgoodenowe.com.

Heather Sandison, ND

Thank you so much, Dr. Goodenowe, for your time today. But just the work—the incredible and very unique work that you’re doing in the world and the charity—I didn’t realize that. Thank you for doing that. It is special and amazing.

Dayan Goodenowe, PhD

Yes, amazing children, it’s like these: leukodystrophy, Canavan disease, Rett syndrome, and Rhizomelic Chondrodysplasia punctata. It’s very exciting, and it’s just amazing to see these children come back.

Heather Sandison, ND

What a massive impact you can have on the next generation!

Dayan Goodenowe, PhD

We’re getting there. Autism is a huge program for us. I guess it’s related to that.

Heather Sandison, ND

Interesting. I think of autism and dementia as kind of flipping sides of the same coin, one happening early in life and the other later in life. 

Dayan Goodenowe, PhD

It’s a dismyelination. Autism is an inflammatory-mediated dismyelination event. So, later on in life, we have the same thing. The problem is that when they’re children, they haven’t built up the plasmalogen stores for their myelination, so we do massive myelination for the first six to eight years of their life, and that’s why autism doesn’t occur in children. If a child doesn’t get autism by age six, it’s quite rare for them to get autism after age six because they’ve built up sufficient stores. But then again, fast forward to our sixties and seventies, and so we start losing like we’re exactly. You’re 100%, Dr. Sandison. It’s a kind of bell curve. If this inflammation happens early in your life, in your brain, it prevents the myelination from occurring. If it happens later in life, it causes an accelerated aging process fundamentally. Then, cognition is one of those early signs that we’re aging, if you will, from a very simple perspective.

Heather Sandison, ND

How exciting it is to have things that we can do to address it. Thank you again for your time, your expertise, and for being with us here today.

Dayan Goodenowe, PhD

Thank you very much, Dr. Sandison. I’m happy to be here.