Is Alzheimer's Really an Autoimmune Disease? Dr. A Explains

I got a bunch of questions about, which is Alzheimer's disease, and is it really more of an autoimmune problem, or where do we think it is coming from? Hey, it's Dr. A. Welcome to my YouTube channel. I've been teaching and researching in the world of integrative and naturopathic medicine for 30 years now. I've been seeing patients for a very long time. I use this channel to try and help answer questions and do patient education. So let's break this down. First thing I want to talk about is dementia as a condition versus versus Alzheimer's as a disease. So while Alzheimer's disease has dementia as one of its primary characteristics, dementia is a finding medically. And when you think of dementia, it could include things like Alzheimer's, but other conditions as well. So someone could have dementia because they had a brain tumor, for example. Somebody could have dementia because they had a head injury. Somebody could have dementia because of a toxic material or too much alcohol ingestion or any number of other things. So dementia is a finding about the memory and the state of the memory secondary to something. Now, a very common reason for dementia is Alzheimer's disease, which is a specific disease type. And what comes up a lot is you might also consider it competing theories, competing ideas about the basis for Alzheimer's disease. So sometimes you read about Alzheimer's and this group of researchers thinks it's this, and these other people think it's this other thing. And then there's sometimes, you know, Oh, this research was discredited because of this. That goes on a lot with lots of diseases, but especially in Alzheimer's disease, we know what the effects are, but the true cause, we look at people's brains after they've passed away. We look at people's brains under functional imaging while they're still alive and a number of other things. So we can kind of characterize what's wrong in Alzheimer's disease, but what's at the real root of it? What's at the base of the cause is one of those things where the more we learn, the more we understand and the The broader the cause seems to get. So I wanted to talk about some of the things you probably heard the most about, and kind of break them down and look at the idea of Alzheimer's disease as a totality of dysfunction that has a pathological basis, and then that gives us a pathological output as far as our memory and behavior, etc. So the first and probably most common idea in Alzheimer's people have been talking about for quite a long time is the beta amyloid or amyloid beta hypothesis. So the The amyloid is part of a larger structure, and it can lead to deposition in the brain. It can lead to collection of other proteins, and essentially it's not supposed to be there. You can have amyloid elsewhere, like your heart or your kidneys and other places like that too, but it's just not supposed to be there. So you can imagine if it's in your neurons in your brain and it gets in the wrong place, it might cause dysfunction in the way that your neurons fire and talk to one another and create memory and all those other things. One of the big supports to the amyloid beta hypothesis is that when people are given anti-amyloid drugs, you do slow cognitive decline. This makes a lot of sense. So if I have a theory that this thing underlying my disease is there, and I have a treatment that can block the underlying condition, and then the person either improves or their disease slows down when I block the underlying problem, that would make a lot of logical sense that that may be part of the problem. Now, one of the things with any of your organ systems, especially with your brain where it can be, it's very complex. It's not just sort of two-way communication. It's multi-leveled and multifarious types of communication. There's lots of feedback. There's lots of crosstalk. When you start to have something physical like amyloid beta deposition and other proteins and things, depending on where that goes, the output may be different among different people. So while generally people might have a dementia picture, some people may have more neurobehavioral issues that go with their dementia. Other people may have more neuropsychiatric issues that go with their behavior, and some people have all of the above. So that does happen. There was, I forget when it was, but a while ago there was some kind of shade thrown on the amyloid beta research, some of the newer research saying, well, maybe not all their numbers were real, or maybe not all their numbers were legit or whatever. And I think the important thing about that is that can happen with individual research projects. It certainly does. And so sometimes maybe a piece of the data is sent over to one person and then it's cross-checked by another person, but Maybe the rest of the group kind of looks at it and, you know, they can take at face value what the, you know, the expert in that area said. Occasionally when this happens, it's something is missed, maybe statistically, maybe as far as the values that are put in. My point here is that the shade kind of thrown on the amyloid beta hypothesis is really at particular research. And maybe that wasn't all done up to spec and it wasn't all the best. But what it doesn't mean is that the whole amyloid beta hypothesis is completely null, is completely, you know, Useless. There's still something there. Now, my personal opinion is because it's a multifactorial disease, meaning there's probably multiple layers of trouble. The amyloid beta hypothesis has a role, and it's probably a moderate to large role, but it may not be the only role. Before we get to another one that's probably the biggest and a little bit newer, at least in the news, I want to talk about an old, old idea, and that is around aluminum and Alzheimer's and the aluminum soda. Speak controversy. So, and this, this goes way back. It was found that aluminum was higher in the brains and the blood of people with Alzheimer's and on postmortem, they would find more aluminum. And one of the things about aluminum is it's ubiquitous in the water supply around the world. Some places are higher, some places are lower, but there's no way to not have some background aluminum in usually your water supply or maybe even your food supply. And aluminum is not a heavy metal, but it is a metal and it's a metal toxic And so what it does is it can get into your tissues. And in tissues where you have very sensitive neurological functioning, what you have is very sensitive, we call ion gating or mineral gates. And you need the minerals to transpose back and forth across the gates in order to create action potentials and neurological information. Aluminum has the potential to essentially mess with those gating or those landing sites for the minerals. So as a mechanistic connection, it kind of makes sense that Too much aluminum may not be a great idea. Now, because I've been working around this research for 3 decades at this point, I always call aluminum one of those sort of ping pong types of research data. And a long time ago it was, well, it's definitely associated. And then a while after that, it went totally the other way and said, oh, there's no association at all. And then it's gone back and forth a few times. And now if you look at kind of the totality of the research that's out there, basically kind of like with the amyloid beta hypothesis, aluminum at the very least does not help your brain. And it is associated statistically in enough papers with people with Alzheimer's. It probably does play a role. Now, what about other toxicant metals? You know, things such as mercury or lead or cadmium, et cetera. And there are association studies, meaning we find that the disease rises in incidence when this metal rises in the bodies of people. So there are association studies that certainly do associate other metals such as lead with increases in cognitive cognitive decline, et cetera. So I think when it comes to aluminum, certainly we want to not have any extra. There is no way to avoid all of it, and you want to do everything you can to just kind of have minimal aluminum exposure. But the other thing is the other metals are not great for your brain function either. Now, the final category I'm going to try and do in a couple of steps, but this is related to diabetes and Alzheimer's. So the first thing is Something we know from statistics is that in type 2 diabetics, you have increasing incidence of Alzheimer's disease. And so they started looking at this and saying, well, what could be the causes of this in a type 2 diabetes community? And one of the biggest causes really winds up being that you get insulin resistance, which is a key cornerstone of type 2 diabetes. And that creates a problem with insulin working at your receptor sites. They're literally resistant to the insulin that's Trying to bind there. Now that then can create insulin excess, which can create a lot of inflammation. So they started to see this association between type 2 diabetics and more Alzheimer's disease. And then a number of years ago, they coined the term type 3 diabetes. So we got type 1 diabetes, which is traditionally insulin dependent. Type 2 diabetes tends to be insulin resistant, meaning you still make insulin, your body just, your cells don't care about it. And then they came up, well, what's type 3 diabetes? Well, type 3 diabetes. is used as a sort of euphemism or medical euphemism to say we have insulin resistance, not only peripherally, but at the brain cells. If you have insulin resistance at the brain cells, then you wind up having a slowdown of glucose going into the cells. And the brain's primary preferred method of getting energy is glucose and ketones, but glucose in this case. And so if I have insulin resistance and specifically in type 3 diabetes, my brain, then I have trouble with the insulin binding at my brain cells. And that means that the gates that let the glucose in are going to slow down. So that means that my energy function goes down. But here's the other side of it. That means then I'm going to have more insulin available and it's going to do non-insulin receptor binding things. And those things are generally not good when you've got extra insulin running around. Well, if it's below your neck and you have type 2 diabetes, it can create obesity. It can create inflammation in your body, like heart disease and kidney function problems. And stuff. Well, in your brain, it's the same. If we have insulin receptors that aren't working right, we're going to trigger a lot of inflammation. So it kind of makes sense that this would also not be good for your brain function. So you have sort of the, a little bit older idea of a mechanical problem of beta amyloid and maybe some metals and stuff, and slightly newer idea of type 3 diabetes, which is just insulin resistance in the central nervous system. And my assumption from watching patients and looking at the research and everything is they're not mutually exclusive. Just because you have 2 hypotheses doesn't mean that one is wrong. They both can be going on. It's the idea that you can have 2 very reasonably positive things. Now, does everybody have to have both? No. Are there probably reasons for Alzheimer's that we haven't discovered? Yes, 100%, probably. But certainly if we put these 2 things together, those are not going to be helpful to you. Now, Now there's something that can be tested beyond like looking at type 2 diabetes and things peripherally. And that is something called apolipoprotein E, E like Edward. So ApoE we call it. And ApoE is a group of apolipoproteins that are receptor categories. So ApoE in the liver, its job, the ApoE family, is to take the fats that you have eaten And they get packaged into this giant ball called the chylomicron in the gut, and they're sent into your lymph, and then the lymph dumps into the blood, and then that chylomicron, this big lumbering thing, goes to the liver, and then it binds at the ApoE site and gets sucked up into the liver for processing. That's where you're supposed to process your fats. Well, if I have genetic problems with ApoE, then I'm going to slow down my body's natural thing of eating the fat and binding it and taking it up into the liver, putting the fat into the free cholesterol pool and doing all the stuff that it does. But in the intervening years, we discover, well, there's different subcategories of ApoE, and specifically ApoE4. We now can look at your genetics, and if you have ApoE4 genetic problems, SNPs, etc., you have 10 to 15 times increase in your probability of getting Alzheimer's disease. Well, how does ApoE4 tell us— not 1, not 2, not 3— that we might have more likelihood of Alzheimer's disease? And the reason that ApoE4 might inform Inform us of that is that ApoE4 has a specific activity in the brain for interfacing with the insulin binding site. So this goes back to type 3 diabetes. And so in the rest of our body, ApoE does a lot of work at the liver. In the brain, ApoE4 is sort of responsible for a bunch of things, but one is sort of maintaining the insulin binding site in the brain. So one of the things that can speed up my insulin resistance in the brain is ApoE4 genetic problems. And so on patients, we will check into your mainline labs, all do ApoE4 testing. So that's something that you can request. But why ApoE4? Because if you genetically damage there, you're more likely to have this insulin resistance in the brain, also known as type 3 diabetes, and that's more likely to be more aggressive. Now we've got all these things. And so then you say, well, am I just sort of a slave to my genetics and all of this other stuff? Well, yes and no. The first thing is there are people for genetic reasons that can develop more amyloid. So the amyloid beta hypothesis, there are genetics involved in type 2 diabetes. And then as I said, with the ApoE4, there's genetics involved in type 3 diabetes. But here's the thing, the world of epigenetics is what modifies the genes. So here's just some basic things and we'll, we'll wrap it up here quickly that you can think about working on in diet, lifestyle, et cetera. The first thing is, although it's not always associated, decrease your aluminum intake as much as you can. There's lots of good stuff online about decreasing aluminum intake. If you have exposure to other heavy metals like lead or mercury, work with somebody to help to depurate and detox those things. If you have type 2 diabetes or you have type 2 diabetes in the family, or you've been told you're pre-diabetic, all of the above, you can eat in ways that decrease the amount of insulin that you're pushing out and help to increase your insulin sensitivity. But you can eat in ways to be, to modulate insulin. So they often talk about low glycemic diets. Well, you can also look up online a low insulinogenic or a low insulin diet. And that's basically eating in a way where your insulin isn't going like a roller coaster all the time. Because the more level the insulin output is from your natural production, I'm not talking about injecting insulin, but from your natural production of your pancreas, the longer it'll take you to develop, say, type 2 diabetes. Now, with the Apo issues, the Apo family is very sensitive to higher fat in the diet. Now, this is not all fats, but if you think about it outside of your brain, the ApoE family is involved in taking kind of raw balls of fat that are made into chylomicrons and helping them up into the liver. Well, if ApoE4 is going to mess with my insulin receptors in my brain, there might be a connection there as well. So what we often recommend to people is on a dietary basis, watching the kinds of fats that they take in, but also increasing the so-called good fats. So like your omega-3 fats that you hear all about and all that. But for some people, like the total quantity of fat that they're taking in is is a bigger deal, especially if you have both genes on ApoE4. You have to be a bit more careful. But the other side of it is everything that would help you for type 2 diabetes dietarily, having a low insulinogenic diet is going to help with central nervous system insulin receptivity, et cetera. So there's many, many things that you can do. I think that all of these different reasons, competing hypotheses, they're not really competing. It's just different roads into the same dysfunction. All right. Well, I hope that answers the question about Alzheimer's and autoimmunity and type 3 diabetes and all of that. I'm Dr. A. Thank you so much for liking, sharing, subscribing, notifications, all those things. We really appreciate all of the new members we have joining on the YouTube channel. And do share this around if you found it to be useful. I'll see you all in the next video.