Catherine Crofts transcript

Written by Christopher Kelly

June 2, 2016

[0:00:00]

Christopher:    Hello and welcome to the Nourish Balance Thrive Podcast. My name is Christopher Kelly and today I'm joined by Dr. Catherine Crofts. Hi, Catherine. How are you doing?

Catherine:    Good, thanks.

Christopher:    I say, I put the emphasis on doctor because Catherine has just passed her Ph.D. How cool is that? Why don't you tell us about it?

Catherine:    Thanks. I just spent the last three years investigating high levels of insulin, hyperinsulinemia and its effects on metabolic disease and trying to work out the best way of diagnosing hyperinsulinemia. I've been so lucky to work with a brilliant group of people including Professor Grant Schofield, Dr. Caryn Zinn and was really, really lucky to get in touch with Dr. Joseph Kraft from Chicago. He is 96 in August and he collected a database back in the 1970s that just sort really did show the patterns of insulin produced in the bloodstream after glucose load and how this could be one of the earliest diagnostic tools for hyperinsulinemia.

    And it's really funny now that 40 years later his work is just starting to be recognized because we're at a stage where we can actually look at hyperinsulinemia and maybe how it sort of just comes in to just so many different metabolic diseases from type II diabetes to cancer to heart disease but also to dementia.

Christopher:    And that was going to be our subject for today which I think is fascinating. It's a topic I know almost nothing about. Maybe a good introduction for both me and the people listening would be for you to talk about your time working on the ward.

Catherine:    A few years ago, I've got to finish my master's thesis. I wanted to do my Ph.D. but I had, my husband told me that I had to get a scholarship to be able to do my Ph.D. full time. That meant that I had to go back to work. And I'm a pharmacist and I spent 15 years at this point working in community pharmacy. But outgrowing community pharmacy, I was now wanting to really get my teeth into a more academic and cognitive side of pharmacy.

    And there was an opening at one of the local hospitals for a pharmacist for the older adult mental health service. And I've had a lot of experience with older adult pharmacy but I don't know much about mental health. But they were quite happy to take on as a challenge. I spent two and a half years working with older adult mental health. Now, while that meant that we dealt with the normal mental health conditions like schizophrenia and bipolar disease, I spent a lot of time dealing with the different dementias. And the challenges that are associated with people all the way through their dementia journey and their families and it really was a case of there was very little we could do for many of these people.

    When I started getting, looking into the insulin side of things -- I left that job. I had a fantastic time there [0:03:05] [Indiscernible]. I really did. I only left that job to go and do my Ph.D. And there was a little bit of soul searching because I was enjoying the mental health journey so much, as to whether I should go and do the Ph.D. or stay where I was. And I did the Ph.D. But when I was looking through, when I was starting to look through all the metabolic diseases that were associated with hyperinsulinemia, the dementia started jumping out as well.

    It's a case of, well, hang on a second. We keep saying there's nothing we can do but they're describing Alzheimer's disease as type III diabetes. They're saying that Alzheimer's dementia is very, very much a disease of diabetes and insulin and glucose. We talked about dementia as most people think about dementia as being Alzheimer's disease but it's about four main classes of dementia. We've got the Alzheimer's disease which is associated with this sort of protein tangles within the brain.

    Then you've got vascular dementia which is sort of associated with the blood vessels. People might have had lots of mini strokes where the blood vessels are getting shrunk and damaged inside the brain because the blood vessels get blocked and just stopped working, bits of the brain die around them. Then you also got Lewy body dementia which is another type of protein deposit. The Lewy bodies that are slightly different to the Amyloid plaques that you find with Alzheimer's.

    But these diseases never happen in isolation. Most people with dementia will have a mixed dementia. One of my consultants, one of the things they always did with anybody who was admitted onto the ward was we got a CT scan of the brain, specialized x-ray of the brain. And we always looked at everybody's brain scan and I can't tell you much beyond that hole is bigger than it should be, the brain is smaller than it should be, and that's a lot grainier than it should be.

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    I can probably tell the difference between a healthy brain and an unhealthy brain. And most people had mixed symptoms on the CT scan. It wasn't just Alzheimer's disease. It maybe Alzheimer's predominant but there's a lot of vascular changes as well or vice versa. So, when we talk about dementia, there's lots of things happening with the brain, and many of them come back to insulin.

Christopher:    And then tell me about how these people interact with the ward? How would you describe their symptoms? What are their problems?

Catherine:    Very much depends on which stage that they've been diagnosed at when they came in to the ward or where in the brain things happen. Now, when I say where in the brain -- I sort of mentioned that you end up with holes in the wrong place or brainy bits where they shouldn't be. Depending on where it is in the brain can end up with different things happening. Anything happening around the substantia nigra or something, you end up with a lot more movements, challenges, meaning that was more the physical disorders.

    But if you get some of the other changes happening in the front part of the brain, the frontal temporal system, action and consequence kind of get missed. So, the consequences for an action just get missed. And these people, you talk to them and they seem to have a completely normal conversation and trying to work out right, why is this person here? And then they try and do something -- there's just no thought, that they just can't put the consequence to the action like banging their way through a locked door trying to get the food that's on the other side of it. The door is locked but that's not going to stop them.

Christopher:    Oh, I see.

Catherine:    Right. I can see really why they take the car keys of you. If you are driving you might be able to physically drive your car down the road but you're not going to recognize that a child has just stepped out or who is about to step out and you'll just bowl straight through. That's why you bowl through that stop sign.

Christopher:    So, is simulated the right word to use? I've heard Dr. Kirk Parsley talk about a simulator and I believe that analogy or metaphor, it came originally from Robert Sapolsky. Just after he said that to me, I thought, wow, that's such a perfect metaphor. And the example that I had was my two--year old daughter putting her teeth on my finger and then looking at me. And you could see like the wheels turning. I could clam down pretty hard right now and really hurt you. And she didn't. She didn't do it. And it was that simulator, that kind of moving through, like, okay, so what's going to happen after that and then after that and then after that and what are the consequences going to be? So, is that the part that's broken in these people?

Catherine:    In a lot of people with frontal temporal dementia, yeah. As the case often, not going to associate, it's almost coming back to the two-year old type thing for some of these people. It's a case of I'm going to bite down on this. And your two-year old is going, "But if we did that, these are going to be the consequences." For those people, that's missing. They just don't see the consequences. But for other people with Alzheimer's, they might lose their words. They might call something by the wrong name or they just might not remember the name for it. They might have difficulty expressing themselves. They might lose their memories.

    And that can be really, really frustrating for a lot of people. That can be really more frustrating for them if they know that they can't do some of these things but they don't know why they can't do it and they always used to be able to do it. And that can be really -- and that frustration can manifest itself in different ways, behavior issues, anger issues. People might go for a walk because they've always gone for a walk. But then they forget where they left or they're looking for the home that they lived in 20 years ago. They're looking for where they were 20 years ago and they just don't recognize where they are.

    So, it's a scary world for a lot of these people because some of them know what's happening, some of them don't. Each person when we were working with them, it was very, very individualized. We're constantly thinking how can we make this person's journey better? We know there's no cure but how can we -- is there anything we can do to slow the progression of their disease state? Is there anything that we can do to improve their behaviors, help re-orientate them? What strategies in place that can be managed? Because these people have families. It was very rare for us to have somebody who didn't have families. Some of these family members would visit every day and would want to know how they're going to take their loved one home again but how they were going to manage with that person at home again.

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    That can actually sort of be really quite difficult when you try to get this person home but you're trying to keep them save and you're trying to keep your family members safe, you're trying to reduce burden on family members by doing everything that you can just to try to keep the family together.

Christopher:    And then what do you think the prevalence of this disease is? So, let's say, Alzheimer's specifically. Is this a rare and uncommon disease or is it…?

Catherine:    No, it's not. And the prevalence is only getting higher. It used to be considered an older person's disease but the scary thing is a lot of people over the age of 60 are starting to get noticeable cognitive changes. I think with the Whitehall Study, when they're saying they can start noticing changes in some people from the age of 48. Now, some people, sort of academics especially, they got a high degree of cognitive reserve. So, maybe you need to have a lot of change before we start noticing in these people.

    But for other people, they may not have such a high degree of cognitive reserve and so changes and problems might be detected earlier. When you talk to an academic who is in their mid-90's, it's a case of, sometimes it's a case of -- it's not just Dr. Kraft. It's a lot of people that I worked with on the ward as well. You can tell that you've lost -- there's a good chance that they've lost their top end but my god what's still there is just fantastic and it is still extremely functional in the scheme things but they probably have lost their top end. But other people, they may not have quite so much reserve to lose. And that's a problem for a lot of people.

Christopher:    And I wonder how many people are under or not diagnosed at all? Like how long has this situation been in the making and it's only when it gets to a certain level or certain point that you actually get the diagnosis and so the disease may be under diagnosed?

Catherine:    Very much so.

Christopher:    I'm really interested to hear about your hypothesis of type III diabetes because I spent a little bit of time on Wikipedia this afternoon and they actually introduced a number of hypothesis and it talked about genetics and they talk about the ApoE gene, which is quite interesting, and then they talk about the neurotransmitter acetylcholine and they talk about Amyloid plaques and they talk about this tau protein, which is very interesting, and they even talk about an infection with spirochaete. But I can't find any mention of insulin or type III diabetes or anything.

Catherine:    There's a few things going on that people just we don't know enough about. So, we've got the etiology but then we've also got sort of ongoing issues. Now, one of the things is that we know that a high level of insulin is involved with a couple of different things, one which is the protein bindings and the tau proteins. People don't really know enough of what's going on with that at this point in time but it's also an issue with -- we've now got a changed regulation of the beta-amyloid plaques and the tau proteins. We don't really know the implications with that because one of the things that it's just not really known at the moment is that the beta-amyloid plaques as to whether they -- there's two theories out there -- as to whether they are protective for Alzheimer's disease or damaging to Alzheimer's disease.

    And one of the latest theories is that it's the particle size of the clumps. If you've got really small clumps of beta-amyloid it might be protective. And very large clumps of beta-amyloid it might be protective. But the medium size clumps might be damaging. All we know at this point in time is just some potential mechanisms that we just don't know enough about. But also we've got changes with synaptic plasticity with another dysregulated system called PSA-NCAM. It's a polysialic acid. It's for neural cell adhesions. And we don't really know enough about that but we do know that cell plasticity in the brain is really important for what's called neuroplasticity.

    And if one part of the brain dies a neuroplastic brain sort of build connections around that and keep going. So, while we've got the links to mechanism, we don't understand enough about insulin and the mechanisms yet except hyperinsulinemia seems to be associated with these problems. But we might certainly know that hyperinsulinemia is associated with vascular changes and with type II diabetes. And so, given that type II diabetes is one of the biggest risk factors for developing Alzheimer's disease and other dementias then it's something that has to be explored.

    But when you start looking at vascular changes within the brain, which is really, really key with all of the dementias, this is really where insulin and changes in the brain really start coming through.

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    Because the brain is a highly, highly, highly vascularized organ. Even at rest, the brain uses 20% of your fuel supply. And to get that, all the fuel, all that oxygen and whatever fuel its using to get to the brain it realize a really, really important vascular system. I'll come back to fuel sources shortly. We've got several things that are happening in the brain and the vascular system and insulin because what we know is when you got high levels of insulin it changes a lot of things in the capillaries. You end up with endothelial microdamage. You get a little bit of vasoconstriction. The nitric acid doesn't work quite so well.

    

    And you sort of get changes to capillary permeability and microaneurysms forming. So, one of the things that insulin does is it prevents a process called fibrinolysis, which is the breaking down of blood clots. So, high level of insulin prevents micro blood clots from being broken down. And those things will stick in the brain and cause a little bit of the brain to die. They'll clog all of the blood vessels in the brain because they're very, very fine blood vessels. Those start getting blocked up. And that's just insulin doing that.

    But then you've got the other challenges happen when you got high levels of insulin. Insulin is elevated usually responds to increased glucose in the bloodstream. It's trying to get that glucose down. So, we might have elevated insulin but we might not see that glucose change in the blood because the insulin is working on the background. But the insulin, sorry, the glucose has been there. And it's also doing stuff in background. And one of the things that glucose does is that increases the thickness of the blood essentially.

    It causes increased blood coagulability. It makes the blood clot a lot easier. And that's really, really find blood vessels, you've got thicker blood that when it clots it clots out and be broken down quite so easily. Now, the brain is also fascinating with the way it takes up glucose. Now, I get all my blood transport and my glucose transport a lot of it mixed up. But the brain lies on what we call GLUT1. And the GLUT1 transporter is there most in cells around the body because it's your basal respiration. And it takes up glucose.

    Now, I can't find out easily if it's sort of reliance, if it's an active transport system. It can slow things down. Or it's very much reliant on the concentration of glucose in the blood. You've got high concentration glucose in the blood and it just encourages more glucose to be taken up into the brain. Other parts of your body like your liver work on that whereas your muscles and things, it's all insulin dependent. It relies on the insulin to get the glucose into a lot of the muscle cells and things.

    But it's possible that high level of insulin because of the high level of glucose. We've got so much glucose going into the brain. But then several things happen within the brain is if you've got cells that had been over fed, there'd been forced to take up glucose because there's too much in the bloodstream, we end up with an overfeeding syndrome and we end up with a lot of oxidative stress in the cells. And that actually causes the cells to die. And it may be implicated with some of the inflammation that's associated with the development of these beta-amyloid plaques.

    And I think that the development of these medium size damaging plaques might be due to systemic inflammation. So, what's hard to say at this point is whether the hyperinsulinemia is a direct contributor to the Alzheimer's or not with what's the happening with the TAL plaques and the beta-amyloid tangles and things. It's certainly not helping. Then you've got the other challenges with what happens within the brain. The insulin within the brain does several things. And one of the things that you think might be doing is doing with cell signaling.

    Now, you mentioned the known neurotransmitter earlier called acetylcholine. And they know that with Alzheimer's acetylcholine is one of the key transmitters for the neuro-signaling within the brain. A lot of the drugs I give people is always to do with increasing levels of acetylcholine in the brain trying to help with the signaling better. But insulin is also involved with the signaling but they just haven't really sort of gotten their heads around what or how because the brain actually will make it sound insulin. We don't know why yet but the brain actually, it's not just the pancreas within the body that makes insulin. The brain does as well.

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    But they're thinking that, well, maybe this is needed for more than glucose regulation. Maybe it's needed for signaling. We just don't know enough yet. But what we do know is that glucose blocks and fuel flux within the brain. And that's sort of -- So, for Alzheimer's type dementia, we've got issues where the insulin may be contributing, and the inflammation of things may be contributing to the plaques that implicated with Alzheimer's disease. But then you've got vascular dementia, which is high levels of insulin causes vascular disease around the body. I guess, there's no question about that.

    So, vascular dementia is very much a disease of high insulin. Most people do not have one of these diseases in isolation. Most people would have a mixed. So, there'll be a mixed progression of Alzheimer's and vascular dementia. It's called mixed dementia. And that will be probably about 75% of the people with a dementia it would be a mixed type and it may even be higher than that.

    So, try to tease out insulin with Alzheimer's or insulin with vascular with most people dealing with mixed, it's going to be -- we're talking a lot more sort of test tube type experiments rather than the real people type experiments to really work out what's going on there. So, we have to sort of work with the epidemiological studies that guard Alzheimer's type III dementia because if you got type II diabetes -- So, Alzheimer's is type III diabetes. Because if you have type II diabetes, major, major risk factor for developing dementia.

    But then you've got the flipside of the coin and it's looking at how people are managed after that. And what happens in the brain of somebody work Alzheimer's or vascular dementia -- from this point onward, we're just going to talk about it as being dementia -- is fuel flux becomes critical. Now, what do I mean by fuel flux is when somebody eats a typical carb laden meal, for the next sort of two hours you'll get a peak and you're a get rise in blood glucose and blood glucose and then blood glucose will have a peak and then blood glucose will drop and you'll sort of bottom out and you start feeling hungry again.

    Now, what I believe happens is that people with dementia can end up with brain challenges at both the top and the fuel flux when there's lots and lots of fuel in the brain especially glucose. And at the bottom end of the spectrum and they're hungry and you've got low fuel flux. I mean, if you think about the term hungry, you're so angry because you're hungry, part of that is because the brain, as I said, needs so much energy. It needs a constant supply of fuel.

    And all of the symptoms that you get with a hypoglycemic episode come from the brain being hungry. It's like I'm saying stuff here guys, we need to start feeding me again. That's when you get the confusion. You can't think properly. You get the irritability. And you may end up with making some poor decisions when you're hungry. If you take that concept and put it into a challenged brain, a brain that is already not thinking clearly in the best of days, and you take away some of the glucose, you got fuel, you got brain cells that are struggling to maintain normal thinking, take away some fuel, they're even more challenged at this point.

    So, you have to start wondering if some of the behavior changes that you see when you have somebody who has an almost rapid behavior change. Sometimes food does make a difference. And maybe that's getting a lot of the glucose back into the cell. The other problem that you have is when you're at the peak and the fuel flux. And you got lots and lots of fuel glucose especially in your bloodstream. Once that happens, a lot of it is toxic to the brain cell because of the overfeeding inflammation and then it can also encourage the production of something called glutamate from glutamine. Now, glutamine is an amino acid. It's used in the brain to make several different neurotransmitters. Glutamate can be a little bit toxic to the brain. And it's another entity that is targeted with drug treatment for Alzheimer's disease to reduce glutamate.

    The flipside of the coin is that when everything is going nicely with fuel flux in the brain and you're in that intermediate stage and you've got even fuel within the brain. You've got GABA being produced from glutamate. Now, GABA is a calming hormone. If you give somebody a benzodiazepine or a chill pill against anxiety, it increases GABA that's on the brain or works on the GABA receptors. So, you can induce a state of calm in somebody with, or at least reduce agitation, if you've got the right amount of fuel going into the brain.

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    Now, they've done a study with both -- they looked at a high infusion of insulin into people with Alzheimer's disease and maintaining the blood glucose steady. I found that they've gotten improvement in symptoms. But they did the same thing and they got people on the ketogenic diet. And they also found an improvement in a very similar stage of symptoms. And I believe that's due fuel flux. So, you've got somebody who's on a carb laden system, their energy is going up-down, up-down, up-down. Poor brain is sort of going toxic-hungry, toxic-hungry. And maybe if we can sort of change the way the brain is being fueled, then maybe that will have some implications for management of people with different dementias. But also if you're not having the oxidative stress on the brain all that slow the progression of some of the disease states.

Christopher:    This is really interesting. So, you're saying that a ketogenic diet may be a useful therapy for dementias?

Catherine:    Yeah.

Christopher:    And has anyone done any work on this? Has anyone looked at it or tried it?

Catherine:    There are some studies in the literature. It does look like it has been tried. It's definitely a viable option. But there are some real practical difficulties with its implementation. As I said earlier, you have people in a state of dementia where it's being recognized that they've got dementia. But often it's being recognized because they've become, I don't know, fixed in their ways or they're behaving really, really rationally. Now, for these people, if you suddenly go, "Right. I know you really love your beer, your pasta, your bread and your potatoes and your sugar, and we're not going to take that all away from you." That's going to be a major problem. That's really going to--

Christopher:    It's just not going to work, right? I mean, you could almost hear the penny drop as I realize what you're saying. Some people would argue that a ketogenic diet is difficult to implement or difficult to adhere to or they might even say it's a hideous diet. I've heard that said before as well because there's just so much fat and it's all unpalatable. But those things can typically be overcome by the types of people that listen to this podcast namely practitioners and athletes. But, yeah, if you're taking someone who has got some kind of dementia, can you, is this even an option?

Catherine:    Is it viable? I don't know. I said all I know is that people can sort of really have a behavior outburst. I've had patients have a major behavior outburst when you tell them they can't go outside into the garden because it's raining, when you can't take their cell phone off them, you can tell them to change their diets. Now, it can work in an institution where they're being managed by a nursing staff and everything else but for somebody who's just being diagnosed because [0:28:05] [Indiscernible] they're really irritable and a change in the slightest in the house and they get a temper outburst, I'm concerned that something's happened.

    You try changing the diet that may not be possible. At the same time though you get people be coming through to the early memory clinic where you got the patient going, "I want to be checked out. I think there are some changes happening. And so I w ant my memory checked. I'm in the early stages of Alzheimer's. Okay, right. I am. What can I do now?" And a lot of these people are looking to make lifestyle changes. Those are the people are the ones who would probably get a lot of benefit.

    It's not to say that people with moderate disease state where you're not going to be able to make a full change to the diet. But really getting these people onto low glycemic index food would make quite a bit of difference. If you can reduce some of that glucose fuel flux and take away a lot of the high Gi foods, you possibly will make some difference. But the people at the early stage of the journey, when they still understand action consequence, you can talk to them then about the changing the diet and see if it works. And for those people, it might really be viable.

Christopher:    And then what would happen if you were to try and sneak in say some of the ketogenic foods like MCT oil or ketone ester or salt or maybe just even coconut oil? Could those things help, you think?

Catherine:    I don't know. Possibly. I mean, for those -- I mean, the key thing is looking at fuel flux. Now, the ketone esters might be a possibility but you'd have to be really careful because I don't know what happens if somebody puts ketones into the system that's glucose laden, are you still going to end up overfeeding? Because the mitochondria doesn't really care where it's getting its energy from to a degree. It just has to deal with it.

[0:29:59]

    

    And so what's going to happen there? My biochemistry is a little bit weak at that point. But if you've also got somebody who's been running on a carb-based system for so long, can they convert the fatty acids to ketones? Because fatty acids do not cross the blood brain barrier and the ketone bodies do. So, you've got to get the ketones into the brain for the brain to use them as fuel. And the brain will quite happily use ketone as fuel. That's one of the things that just makes me cross, when you see that the brain has to run on this amount of glucose a day and it can't run on ketones.

    So, no, fatty acids will not cross the blood brain barrier. Ketones will. But if you've got a liver that's never been asked really to convert fatty acids to ketones for so long, you don't know how long it's going to take to get it up to running or if it can get it up to running? So, we just don't know enough about this yet. Would it hurt to try? No, not in the slightest. As long as you're being moderate about it and just don't suddenly stop doing that sort of thing. Also it wouldn't hurt to try and reduce some of the sugars that are in people's diet. Try and switch out some of the sweet fruits for berries or sweet vegetables like bell peppers or capsicum, reducing some of the really sweet treats.

    I mean, it's [0:31:26] [Indiscernible] where I was working was always, what we call in new Zealand a ginger kiss but it was cake with some butter cream, small cake with some butter cream on the middle of it. Looking back at it now I've sort of go, oh, that was probably the worst thing in the world for these people to have. Probably they could have had some cheese, cheese and crackers instead of something sweet. The crackers would at least have been a step in the right direction.

Christopher:    Right. So, these people that are being fed a diet on the wards, is it not then quite easy to manipulate it?

Catherine:    You'd like to think. Have you ever tried to change a hospital ward's diet?

Christopher:    It must mean the decisions -- where do they get the diet from in the first place? Where does it come from?

Catherine:    To be honest, I don't know. I mean, we've got the dietician on the ward who are making a lot of changes but they were being fed -- for most people, they didn't need any special diet to be requirements, so it was the standard hospital food. But also, occupational therapist would often have people making pipelette and things in the kitchen. And it was time to give a lot of people a sense of normality. Pipelette is relatively -- pipelettes are sort of thick mini pancake, hot cake type things. so, it's a case of, one, is it about can it be safe in the kitchen but, two, it's a really good activity for them to do that's sort of keeping the brain and body engaged in normal day to day activities. But these things will take slow, will be slow to change. So, some of the stuff I have worked with since have sort of gotten old. Maybe we should rethink that but I haven't been back for a few years to see if anything has changed.

Christopher:    So, tell me more about the role of using your brain then? Is it just a simple to understand as use it or lose it and that's why they recommend that you should do puzzles and soduku and other things like that that would engage your brain and maybe that can help with the onset of dementia?

Catherine:    Possibly. They don't know enough about it but they're sort of going maybe it's a use it or lose it, but maybe the people who aren't using it aren't using it because they're losing it, not because of lack of trying. But one of the things to sort of come back to is, I think, with neuroplasticity. It's having cells that can -- so many of the neurons in the brain, they talk to so many other neurons to get a cohesive message going through. Now, if a little bit of the brain has died, the neurons that used to talk to that part of the brain are going, "Ah, can't talk to that bit of the brain anymore. Where should I be sending this message?"

    And they can develop new connections. And this is, I think, with neuroplasticity. The brain will create new connections around something where something has died. I mean, if you think about a person who has had a minor stroke. A bit of the brain has died. They lose the ability to smile. They lose the ability to use their hand in certain ways. They lose their ability to sort of walk, to talk. But for some of these people with probably a great deal of luck of many cases but also they've got a neuroplastic brain and they get the right assistance from the occupational therapist, the physiotherapist and everybody else, they can regain their ability to do a lot of these things. And that's the brain making new connections. That's the neuroplasticity in place.

Christopher:    Okay. That's really interesting. So, is that the same process then when you see someone that's had a traumatic brain injury?

[0:35:02]

    Maybe they've crashed their bike or been in a car accident or something like that and they lose some of their brain function. Is it the same process then that they're relearning, to almost relearning to do things again like a child?

Catherine:    Yes, it is. It's that brain having to make a new connections. Well, this is to the best of my understanding. It's the brain making new connections. Because once a bit of the brain has died it's not coming back. But there's a lot of reserve in the brain and maybe you can re-train other bits to do the same job.

Christopher:    And one last kind of weird slightly maybe technical question that you want to talk about but I just have a thought. So ,we  know that people who are ApoE4 carriers they might not do well on a high fat diet. And ApoE is also implicated in Alzheimer's. So, do you think -- are we running into a problem here where you can't really put these people onto a high fat diet because of this gene that may be implicated in the disease in the first place?

Catherine:    There's so much that we don't know about Alzheimer's. We don't know why it happens. It's a multi modal system. So, for some people, high glucose, yeah, definitely a problem. We get those people onto a lower glucose system. I mean, the way I look at it is it's not an either-or system. The body is designed to run on two engines. The mitochondria within the cell doesn't mind if it's getting its energy from glucose. It doesn't mind if it's getting its energy from ketone bodies. And it can use a few other bits and pieces there in between to produce ATP.

    All the cell cares about is that it's getting a steady supply of ATP to create energy, very, very simplistically. What we have to do is manage the fuel that's going into the mitochondria so that we're not causing overfeeding which causes many of the other problems including insulin resistance, hyperinsulinemia, and then the body just does not do well on glucose. So, I would say for people who have got the ApoE gene, the early you can identify them the better. Because then you can work out where they fit in the hyperinsulinemia state and how much carbohydrate restriction you need to put in place to keep their insulin levels down to a healthy balance.

    It's all about finding your healthy balance. Now, for a lot of people with ApoE, if you find it early, you may not need too much the carbohydrate restriction to prevent the other metabolic changes that lead you towards type II diabetes and that that carries for Alzheimer's disease. And that way you're going to be able to keep these people on a whole food low GI diet. It's going to be higher in carbohydrate and lower in the fats that they don't want to take on board because of that gene system.

    We've spent so many years in a one diet fits all which in reality is one diet fits none system that we forget that we need to be tailoring diets to suit the individual not forcing the individual to fit into a dietary system. So, does that sort of go along with answering your question?

Christopher:    Yeah, it does. So, I was going to twist your arm and ask you kind of as a takeaway message for people who may be are caregivers or know somebody with some type of dementia or specifically Alzheimer's, with the preface that this is not medical advice, we can't do that over the internet, just some things, some take home points that people can think about what you've learned. I think you've started with that. So, start thinking about the glycemic load of the diet. But is there anything else?

Catherine:    Well, as I said, I'm a pharmacist. I've been practicing in the community for the better part of 20 years. My take home diet message for just about anybody -- I mean, I had one of my pharmacy students look at me at the end of a very busy six-hour period and going, "You don't like sugar much, do you?" About every second person got told take away added sugars from your diet and eat more non-starchy vegetables. So, I'm really pushing for whole food diet where possible. Limit your added sugars.

    I think that's a message that everybody should take on board. Limit your added sugars. That's honey, that's your agave, that's your coconut sugar, I'd say your date sugars. Reduce your sugar load especially if sugar is from the fruit juice, especially from added sugars. It doesn't matter if they're from a healthy source or not. The body can't deal with it. Limit your sugar intake. Make the largest part of your diet non-starchy vegetables. From there, that's possibly where you need to be talking to your health care provider or dietician as to what's going to work best for your individual make up.

[0:40:09]

    But even people with Alzheimer's disease who can be reluctant to change, if you can reduce carbohydrate, sort of the sugary sources, sources of sugar, not just sources--

Christopher:    They do happen a lot. But, yeah, I understand what you're saying.

Catherine:    If you can reduce the sugar intake and increase the vegetable intake that might be a very good start. From there, we need to individualize diet.

Christopher:    That's been there.

Catherine:    But also if you're at the early stages and you're thinking, well, maybe. Yeah, definitely. Do your own homework. Talk to people. Maybe a carbohydrate restricted diet is best for you. But I'm going to say do your own homework on that and talk to your healthcare provider especially if you're in the early stages of -- you've got early memory loss and even the early cognitive changes.

Christopher:    That's excellent advice. For everybody listening, if you've enjoyed this conversation, then it's almost a continuation of the discussion of insulin because we're going to talk about the Kraft test which I have done that measures insulin in response of a glucose load over time rather than just static fasting measure and Catherine is going to talk about why a fasting insulin measurement is almost useless and why you need to see the dynamic response. And that will be part of the Keto Summit that's coming out for this autumn.

    So, if you look in the show notes, for this episode, I have a link to the Keto Summit that you can sign up for. And, yeah, I think I've already mentioned a list of the names on the summit is really quite phenomenal and I'm really, really enjoying this interview. I'm hoping that you'll sign up and get access to that because there's some really great content.

    Well, Catherine, thank you so much for your time. I really appreciate you. And I think it's so interesting to hear a pharmacist talk about food like that. But when you get to the end you'd expect the pharmacist to have some pharmacological solutions to these problems that you're discussing but you didn't really mention, in fact, you didn't mention a drug the whole episode which is quite extraordinary.

Catherine:    I think my job -- Thank you very much. I've really enjoyed talking to you about this. But I think my job is to get people off the pills, not to start them on it. And I'm looking forward to coming back and talking to you through your Keto Summit as well.

Christopher:    Awesome. Thank you very much.

[0:42:29]    End of Audio

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