In this episode, I’m speaking with Dr. Heather Sandison, a naturopathic doctor, published researcher, and the author of a new book you’ll definitely want to read, Reversing Alzheimer’s: The New Toolkit to Improve Cognition and Protect Brain Health.
Dr. Sandison’s work is extraordinary in many ways, but, in my opinion, one of her most impressive achievements is creating Marama Memory Care, the first residential memory care facility to have the goal of returning cognitively declined residents to independent living!
I loved speaking with Dr. Sandison, and I know you’ll learn a lot from this podcast. Enjoy!
Table of Contents
In this podcast, Dr. Sandison and I discuss:
- The true underlying drivers of chronic illness, and dementia specifically, and why the conventional approach is not working
- An incredibly surprising role of amyloid beta plaque (thought to be the major contributor to dementia) that no one is talking about
- 6 factors Dr. Sandison addresses in her Alzheimer’s patients to achieve cognitive improvement at the cellular level
- 3 reasons why Alzheimer’s research and standard treatment has been a massive failure…this is a must-listen for any person dealing with neurodegenerative disease
- Details of the now infamous 2006 study that seems to have fabricated research on Alzheimer’s connection to amyloid beta proteins
- How faulty science led to a misguided paradigm of Alzheimer’s treatment and the development of risky, expensive drugs that don’t have a substantial positive effect
- Why inflammation isn’t a root cause of disease and the triggers we can be aware of instead
- The thoughtful details of Dr. Sandison’s research and how what she found completely upends everything we thought we knew about Alzheimer’s
- Actionable, accessible steps you can start TODAY to prevent or even reverse dementia…plus movement and mindfulness tips you’ve never heard before!
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Transcript
Ari Whitten: Welcome back to the Energy Blueprint Podcast. With me today is Dr. Heather Sandison, who is a renowned naturopathic doctor specializing in neurocognitive medicine and the founder of Solcere Health Clinic, San Diego’s premier brain optimization clinic, and Marama, the first residential memory care facility to have the goal of returning cognitively declined residents to independent living. She has dedicated her career to supporting those suffering with dementia and is the primary author of the peer-reviewed paper “Observed Improvement in Cognition During a Personalized Lifestyle Intervention in People with Cognitive Decline,” which was published in the prestigious Journal of Alzheimer’s Disease.
She hosts the annual Reverse Alzheimer’s Summit where she shares cutting-edge and tried-and-true insight into what’s possible for those suffering with dementia. She is excited to shatter common misconceptions about Alzheimer’s and share what she has learned about keeping your brain sharp at any age. She’s also the author of the brand-new book Reversing Alzheimer’s: The New Toolkit to Improve Cognition and Protect Brain Health, which I strongly encourage you all to pick up. With no further ado, enjoy this wonderful conversation with Dr. Heather Sandison. Dr. Sandison, welcome to the show.
Dr. Heather Sandison: Such a privilege to be here. Thanks for having me, Ari.
Why the current approach to Alzheimer’s isn’t working as intended
Ari: Yes, it’s absolutely my pleasure. I really enjoyed our last conversation, and I was just reminiscing with you that the first time that I encountered you was five or six years ago, something along those lines, just down the street from where I am right now in Encinitas, California, at the public library, and I saw a really nice presentation that you co-hosted and presented with Daniel Schmachtenberger. We didn’t officially meet, but we’ve known each other. I’ve known you for quite a long time at this point and heard you speak, and I’m a big fan of the message that you’re promoting in the world and the work that you’re doing now, especially with the release of your new book, Reversing Alzheimer’s.
Dr. Sandison: Thank you. Yes, Daniel, that work that he introduced me to, it really is the framework on which I do everything, whether it’s the residential care facility or the clinical medicine that we do with patients or the coaching that we do with clients who are at home struggling to care for a loved one with dementia. The ideas that he imparted on me, what he really taught me was this rethinking of the paradigm of complex chronic disease.
The big picture things that Daniel really imparted on me was this paradigm shift in how we think about complex chronic disease, that when we oversimplify things and suggest that a single-molecule intervention is going to cure a disease, we often come up short. Particularly in the case of neurodegenerative diseases, we find this over and over again, right? This paradigm, that we’re going to have this molecule that’s going to get rid of amyloid and we’re going to cure Alzheimer’s. Despite billions of dollars in research funding and decades of super intelligent people’s time, that hasn’t panned out, that hasn’t worked.
What we do see works is this more complex system science approach, that I don’t want the word complex to alarm anyone. Really, we can do this systematically. We can look at the brain and at the body and we can say, “What causes imbalance or dysregulation?” If imbalance is the cause of disease in this case, this can be applied to any complex system, whether it’s a financial system or a government system or an educational system. If we think of the brain as a complex system and there’s imbalance in it, it’s going to lead to dysfunction or dysregulation.
What is imbalance? It’s too much, too little, in the wrong place or at the wrong time. Fundamentally what we’re looking at here, what are the causal-level factors? What are the primary factors that are going to create dysregulation and imbalance? There’s oftentimes we can look downstream. We can say, “Oh, inflammation is the cause of dementia.” Yet if we can ask why is there inflammation and come up with an answer, then that’s not the cause. The cause is one step before that or maybe a couple of steps before that, depending on what we’re talking about. Amyloid is much like that as well.
Amyloid, these molecules that we think of as the cause of dementia from a conventional perspective, they are a response. Amyloid is actually antimicrobial. This will pop up to protect us from things like herpes simplex 1 or from Lyme spirochetes or from gingivalis, gingivitis, causing bacteria. What we want to keep doing is going back to why is this happening? What’s triggering it? Can we create balance at a causal level? Those six factors, there’s basically six things that I would argue when they’re out of balance, they cause neurodegenerative diseases and many of the complex chronic diseases that we see associated with aging.
Those six things are toxins, nutrients, structure, stressors, infections, and signaling. When we look at those in a very systematic way with our patients, with our residents, with our coaching clients, we often find that when we address them, create more balance, we get improvement at the cellular level and then of course where it really matters, which is in cognition.
Ari: Excellent. There’s so much there that I want to dig into. I was actually taking notes to make sure I can come back to some of these things that you mentioned there. One thing that you said there that I really liked and actually happens to be something that I’ve been writing a lot about in my book is this paradigm, this culture that we have created in medicine where we take these, what are, as you said, complex systemic problems and we are insistent on trying to look for the one mechanism or the one molecule that is the thing that “causes this condition.”
Based on that idea that we’re going to find this one mechanism that is problematic and causing this problem, then what we do is we go to a chemistry laboratory and we synthesize man-made chemicals that are specifically designed to target and interrupt this specific one mechanism that we believe to be causing this illness. There’s two aspects to this. On the one hand, you kind of understand how we all got convinced that this is a good way of approaching things because it was hugely influenced by the antibiotic revolution, which really was a case of, “Okay, there’s this one problem, this organism that’s causing this disease. If we just develop a chemical that kills this organism, we can cure the patient.”
It does work in that context or historically worked in many different infectious diseases where that actually turned out to be a good approach, but then based on this, we sort of applied this to all illnesses, that this is the model that we need to think through, what’s the one thing that “is causing this disease”? What’s the one chemical that we can use to fix this cause of the disease? It’s been just such an enormous failure on so many levels over and over and over again for basically every chronic disease, 8 out of 10 of the diseases that kill us are diseases of lifestyle. This model has just been a massive, like unbelievable-scale failure over and over again for these things, and yet, what do we do?
We go, “Okay, well, I guess we haven’t found the one mechanism and the one right drug yet. Let’s keep searching for the one mechanism and the one right drug to fix this disease.” It’s just kind of astounding to me. I mean, obviously, it’s heavily influenced by financial incentives, but I’m wondering if you can go deeper into that story and that sort of paradigm and why it’s problematic.
Dr. Sandison: Yes, I think you’re absolutely right. The incentives, if you follow the incentives, it tells the story. When we think about the way that we approach Alzheimer’s and how– With this complex system science approach, looking at it from a holistic perspective, I’m trained as a naturopath, what we see is we get great outcomes. Not only do people end up with better cognition, more independence, more ability to live fulfilling lives as they age, but they also resolve their hypertension and they also resolve their weight issues and their bones get stronger and their mood gets better and their diabetes resolves. What we’re doing is really creating more health.
Yes, our focus and the nuance around what we’re doing is very much directed towards a family who’s affected by dementia and Alzheimer’s. However, what we’re doing is really about whole brain, whole body health. When we take these single molecules, you mentioned antibiotics, and I think this is such a great contrast to what we’re suggesting because when I talk about my reversing Alzheimer’s approach, Dr. Bredesen’s approach, this isn’t a cure. This is a lifestyle. What we see is that many people who jump on the train, who get on it with us, who dive in fully, who do the approach, they get better, but if they get off, it doesn’t last, the symptoms come back, so it’s not a cure.
Like you mentioned antibiotics, if you have a urinary tract infection or a sinus infection and you take antibiotics, you’re cured. You don’t typically have to think about it unless something else is going on. Typically, that can be a thing of the past. You don’t have to revisit it. This is not that. This is about a cellular function. It’s not about a single organism causing this disease. It’s about a milieu of things, and that’s why we want to think through this.
For the individual with precision medicine, there is not one path that you take to most complex chronic diseases. It’s multiple things that add up, that stack up, that spiral in a negative direction towards cellular dysfunction. What we want to do is turn that around. In the book, I actually talk about some of, I think, what you’re alluding to. What happened with the story of Alzheimer’s is actually this phenomenal book that any Alzheimer’s nerd out there would read quickly on a plane ride. It’s called How Not to Study a Disease: The Story of Alzheimer’s by Karl Herrup. He describes these three elevations.
The first one was in 1906, he was the doctor for a patient, Auguste D., who had Alzheimer’s, the original case of memory loss. Then when they did the autopsy, they saw these plaques in her brain. Then his teacher put that case into a textbook. Now, it was a single case that should never be in a textbook because usually what we want to do is get sort of a consensus. You want multiple cases. You want there to be a trend, not just a single outlier case, but he was trying to sell a new edition of his textbook, and so he included this case. This was the first elevation. Now, there were a couple of others that happened in the ’70s as the National Institute on Aging came around.
If you talk to doctors who were in the ’70s and ’80s, they’ll say, “Why is it called Alzheimer’s and not senile dementia?” The people who were practicing in the ’80s, ’90s, like in the last century, they’re like, “Why is there this distinction with Alzheimer’s?” It’s because of marketing and the desire to get funding from the National Institutes on Aging, not because of any science.
Ari: Wow.
Dr. Sandison: Then again, later on, the incentives around the pharmaceutical industry are to look for these single-molecule interventions because they can patent them, and so then you can fund the drug trials that are necessary to get through FDA approval. You need to be able to patent the medication in order to afford the millions or billions of dollars that it costs to get up to that point, right?
How one factor alone has shaped the treatment of neurodegenerative illness
Ari: Can I just interrupt for one second, because what you just said is so important and so profound that I don’t want it to be lost in the mix of what you’re saying, because just that one thing that you just pointed out is like, I want people to understand how that one factor alone is so hugely responsible for shaping our entire system of medicine.
Dr. Sandison: Right. If you need to have funding to get through these very expensive trials, Dr. Bredesen, my mentor, and I both have done clinical trials. They’re small. I had 23 participants in my trial, he had 25 participants in their trial, and they were both funded by philanthropists. Because we can’t work inside the system because there’s nothing to patent on the other end of these trials. That’s part of why it’s slower. It takes longer. We were funded for our trial in 2018. We didn’t publish until 2023. COVID had something to do with the delays there, but not all of it.
It often will take 18 months to get IRB approval, Internal Review Boards, which are very, very important in the case of Alzheimer’s because they’re there to protect vulnerable patients in these human trials. There’s a lot of red tape, there’s a lot of hurdles to get through, and a lot of them should be there. Now, in the case of Alzheimer’s, there’s another really important part of the story. In 2006, there was a paper that was published that basically connected the dots between amyloid and cognition. Before that, this hadn’t really been done.
With amyloid, one of the things we want to understand is that amyloid is present in all of us. If you take babies, infants, to centenarians, less than 2% of the population doesn’t have amyloid. Then when you get to those later stages of life, there are people with perfect cognition who have lots of amyloid, and there are people with poor cognition, with dementia, who don’t have any amyloid.
Ari: Isn’t amyloid also a case of, like it’s much more dynamic than we’ve been generally taught to conceptualize, meaning, don’t we accumulate some bit of amyloid on a daily basis and that it’s cleaned out on a daily basis?
Dr. Sandison: Yes, especially if we’re getting sleep. If we have sleep deprivation, then we get a measurable accumulation of amyloid even in one night and then, of course, if you extrapolate that over decades, that’s going to lead to a measurable and significant accumulation of amyloid. The amyloid is an indication that something is dysregulated. It’s not causal, it is certainly correlated, but there’s also a lot of exceptions to that. It’s not a clear-cut line. When you get rid of amyloid, you don’t actually get better cognition.
We would have solved this problem if that were the case. What happened in 2006 was there was a mouse study, and I don’t want to go into all of the drama, but basically it was the images that connected these dots [crosstalk].
Ari: Actually, I had this on my list to ask you, so by request, I would actually like you to go into all this drama because I think it’s also important for people to understand just how deep the corruption and fraud within the field of medical science can be, and how influential those financial incentives can be in corrupting good science.
Dr. Sandison: I don’t want to, I don’t know that I personally want to– I don’t want to vilify someone. I think that the vast majority of people who show up to do this work around Alzheimer’s are dedicated, smart, caring individuals who really want to reduce the suffering associated with Alzheimer’s. I think that most people, the vast majority of people come to this work with that intention, and in this case, there was a paper published that was highly influential. It’s been cited over 2,500 times, and it was used to justify more dollars, more taxpayer dollars, more NIH funding to go towards this amyloid hypothesis.
The refrain in Alzheimer’s research for a long time was, if you’re not studying amyloid, you’re not studying Alzheimer’s. If you weren’t in that– They refer to this as amyloid mafia. Like if you weren’t in that group, you weren’t getting funded, and that’s not good science. There’s this idea of the null hypothesis. You’re not trying to prove something. You’re trying to prove that [unintelligible 00:16:33] you might be right. Basically, you’re trying to keep your mind open.
Ari: That dynamic, which is really a psychological dynamic and sort of a cult dynamic where you’re sort of part of the in-group or the out-group, depending on the paradigm in which you view a problem, I think those kinds of dynamics exist across the board in the way basically all diseases are, studying and the pursuit of treatments for all diseases. It just so happens that with Alzheimer’s, you have this unique situation where the very sort of foundation of that way of viewing the disease and trying to cure the disease has been exposed as a big fraud.
Now it’s really in our faces. It’s become very obvious just how problematic those sort of psychological cult dynamics, in-group, out-group stuff, even to the point, as you said, of whether you get funding or not, how influential that has been and what a big mistake it’s been, but I think those same kind of dynamics exist probably across the board in the way a huge number of diseases are being studied.
Dr. Sandison: Yes. I mean, I don’t know. My focus is so much on Alzheimer’s. However, this paper that I’m referring to is in the process of being retracted by every author included on the paper except for the one at fault. That particular gentleman is still employed at the university that he has been at for decades, and he’s still receiving NIH funding. That, I think there’s an injustice there, right? There’s been misdirected funds. This seems very clear. Many people have looked at his images.
There’s other papers that also I think are in the process of either retraction or have been flagged as having sham images included in them. I am disappointed because this came out a year or two ago. This came to light, and there hasn’t really been justice served. There was this amusing article that I read the other day where basically there are other people who misused NIH funding to like go to Fiji or like to go to strip clubs or gamble, and they have been seriously reprimanded. There has been justice served.
I think some of them maybe even ended up, I don’t know exactly what it was. I don’t know that they ended up in jail, but there was like a justice that was done. When I think about, and the point of the article was really to come to the conclusion, actually that paper that was cited so many times, that was used to justify so many taxpayer dollars, that was used to direct the– kind of how the research dollars were spent and what was focused on, that amyloid would be focused on more versus other things that might have gotten us more traction. There are people suffering today with dementia that might not be if that hadn’t happened 20 years ago.
If we might’ve used all those dollars in a much more resourceful way because we had better science. I think that, like that fires me up, like that gets me mad, like there’s still not justice there. Anyways, what are we doing that– Actually, I like to talk about solutions more than that stuff.
Ari: Well, hold on, hold on second before we go there, we’ll definitely get there, but there’s another layer to this evidence around the amyloid stuff, which is important, and I think it’s also worth stating that the paper that you’re referring to, this wasn’t just, “Okay, yes, this was a case of these scientists lied or misrepresented something, and now they were caught.” It was that this whole idea, this whole hypothesis of what’s causing this disease had a massive influence on the whole researchers around the world of how they view– and the education of the public, right?
Like hundreds of millions or billions of people became indoctrinated into this paradigm that Alzheimer’s is caused by these amyloid plaques, and then that influenced not only the public, it influenced scientists, pharmaceutical companies, everybody is now pursuing trying to cure this condition by developing drugs that block the formation of amyloid plaque, and I think that’s another interesting layer to this discussion that I’d like to have you speak to, which is that they did develop drugs that were successful in blocking amyloid plaques, and what happened with those.
Dr. Sandison: Yes. Right now, there are the monoclonal antibodies that are available, and donanemab, the Eli Lilly medication is, I think it’s about to be approved by the FDA. That’s been delayed a little bit. Leqembi, or lecanemab, is available right now and FDA approved and available through Medicare if you meet certain criteria, and then aducanumab, or Aduhelm, that one has been taken off the market.
These are all in the same category of drugs, and these are these first-generation monoclonal antibodies that take amyloid out of the brain, and what we see with this approach is that these are each increasingly like marginally better than the next, so Aduhelm being the first one, Leqembi being the second one, and then donanemab being the most recent, and what we see is that they are each slightly less risky. Maybe they slow the progression of the disease a little bit more, but none of them meaningfully improve the patient in terms of their cognition, so when you take amyloid away, you don’t get an improvement in cognition. No one gets better.
What we do see is that you get a slowing of the disease process by about 30%, and so from my perspective, I’ve worked closely with families for years now, and drawing out a torturous process is not typically that valuable. Now, for some people, this will be, “It’s an IV that you can go get, you don’t have to do much more than that, although you do need to be close to a major medical center because the risks are brain bleeding and brain swelling,” and this happens in about 30% of patients, and so you need to be near a major medical center so that you can have the MRIs done to double-check that you’re not having these side effects happening.
Ari: And potentially death, right? I think I remember Dr. Bredesen, when I spoke to him about this, he said, “Yes, it can slow the disease process by 30%, but you have this huge risk of side effects and potentially death from the drugs themselves.”
Dr. Sandison: Yes.
Ari: Correct me if I’m wrong on that.
Dr. Sandison: I mean, I think that when you’re studying a group with Alzheimer’s who is older, often when you do studies with thousands of people, there are deaths because people are at that stage of life, and I can’t speak to, precisely like the increase in the risk of death. I do know that there’s an increase in the risk of hemorrhage, brain bleeding, and brain swelling because you’re basically ripping the amyloid out, including from the blood vessels. There is certainly risk associated with these medications, and they’re expensive. They’re really expensive. They’re used in mild cognitive impairment.
When we say mild cognitive impairment, there’s nothing mild about this. Alzheimer’s has these four stages, the pre-symptomatic stage, which is before you even notice that there’s anything going on, and that can often last for decades. Then there’s that symptomatic stage where you’re aware of it, that you notice or maybe your family starts to notice that you’re not remembering names or you’re not remembering the words and nouns as well as you used to. That’s a subjective cognitive impairment. Then we have this mild cognitive impairment, which is actually when it’s measurable and you’re on this progression towards Alzheimer’s.
Again, it’s not mild. It’s highly impactful. People are losing their jobs. They’re not able to take care of their financial health. They’re not able to potentially like plan a trip. Like your life is impacted. You can still have a conversation typically, but you’re on that slippery slope towards Alzheimer’s. With these medications that are approved for that mild cognitive impairment stage, so this isn’t like a last-ditch effort when somebody has severe Alzheimer’s, that’s when we’re going to decide to spend the money and take the risk.
This really is something that you do when you’re still going to birthday parties and enjoying Christmases and going on trips with your spouse that you waited until retirement to take– I think that a lot of people come into my office and they’re like, “Okay, well, we’ll try this. Then if it doesn’t work, we’ll think about Leqembi.” It’s like, it doesn’t work that way. You don’t wait until you get further progressed to then try these medications. I think there’s some misconceptions around them. Then many people are coming out of pocket, although it’s covered by Medicare. I think that the average cost per patient out of pocket, it’s still over $8,000 for these medications. It’s not a small amount of money.
The value of the current Alzheimer’s medications
Ari: What’s your overall take as far as the value of these medications?
Dr. Sandison: I hope that they’re a first crack at it, the first-generation medications, and my hope is that over– As taxpayers, we’ve spent so much money going down this path. I do hope that there’s some value that comes out of them and that they can be used in conjunction with the lifestyle medicine and the functional medicine, that we get better results with.
Ari: One of the challenges with that hypothetical scenario that you’re alluding to there is psychologically it’s problematic because to the extent, just as the way human psychology tends to operate, to the extent that people perceive there to be drugs that are effective in treating a particular condition, they are less inclined to also take action on the lifestyle dimension of things. There’s another element to that, which is, I’ve found, and there’s a lot of research to support this, that most people, particularly those that don’t have a strong background in scientific literacy and statistical literacy in particular, have enormous difficulty in understanding the nuance of the magnitude of effect size.
For example, with statin drugs, there’s a lot of research showing that people overestimate, after being educated by a doctor or hearing advertisements in magazines or on TV for statin drugs, people who take statin drugs have been shown to overestimate the magnitude of the effect size in reducing their risk of heart disease by over a hundredfold. This is not a small, a trivial thing. Like people who take these drugs think that they are massively slashing their risk of getting this disease or even think that maybe the drug is curing them or completely eliminating or close to completely eliminating their risk of this disease, when in fact it’s, in the case of heart disease and statins, absolute risk reduction is about 1.3%.
There’s this enormous gap between the people’s perception and the actual magnitude of effect, and because they perceive it to be so much more effective than it actually is, it becomes like, “Well, I’m taking this drug. I guess I don’t need to worry about my diet and lifestyle anymore because my drug, all this amazing science and technology came up with this drug that cures this disease. I’m taking it, so I’m protected now.” You know what I mean?
Dr. Sandison: Yes. I think that there’s a risk there too of, “Okay, I’m taking my statin, so I can have an extra cocktail or I can have an extra three, or I don’t have to get exercise or I don’t have to change my diet.” What we see is that those lifestyle decisions are absolutely foundational. I think we live in a society, again, just going back to the incentives, there are big food companies, the food industry is responsible for our poor health outcomes. I think if we could change anything to increase the health of our society, it would be to change the food system and have fewer, especially ultra-processed foods, but generally just having less processed food I think would be helpful.
Going back to whole food diets. Then also to society, the way that we’re set up, there’s no incentive to exercise other than our own health and well-being. We’re incentivized to work harder, to work longer hours, to eat cheap, processed, convenient food that’s not good for our health. The insurance system and the way that that is set up is not designed for health. It’s designed for insurance companies to make money.
There is a lot– We’re swimming upstream if we want to be healthy. It’s really a choice that we have to take responsibility for. Our priorities have to be reflected in how we choose to spend our time, what we choose to put in our mouths, how much movement we choose to get each day, what time we go to bed, who we spend time with, how we manage our stressors. Really those small choices that we make every day are what determine the trajectory of our health as we age.
Inflammation
Ari: Yes. Well said. I want to come back to something before we move to sort of the more practical side of things. I know you’re itching to get there, but– And sorry for slowing down. There’s just a lot of stuff I want to cover before that. One of the things you said earlier in passing was speaking about inflammation. You mentioned that we need to look one step above inflammation, what’s upstream of that. I think this is a really important point because so many, especially now, I think, within natural health and functional medicine circles, it’s become very trendy to speak about inflammation as the “cause.”
This is sort of analogous, I think, to seeing amyloid plaques as the cause, right? It’s like we have this tendency with the way our whole paradigm and culture is structured with regards to how we look at human health and disease, that we think that the smaller and more micro of level we are peering into the human body, the closer we are arriving to truth of the “causes” of things.
As soon as we look at things at a microscopic level and we find something that’s correlated at that microscopic or cellular or biochemical level, we go, “Ah, that’s the cause. We found amyloid plaques in the brain, we found tau proteins in the blood, we found this profile of inflammatory cytokines, this is the cause, let’s treat this.” We confuse the micro-level correlates of disease states with the causes of disease states. I’d like you to speak a bit more about inflammation and why there are so many people that conceptualize inflammation as the cause of things and how you think it’s better viewed.
Dr. Sandison: Yes, inflammation just like amyloid or just like many of the diagnoses. This is sort of this, we’re going to label what’s going on, there’s inflammation. When you think about that, like you and I, we’ve both been inflamed. Inflammation is a natural process. This is part of the body’s divine design. If I twist my ankle, I want inflammation to occur because that’s part of the healing process. If I get an infection, I want inflammation to occur. It’s part of the healing process.
Now, if that inflammation lasts for a really long time, we want to understand what happened. Is there a signaling pathway that’s off? Is there a self-perpetuation of a cytokine storm that’s going on that maybe needs to be interrupted? Typically, inflammation starts because something triggers it. If we miss the opportunity to ask what was the trigger, we miss the opportunity to get real healing.
Inflammation, I listed just a couple of things that can happen; an infection, an injury, a traumatic brain injury in the case of the brain, that can put us at risk for dementia later on. An infection, like this is a great opportunity to talk about COVID, right? COVID creating these cytokine storms that when we put that on top of inflammation that was already existing, with COVID, it’s this great illustration of some people die from COVID, other people have long-haul COVID, other people never even have a symptom.
What’s the difference? It’s that, this is where a lot of people understood the idea of comorbidities, other things going on in this environment, in the host, when that virus came into the host, what was already there, what was the milieu of inflammation and inflammatory factors that might’ve already been there. High blood sugar, high blood pressure, stress, potentially structural issues, like not getting enough air into the lungs and not getting enough oxygen in the brain at night because of sleep apnea. This is going to create a much more inflamed state.
Then when we add another trigger on top of it, it can get out of control. This also happens with dementia and Alzheimer’s, is when we already have some inflammation in the system for whatever reason, and then we add a couple more, now we have so much inflammation that’s out of control. We can add fish oils and we can add some turmeric and we can add all of these like anti-inflammatories.
Ari: Why not take anti-inflammatory drugs if the cause is inflammation?
Dr. Sandison: Yes, or steroids. Steroids are something that we’ll use. What they do is, steroids in particular, they suppress immune function. They make us more at risk for other infections. Over time, they can create bone loss. They can, adrenal issues. There are many, many, many things that can go wrong when we add anti-inflammatories. Again, we miss the invitation to say what is causing this and and how do we get to the root cause and get real healing?
Dr. Bredesen’s and Sanderson’s research on reversing Alzheimer’s
Ari: Yes. Well said. You said in passing earlier, you were describing the study design that you did with 23 participants and Dale Bredesen’s research and this was in the context of speaking about kind of in pharmaceutical companies, they have much more funding to conduct much more massive-scale studies, and there’s an interesting sort of dynamic that emerges as a result of those, that financial picture, which is that we end up accumulating a much larger body of evidence on the drug interventions than on, let’s say, lifestyle interventions like you’re doing, what Dr. Bredesen is doing.
I’ve noticed sort of a funny dynamic that emerges from that, which is when you go and you have discussions with people who are in evidence-based circles, they’ll say, “Oh yes, but Dr. Bredesen’s research, or but Dr. Sandison’s research, oh, that was just a very small-scale study, it was a pilot study, it doesn’t have the statistical power, it doesn’t have the weight of the evidence, like this large body of research on the drugs, so therefore the drugs are the really ‘evidence-based thing,’ and these lifestyle interventions are still as of yet largely untested and unproven.”
They’re sort of like, they’re put in the category of like pseudoscience and unproven treatments as a result of basically just the financial dynamics creating a situation where there’s a much larger body of evidence on the pharmaceutical interventions, even though they’re actually much less effective.
Dr. Sandison: Yes, so the outcomes, there is power analysis that goes into these. We had to have a sample size large enough to create an effect, so there certainly are statistics that are meaningful that are here. Maybe I’ll just take you through the research that supports what’s in my book, and people can decide for themselves, right? I think I always go back to, this is common sense, it’s just not common practice. If you can hear the exasperation in my voice, it’s there, like I own it. Like we’re talking about diet and exercise and sleep and stress management.
How do you feel when you get the right food and the right company and the right stress management and you’re well rested and you get some exercise, right? We all feel better when we get that, and our parents suffering with dementia tend to do better too. This is not rocket surgery, and there is science. Dr. Bredesen’s group, we were all doing this– There’s three studies that I want to point out, and we were all doing this research around the same time, but they started a little bit before me.
They took 25 participants through a nine-month intervention, and it was a feasibility trial, so they took participants with MoCA scores down to 19. The MoCA is the Montreal Cognitive Assessment. This is out of 30, it’s a one-page worksheet where you draw a clock, copy a cube, identify some zoo animals, and then you end up with a score out of 30. Perfect is 30, normal is 26 and above. They took participants with MoCA scores down to 19, so in that mild cognitive impairment stage, but they all had some sort of cognitive impairment. What they saw after this nine-month intervention in these 25 participants was that 84% of them improved their cognition.
They published in the Journal of Alzheimer’s Disease in July of 2022, and Kat Toops is the lead author on that paper. A year later, in August of 2023, I published my trial, very similar, 23 participants, six-month intervention, so a quicker intervention, and we only took participants with MoCA scores between 12 and 23. Again, normal is 26 and above. Our participants had impairment, more impairment, they were further progressed along the disease state, and we only did six months, and we saw that 74% of our participants improved.
The most recent trial came out on just June 7th of 2024, and this is Dr. Dean Ornish’s trial, and this was a 49–, I think there were 51 participants total, but two dropped out, and they did a 20-week or a five-month intervention, and it was a randomized controlled trial. This is the first randomized controlled trial looking at lifestyle interventions alone. In the trials that we had done, Dr. Bredesen’s group [unintelligible 00:39:34], there’s three doctors who had sites in that initial trial, Dr. Bredesen’s group, and then mine, we did the combination of lifestyle medicine with functional medicine. We looked for toxins, and we looked for infections, and we looked for nutrient imbalances.
We did a lot of the testing, and in Dr. Ornish’s trial, they did mostly lifestyle interventions. They did use some supplements, and they listed all the supplements in the trial, 20 weeks, and they had a control group that did not get that intervention and then an intervention group that got that intervention. The conclusions they drew, I got chills. It was just so exciting because when you have a randomized controlled trial, you can make that connection between the intervention. It’s much more clear. You can draw the conclusions that the intervention is having the effect.
The conclusion that they drew was that comprehensive lifestyle changes may significantly improve cognition and function after five months in many patients with mild cognitive impairment or early dementia due to Alzheimer’s disease. This trial– Yes, we will always need more research, we will always want to learn more, we need more randomized controlled trials, and Dr. Bredesen’s group is in one right now. I think they’ve completed recruitment for that.
I’m looking forward to seeing those results, preliminary results look good. This randomized controlled trial is the first. This is the first really stating that lifestyle interventions can have an impact on dementia. When we look at any of the drugs that have ever been tried, they don’t improve cognitive function.
Ari: That’s what I was going to say, I just want you to point out this distinction between what you were talking about before with the drugs, which was a 30% slowing of the rate of decline versus an improvement, because I think those two things might be conflated in people’s minds.
Dr. Sandison: Right. What’s going on here is if you take someone on their way towards Alzheimer’s or dementia, the average is that they’re going to drop that MoCA score by two to three points per year. If you start with a MoCA of 20, a year later you’ll be at a 17 or an 18, and then so on. Each year you may drop. Now, there’s variables, things happen, and sometimes it will be a little bit better, sometimes it will be a little bit worse, sometimes it will stabilize, but what happens with the medications is that on average, instead of dropping from a 20 to an 18 or 17, you’ll drop from a 20 to an 18 or a 19.
You’ll drop by two points instead of three points, or by one and a half points instead of two or three points, something in there. You basically get a slowing of that disease process. What we see with Dr. Bredesen’s approach is that you get an improvement of about three points on average. We have some patients that get an improvement of 10 points. They go from a MoCA of 20 to a MoCA of 30. We have patients, some of them get five or six points and some get one or two points and they kind of stabilize, but the average is about a three-point improvement. Compared to no treatment at all, this is about a six-point difference. You’re not declining.
With the medications that are available today, there is a decline in cognitive function. You don’t change how someone interacts measurably. They’re not getting that one last Christmas or that last anniversary or that last summer. What you’re having is potentially there’s less care that they need as they progress down this disease state. With these interventions, you see actual improvement. What we see at Marama is that, our goal there with our– We have this immersive experience, in a senior living environment, people can move in, and instead of memory care, our goal is memory recovery so that they can return to independent living.
We had our first resident, she moved home with a MoCA of 30. She came in with a MoCA of 24, she didn’t wait until it was really progressed, but she had measurable impairment, moved in with a MoCA of 24, and six months later, she moved home with a MoCA of 30.
Ari: Wow. Beautiful. I think all of that– I was thinking, this morning I was listening to a podcast and somebody was–, actually it happened to be on Alzheimer’s and dementia. He mentioned that a lot of the descriptions that you read of these diseases online, like on WebMD or Mayo Clinic or Cleveland Clinic or whatever, describe them as “incurable diseases.”
This label of incurable disease implies in our minds that once you get this disease, oh, it’s like this binary state, first of all, you’re either healthy without the disease or you have the disease. Once you have the disease, it’s an incurable progressive condition. You’re just going to go downhill, worse and worse until you die. I think what you’re really getting at here that I want to emphasize, and maybe you can add to what I’ll say here, is that this whole picture is way more malleable than that. It’s way less binary.
It’s much more of a spectrum, first of all, and you can move in different directions on that spectrum. You can move– The word cure I think is problematic in and of itself, as you were speaking to earlier, because we all have this idea that’s like, you have this disease or you don’t, this binary on and off thing. Then the cure is something that you take for a short period of time, that fixes you, you no longer have the disease, you can go back to the way you were living, disease-free now.
It just– The picture isn’t really that. This whole idea of finding the cure that we’ve all been indoctrinated with since the time we were children is itself problematic. The key point here is, as you just explained with your patient, that, okay, there was some decline, there was some movement towards dementia, and we reversed that. We effectively made it, so there isn’t dementia anymore. If we understand that dynamism, that malleability of these processes, I think that’s a really empowering thing for people to realize, “It’s not a binary on and off, and I can do stuff about it to actually reverse this direction.”
Dr. Sandison: Yes, it’s a very hopeful place where I sit, and we see patients even– It’s much easier to reverse the disease process when it’s earlier on, when people are younger, when the disease has not created as much structural damage in the brain. As it gets more progressed, it’s harder, but the good news is that there’s hope. I have seen people even with severe cognitive decline in diagnosed Alzheimer’s improve their cognition. They’re not necessarily going back to work. I will repeat what you’ve said again, this is not a cure, it’s a lifestyle.
The good news is that there’s hope. The bad news is it takes work. You have to do it. It’s not going to be for everyone. If you’re the type of person that’s waiting for a medication, a pill to swallow or an IV to take to cure you, that is not what I have to offer, but if people are willing to make the changes, if they’re willing to significantly change their diet, and you do not have to do all of this. In our clinical trial, not one person who improved did everything, but they did make significant changes to their diet, to their exercise habits, to their sleep, to their stress management practices.
They took supplements, they looked at their testing, they looked at their labs. In the Ornish paper, one of the big differences in their lifestyle approach compared to ours is that we suggested an organic ketogenic diet, and they suggested a vegan diet. I think that you can do either, but I do think you need to commit to one or the other and significantly reduce or eliminate altogether processed foods in the diet. In an ideal world, probably be switching back and forth between plant-based and a ketogenic diet so you get that metabolic flexibility and the benefits of that.
I think that there’s choice in this. You can make it fit for you. Do fun things. We find that fun is a really important consideration. It’s for brain exercise. First, we have to want to do it. We have to continue to do it. This can’t be the thing that we do once a week. This has to be the thing that we do six to seven days a week. This has to be the lifestyle that we choose to adopt long term. That’s when we see the benefits. It takes work, but don’t let anyone tell you there’s nothing you can do for Alzheimer’s. That is just factually inaccurate at this stage. We know better.
Ari: Yes. Heather, are you okay on time? Are you able to go 10 minutes longer or do you have a hard cutoff in five minutes?
Dr. Sandison: I do.
Dr. Sandison’s top brain health tips
Ari: Okay. Let’s finish with a few of the top brain health tips that you can recommend to people. What do you think are the biggest needle-movers for, let’s say, people with early signs of cognitive decline to start to reverse that and get themselves back to full brain health or in the situation of understanding that these are long-term disease processes that often take decades of actual decline in the structure and function of your brain before you actually even notice symptoms or get a diagnosis, what are the things that people can do, the biggest needle-movers to ensure that people don’t end up with dementia?
Dr. Sandison: In the book, the first chapter talks through, if you can only do one thing in each of these categories of brain health, what it would be. I think that I’m going to skip those for your audience, but many of you who are listening, you are super well-educated. You’ve already heard these things. I’m going to give you some things that you probably haven’t heard of, but I want you to know that in the book there are very accessible, quick, easy things to impart on somebody who maybe has never been introduced to functional medicine or isn’t even aware that there’s something you can do for cognitive function.
What we want to do is make this accessible. You can have all the information in the world, but if you don’t put it into action, it doesn’t have an impact on your health. What I want to share with your audience today is if you were to take it a little bit further, because I know that everybody here is super well-educated. Organic ketogenic diet, which we could spend an entire week talking about what that means, but I know that all of you who are here are familiar with that. You kind of know what that looks like. Adding coconut oil for the MCTs, getting the beta-hydroxybutyrate and the ketones available for your brain.
Your brain prefers ketones to sugar for fuel, and so the more that we can be in ketosis, typically the better our cognition is. That has kind of a brain rescue benefit. Then two, exercise. What I recommend for exercise is something called dual-task exercise. D-U-A-L. Two things at the same time where you’re exercising cognitively at the same time as physically. Super simple would be walking and talking.
More advanced, learning a new sport like playing pickleball where you’re engaged physically, you’re engaging intellectually because there’s strategy involved, you’ve got hand-eye coordination, there’s social engagement, you’re outside, you’re getting vitamin D. You’re checking multiple boxes at the same time. Even just going to a challenging dance class. Even just going to anything where you’re cued by an instructor and you have to cognitively keep up with that, or you can get into, if you get really fancy with this, you can do some sort of brain training while you’re exercising, whether it’s math problems or memorizing a poem or something like that while you’re exercising, getting physical activity.
You want to be about 75% of capacity, both physically and cognitively. Not so hard that you give up, but not so easy that you’re checking out. Diet, organic ketogenic. Exercise, dual task. Sleep, you want a minimum of seven hours of sleep. Aiming for, I always hesitate here because I don’t want people to be so fixated on these numbers that they end up not sleeping, but just to use as general guidelines, minimum seven hours of sleep, an hour and a half of REM, an hour of deep sleep. I wear an Oura Ring. I track it. Don’t get too fixated on the numbers, but prioritize your sleep. If there is any sign of cognitive decline, get a sleep study.
Do not wait to find out you have sleep apnea in five years because each night of sleep deprivation and hypoxia is damaging to your brain. It’s like a traumatic brain injury each night, so make sure that you get that treated, and mouth tape. Mouth tape is one of my favorite things. It treats mild sleep apnea, helps with anxiety, helps with cognition, helps with sinuses. I mean the litany of things that helps with is long. Consider mouth tape if you have any issues. Organic ketogenic diet, dual-task exercises, prioritize your sleep, understand if you have sleep apnea right away and treat it. Then stress management.
There is an exercise, a meditation called Kirtan Kriya, it’s a 12-minute–, the Sa Ta Na Ma. That one has a huge amount of literature, review articles published on why it’s so beneficial for cognitive function and for many other things, for blood sugar regulation, for many of the things that are causal level when it comes to Alzheimer’s and dementia. Blood sugar regulation, inflammation, for stress management, adrenal balancing, spiritual fitness, telomere length, like all of these things that are associated with aging. Totally free. Only takes 12 minutes. There’s no reason not to do it.
Ari: Dr. Sandison, thank you so much for coming on the show. This was an absolute pleasure. Thank you for sharing your wisdom on this topic with my audience and let people know you just have a new book– you have a new book that just came out, I should say, called Reversing Alzheimer’s. Let people know anything else you want to let them know where they can find you, where they can follow your work, and where they can get your new book.
Dr. Sandison: Ari, it’s always fun to see you. Thank you for the great conversation. You can find me at drheathersandison.com. Follow me there. Join our newsletter. We’ll keep you updated on the science and all of the incredible things that we are doing to hopefully reduce the suffering associated with Alzheimer’s.
Ari: Beautiful. Thank you so much for the work you’re doing, and I look forward to our next conversation.
Dr. Sandison: I do as well. Thanks, Ari.
Show Notes
00:00 – Intro
00:27 – Guest Intro Dr. Heather Sandison
01:52 – Why the current approach to Alzheimer’s isn’t working as intended
12:30 – How one factor alone has shaped the treatment of neurodegenerative illness
26:15 – The value of the current Alzheimer’s medications
30:50 – Inflammation
35:35 – Dr. Bredesen’s and Sanderson’s research on reversing Alzheimer’s
48:25 – Dr. Sandison’s top brain health tips
Links
Learn more about Dr. Sandison’s work here: https://www.drheathersandison.com/
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