Dementia Prevention & Reversal: Current Research

Now you can take a couple points off here and there, so you don’t have to get it perfectly right to still have normal cognitive function. So anything over 26 is normal. Once we drop below that, we’re starting to measure cognitive changes, and anything below 17 can be diagnosed typically as dementia and maybe even Alzheimer’s. So we use this tool sometimes in research, sometimes just clinically, but it’s informed a lot of what we do here at Solcere and also at Marama. You may know somebody who’s taken this and be somewhat familiar with it, but I wanna have you understand what this tool is. And you can also ask your doctor or some trained professional to perform this for you. Usually you want to do training and there is training available online, so you can sign up for that, and then you could do that if you’re a caregiver for the loved ones or those that you care for. I wanna tell you about Linda. Linda was the first patient who I saw after returning from being trained by Dr. Dale Bredesen. 

So I was a bit of a skeptic. I’ve shared this with many people but I went to Dr. Bredesen’s training, because it made sense to me. I’m a systems thinker and I like connecting these dots and understanding the feedback mechanisms. And I knew from my naturopathic training that there’s not a one-size-fits-all for a complex disease. Lots of this needs to be individualized. And it made sense to me that as we stacked interventions, the way Dr. Bredesen explains, instead of trying to simplify or find that one magic bullet pill, if we could stack these interventions on top of each other, we could be more confident about potential miracles that we might see happen. Now, that being said, even though it made sense conceptually, I had never seen it work in practice. I had never seen a dementia patient return their cognitive function or regain cognitive function, and so I didn’t know if it would work. And Linda came to me with her husband. They had read Dr. Bredesen’s book, “The End of Alzheimer’s”, and they were less skeptical, more confident, more enthusiastic, and more certain this was gonna work than I was. But I took them through the process. 

They taught me a thing or two. So we did Dr. Bredesen’s intake. I had lots of experience working with toxins and hormone replacement, and many of the elements of Dr. Bredesen’s work, I just needed to put it all together in the context of cognitive decline. So with Linda, she came in that first day and you’ll see part of her MoCA worksheet here on the left. She had a MoCA of 2 out of 30. This represents very severe disease. So she could answer with yes or no responses to relatively simple questions. But if I asked her, what did you have for dinner last night? Before she could formulate an answer or kind of remember what she had had, she’d forgotten what the question was. Same thing if I asked her about exercise or what her day to day life was like, and this was heartbreaking to watch her husband lose her. She was losing her mind. And I could tell she had this great big smile and these loud, fun clothes, I knew there was so much personality in there. And it affected her handwriting, so she had very small, kinda shaky handwriting that was at a steep slant. And she had been a school teacher, very proud of her handwriting. So this was a heartbreaking situation, and I was so impressed by how Linda and her husband just committed and did it all. 

They got out of a moldy bedroom. They committed to an organic ketogenic diet and they started right away. They started ballroom dancing several times a week. She took all the supplements, started on hormone replacement. She got all of her amalgams, her metau fillings out of her mouth, got a deep cleaning, and took care of some infections in her mouth. This was impressive. They did all of this in a matter of days after seeing me the first time. And I saw them for a follow up six weeks later. Now in just six weeks, Linda had significantly, measurably reversed her cognitive decline. She had reversed the disease process. Now this doesn’t happen every time, but this miraculous recovery made me think, if this is possible for Linda, what is possible for so many others out there who are earlier on in the disease process and who are younger, who might have even more ability to heal and prevent decline and even regain full cognitive function? I was so delighted. I was actually in disbelief first. I thought we had done something wrong. 

I thought that maybe we had measured it wrong the first time, or maybe I wasn’t- My brain didn’t compute that this kind of miracle could be possible, but you can even see for yourself here that the way she’s drawing the box, she’s copying this cube, although it’s not perfect, it’s different, it’s starting to get a little closer, and same with the clock. She’s adding numbers to it that she hadn’t been before. I mean, this is really impressive change in just a matter of weeks. And so seeing again that this was possible for Linda, I, really, since that day, it had such a big impression on me that I’ve committed my life to showing people that a lot of the suffering associated with dementia is optional. It doesn’t have to happen, that we can take action today to reverse this awful disease and prevent it. So I wanna tauk a little bit more about what we know about the science, and I’ll start by tauking about the language that we use here, because unfortunately, it’s caused a bit of a problem. Doctors will say mild cognitive impairment, when really this should be called advanced staged Alzheimer’s, right? Stage three cancer is not mild cancer. That is metastatic cancer. 

That is a really big deal. And so is mild cognitive impairment, and we should be treating it as such. So it starts with a presymptomatic stage, and there’s some argument in the field around what we would use to diagnose a presymptomatic stage and whether or not there’s utility in finding beta amyloid plaques or tau proteins. But we certainly know that we want to prevent dementia and that there are changes in the brain that happen. There can be inflammation and potentially the plaques and tangles that set us up and put us at risk for developing cognitive decline. The thing we really care about is not whether or not we call it Alzheimer’s or whether or not these plaques and tangles are in our brain, but how well our brain functions and serves us day to day. And so in that presymptomatic stage, this is when it is easiest to prevent the disease from happening at all. So some people are gonna be at higher risk because of genetic predisposition, which we’re gonna learn more about this week. Then subjective cognitive impairment is another great time to intervene. And this is, it lasts probably about five to 10 years. 

This is when someone says, “Oh, my brain doesn’t work the way it used to. I would’ve been able to remember that name or where I put that thing or how I would get from here to there 10 years ago or five years ago.” So if you were saying that, or if one of your loved ones, you hear them saying, “Gosh, my brain isn’t working right the way it used to”, get them signed up with a Bredesen doctor, get them engaged in this process, make sure they have access to the summit, because now is the time to intervene. Mild cognitive impairment is severe disease. This is when it’s measurable, and this is relatively late in the pathophysiological process, so a lot of changes have already happened in the brain and toxins have already been present, infections may have been present, nutrient imbalances may have been present for decades before. We really, we can intervene here, and I would encourage you to, I would never tell anyone there’s not hope even for final or late stage dementia. I’ve just seen too many people get improvements even at that stage. However, the earlier we can intervene, the better, and I think that this word mild, when we tauk about cognitive impairment, discourages people from getting the help that they need and deserve. Final stage Alzheimer’s includes immense amounts of suffering, losing activities of daily living, losing so much of yourself. 

It’s just absolutely awful, and if I can prevent one person this week from going there, from having to deal with that, it’s been worth it. So typically, this underlying process has been present for even two decades, 20 years. And now we know enough where we can intervene in those 20 years so that you don’t have to suffer with this late stage Alzheimer’s disease. There are some other problems that have come up in the field that I think have prevented people from getting the help that they deserve sooner. So certainly, the amyloid plaque hypothesis has been a big part of the Alzheimer’s debate for the last four or five years, especially. In the 90s, 80s, 90s, early 2000s, if you were not studying amyloid plaques or tau proteins, you were not studying Alzheimer’s. We now realize that after billions of dollars of investment and decades of smart people’s lives, being dedicated to finding a solution to the beta amyloid plaque problem, assuming that dementia was caused by amyloid plaques or tau proteins, we now know that this was a bit of a dead end, and unfortunately, you know, we’ve wasted a bit of time and there are still people who are doubling down on this hypothesis. 

I’m glad that people seem to be opening up to more of a multifactorial approach, even across the conventional spectrum, but it’s slow going. And we really need to shift focus because it’s dominated the conversation for far too long. What we know right now is that if you take the brains of anyone on the planet, basically the entire population, less than 1% will not have amyloid plaques or tau proteins present. So this is any age, any place in the world, less than 1% of the people on the planet do not have beta amyloid plaques. That means we all do, so they’re there for a reason, and we believe that they’re there to protect us. They’re highly antimicrobial and they’re inflammatory. So typically they are formed in response to an infection or a toxin or something that is potentially putting our brain at risk. Now, the other thing is that people who are over the age of 65, so the seniors among us, if you look at their brains, there are many of them, 30% of them, regardless of cognitive function, have enough amyloid plaque deposition in their brains to be diagnosed with Alzheimer’s. So if we’re not measuring cognitive decline, why do we care so much? There’s a connection between amyloid plaques and dementia. 

Don’t get me wrong, there’s definitely something there, but that is not the full story. Getting rid of amyloid plaques does not improve cognitive function. And so we need to look outside of that. We need to understand what is driving plaque and tangle formation, rather than just trying to get rid of the plaques and tangles that are the result of other imbalances upstream. So I hope you’ll join me this week as we dive into all of those factors. Another problem that we see over and over, and it breaks my heart every time I hear it is that people go to a neurologist and the neurologists continue to say that nothing can be done. They say here’s some Aricept, here’s some Namenda, they don’t work very well, get your affairs in order. This is going to be a downhill slide. And we know right now that there are so many factors that can lead to improved brain function. Not everyone is going to regain full cognitive capacity, and I will not use the word cure. For anyone who has cognitive decline, they are going to be at risk for developing cognitive decline if they fall off the diet, if they have a traumatic brain injury. You know, there’s a litany of risk factors. If they’re smoking or drinking excessively, all of those things can put someone at risk back on that slippery slope into cognitive decline. And yet there are things we can do, that we need to be talking to our doctors about, so that we can regain control of our brain health and keep our cognitive function into our seventh, eighth, ninth and 10th decades. 

Another issue has been in the research world. So the IRB approval, IRB stands for internal review board. So this was created in an effort to protect vulnerable populations of human research subjects, like those suffering with dementia. I’m so grateful for the IRB. We work with one on the clinical trial that we are doing here at Solcere and they are phenomenal. They protect our research subjects and our study participants and we are so grateful for them. It wasn’t until five or six years ago that IRB started approving these multifactorial interventions. So Dr. Bredesen has had funding to do a clinical trial for years, over a decade, and yet he couldn’t find an IRB who was willing to support and approve a research trial that included so many interventions all at once. In our hierarchy of research, they want things to be controlled, they want the variables to be limited, and I understand where that perspective comes from, and yet as a clinician, as someone who’s seen people suffering in real time, I wanna give you everything I possibly can so that your brain can be better today. And we know enough, especially we know enough about safe, low risk interventions. Now, that being said, now that we’re finally starting to collect some data, I joke that everything goes at the snail’s pace of research around here, because it takes a while. We wanna do it methodically. We wanna do it right before we draw conclusions and we might be wrong. Any good scientist accepts that they could be wrong about their hypothesis. That is why we test it. 

And so all the critics are right. It’s true, there is not enough data. There is not enough research, not enough has been published in peer reviewed, highly respected journals. And there are politics behind the scenes, and there are reasons for that, and it’s happening. It’s going slowly, but it is happening. And yet we know enough today to get started. And that’s because many of these interventions are very low risk. They involve lifestyle changes and choices that really are common sense, just not common practice. And so I’m here to encourage you to stick with me this week, learn as much as you can and get these things started in your life immediately. So here’s some current research that came out of the “Lancet”. The “Lancet” is a highly respected journal in the UK, and this is the 2020 report. This got a little stuffed under the rug because of COVID. You know, COVID was so distracting that year, but this was, the “Lancet” Commission published this 2020 report on Dementia Prevention, Intervention, and Care. And in the executive summary, they said, “Overall, a growing body of evidence supports the nine potentially modifiable risk factors for dementia modeled by the 2017 “Lancet” Commission on dementia prevention, intervention and care. 

So they had a 2017 paper that they published, and then they updated it in 2020. And what they said was that those modifiable risk factors, there were nine of them. They were less education, hypertension. So not having a college education, not having enough education. Basically you don’t have enough cognitive reserve as you age. So not having enough education, having hypertension, hearing impairments, smoking, obesity, depression, physical inactivity, diabetes, and low social contact or being isolated were all modifiable risk factors. So not genetics that are not modifiable, but these are all modifiable risk factors, things we can change, and they are now adding three more risk factors for dementia with newer convincing evidence. These factors are excessive alcohol, traumatic brain injury and air pollution or toxicity. They have completed new reviews and meta analyses and incorporated these into an updated 12 risk factor life course model of dementia prevention. Together, the 12 modifiable risk factors count for around 40% of worldwide dementias, which consequently could theoretically be prevented or delayed. So this is coming, excuse me, from one of the most reputable journals in the world. Excuse me. I’m so sorry. This information is coming from one of the most reputable journals in the world, and what they’re saying is that 40% of worldwide dementias could be prevented, or at the very least delayed. 

Now they don’t even know what we’re doing at Solcere and Marama, and I don’t think that they’re factoring in what Dr. Bredesen’s doing, where we are actually even reversing dementia, when we take all of these factors and we intervene in a systematic way. And so another thing that they mention in their executive summary is that their new life course model, what they’re presenting here and the evidence synthesis, so they take all the data, they take lots of clinical trials and they do meta analyses. So we’re starting to go up the hierarchy of literature, and then these guys are creating a recommendation basically after they synthesize the data and the evidence, and that this has paramount worldwide policy and implications. They say it is never too early and never too late in life for dementia prevention. Early life, younger than 45 years, risks such as less education, cognitive reserve, and then midlife and later life risk factors, influence reserve and triggering of neuropathological developments. So what they’re basically saying is that it’s never too early and it’s never too late to prevent dementia. That there’s so much we can do and including these 12 risk factors. They also say, similar to what I presented in the problem slide, that amyloid beta and tau biomarkers indicate risk of progression to Alzheimer’s dementia. However, so they’re associated with risk of progression to Alzheimer’s. However, most people with normal cognition with only these biomarkers never develop the disease. So this is that 30% of people over 65 who have enough beta amyloid and tau biomarkers to be diagnosed with Alzheimer’s. They are not in a pre-symptomatic state. 

They are not sick people who aren’t showing symptoms yet. They are healthy and that’s okay, and it doesn’t necessarily mean that they will progress to Alzheimer’s, although they could, and so we want them to make these modifiable changes in their lifestyle to prevent or to reduce their risk. Dr. Bredesen also has done, has published several papers. So this one on the left, this is a 25 participant trial and where the “Lancet” was taking the sum total of a lot of research that’s out there about dementia, what Dr. Bredesen was doing with Dr. Kat Toups, who’s the first author on this paper, what they did was they took 25 participants and there were three different sites where different doctors took their patients who had cognitive decline through the Bredesen protocol for nine months. They had the supportive health coaches, they had the supportive exercise coaches, they got on their toxins out, they were able to get on supplements, they were able to get on medications as appropriate. So they worked one on one with their Bredesen trained provider to get the best of his protocol over the course of nine months. And what they saw when they measured it is that 84% of those 25 participants improved their cognitive function. 

Only one of them had no change at all, and 12% declined. And so what we expect is that everyone will decline by about three points on their MoCA score, on that 30 point scale. So if you have a MoCA of 23, we expect you to go down to a 20 in 12 months. And what they saw in this trial was not only did people not decline by three, by two or three points, they improved by an average of three points. So this is like a six point difference on a MoCA scale. This is incredible. This is groundbreaking, earth-shattering, incredible information. And now these patients had a lot of handholding, they had a lot of support, and I will say that this is very consistent with what I see in my clinical practice, so that if we work hard, if people have the support, the vast majority of them get better. And then this trial on the right, it was also published through Dr. Bredesen’s group and some people who work with him, and this is based on the ReCODE protocol. So these are people who did not have all of the handholding that everybody on this left side did. They had just access to an online AI platform, lots of education, lots of engagement, but all of it was not one-on-one with other people or with trained clinicians. It was only through ReCODE. And so these were people who were interfacing with an online program, and some of them were engaged with doctors and health coaches, but not all of them. So everyone who was involved in ReCODE, of everyone who signed up, 51% of them improved. 

Again, no one is meant to get better, right? If you listen to some of the neurologists, there’s nothing you can do, and you should expect a precipitous decline. Well, 51% of people who didn’t even have all the support, they just had the information, so started making lifestyle changes, had improvement. Now, of course, we expect more people here to decrease and not have as much change at all. However, this is still really impressive, that 51% of participants improved. And so I highly recommend that you reach out to Apollo and get more information from them. They are partnered with us on the summit as is Dr. Bredesen and they really provide some phenomenal educational resources and the papers are available. The original research of both of these trials is available on their website. So I was very, very fortunate to receive a grant to do a similar trial to the one that Kat Toups and Dr. Bredesen did, where we were able to take 25 participants through my version of Dr. Bredesen’s protocol here at Solcere. And we called it the Integrative Therapy for Holistic, Natural Cognition and Lifestyle Rehab, or the ITH NCLR trial. This is a prospective observational study where we were really just assessing feasibility. Could this work? Do people follow the protocol? It’s a very complex protocol, and this is in a population as you well know where they’re cognitively challenged, and so it’s a lot to ask people to change their diet, change their habits, prioritize sleep, prioritize exercise, take all the supplements, take some new medications. This is a lot to ask someone, start meditating, and we did it. So we just have recently finished collecting the last of our six month data. We took 25 participants through six months of intensive protocol to reverse their cognitive decline and Dr. Bredesen’s group, they did it for nine months, so they had a little bit longer trial and they took participants with MoCAs down to 19. So a little bit earlier on in the disease process, not as severe disease. We took participants from MoCAs of 12 to 23. So they had to have significantly measurable cognitive decline to be included in our trial. 

And then we had only six months to show change. So I’m very excited to be publishing that research this year. It has not been peer reviewed yet. Our paper is not finalized, but as soon as it is, as long as you’re on our email list, you will be one of the first to hear about it when it’s out there and ready to be read. And I hope that you will help us share it widely, because the reason that I’m so dedicated to this is because I know that there is suffering happening in the world that doesn’t have to. And so getting the research out there, getting the knowledge out there, showing people what’s possible will be what inspires them to intervene earlier and to prevent this disease so we can make it a rare disease. I believe that Alzheimer’s is optional from what I have seen clinically, and I want everybody to be able to take advantage of that information and that opportunity. I hope that you’ve gotten a ton out of today, and I know that there are often lots more questions after a day like this, where there’s so much information being shared. Please comment in this section below, in the comment section below, and let me know your feedback. Let me know what questions have come up for you. Let me know what you loved about today and what you’d like to see more of. I read all the comments and really appreciate engaging with this community. You are a delight to serve. Thank you for the privilege and opportunity.