Insights on Healing Parkinson’s from an Expert Neurologist

David Perlmutter, MD, FACN, ABIHM

Dr. Sharlin. Thank you so much for having me. I am honored to have the opportunity to participate in this summit. I think it is very important.

Kenneth Sharlin, MD

As a fellow neurologist, Dr. Perlmutter, I am curious about your journey and how it incorporates things like food, movement, stress, resilience, sleep, and thinking about ketosis and uric acid in the microbiome. How did all those things happen? Those are things that we do not study in medical school, rather than maybe.

David Perlmutter, MD, FACN, ABIHM

Or Neurology school, for that matter. I was out in practice for several years and finally had the revelation that I was treating symptoms of the disease. I was not treating a disease. I was not treating Parkinson’s, or Alzheimer’s. Epilepsy, headaches, you name it. I was simply treating the manifestations. I had found that to be less than fully rewarding. I did not want to spend the rest of my life just focusing on the smoke and ignoring the fire. Fortunately for me, around that time, which probably would be about 25 or so years ago, we began to see evidence in the literature that people were indeed exploring the role that lifestyle choices played in predisposing people to neurological problems of one sort or another. Even the notion that lifestyle factors could affect one’s risk of something like Parkinson’s or Alzheimer’s back then was beginning to be spoken about but was pretty much off the table in terms of mainstream neurology. Unfortunately, through your eyes and my eyes, it is still pretty much off the table. 

We do not, even in the journal, see very much activity. Interestingly, what I have found is that even when these studies are published that deal with the impact of exercise on reducing the risk of neurodegenerative diseases, our colleagues do not see them. They are invisible to them. Articles are published. Living in it, I realized that my destiny had more to do with treating the fire than the smoke, trying to figure out why people were getting sick in the first place. That very much opened the door to the notion of disease prevention. That has been my focus for the past quarter century: the idea that these compelling, challenging, devastating neurological conditions, neurodegenerative conditions, may significantly be preventable. I think the challenge is mainstream, for sure. That is good. I am fine with that. Always have been. But it offers up an opportunity to be, in my case, more fulfilled in terms of what I do on a day-to-day basis. It is a pretty narrow group of us who are involved in getting the message out that each person is the arbiter of his or her brain’s destiny. 

Kenneth Sharlin, MD

Yes. 

David Perlmutter, MD, FACN, ABIHM

We tend to want to live our lives. We are convinced that we should live our lives however we want and that there is going to be a pharmaceutical fix for whatever maladies befall us. The reality is, as it relates to neurological conditions and neurodegenerative conditions like Alzheimer’s and Parkinson’s, there is very little out there that treats the problem. Yes. As it relates to Parkinson’s, we can manage symptoms pretty well, but the disease continues relentlessly and is inexorably worsening with time. 

I think it is important to get our arms around the notion that what you and I are going to talk about today is the actual way that we understand Parkinson’s in terms of its genesis and what is causing this problem. This can help people resist the opportunity to get the disease and even help them in terms of slowing the progression of the disease once it has manifested. We are targeting the cause, not just focusing on the symptoms or manifestation. That has been very exciting for me.

Kenneth Sharlin, MD

Yes, 100%. If I can slightly paraphrase some of the things you said, as you pointed out, your focus has been especially on prevention. As such, most of the things that we talk about in terms of prevention in the language of functional medicine can be mediators that ultimately change the trajectory of the person who has the disease now.

David Perlmutter, MD, FACN, ABIHM

I am glad you said that because I think back on a criticism somebody levied towards me once and said that, yes, whatever you want to talk about in terms of Alzheimer’s prevention, that has been validated. But to apply those to treating an Alzheimer’s patient does not make any sense. I had to roll my eyes. Why would it not make sense? There is merit in focusing on prevention. Desmond Tutu once famously said that, yes, it is important to pull people out of the river, but it is equally important to determine why they are falling in the first place. That is where our emphasis is. That is what we want to explore because we keep people from falling into the river of neurodegenerative conditions. You do not have to worry about pulling them out.

Kenneth Sharlin, MD

Yes. Yet we have about a million or so people suffering from Parkinson’s, one of the fastest-growing neurodegenerative diseases that we know. We are still not in this; there are six times as many people with Alzheimer’s, but we still have a huge problem on our hands. It is good for the folks looking for solutions to know that there is much that they can do.

David Perlmutter, MD, FACN, ABIHM

Yes. I would just like to get this out and this opportunity to indicate that I think we have been dramatically underestimating the number of individuals with Parkinson’s. I think that we now see literature indicating that we may have underestimated it by as much as 50%. It is a much bigger issue than we have paid attention to. Well, we have been paying attention to this in recent years. It is a much bigger issue. Based on some of the things that I think you and I are going to explore today, we can understand why that is.

Kenneth Sharlin, MD

That is right. I can also piggyback on an earlier point because I think it is going to be critical for the viewers of this interview. I completely agree with you that we are seeing in the peer-reviewed literature articles about the microbiome and fill in the blank, whether it is MS, Parkinson’s, or Alzheimer’s. articles about gut permeability, lipopolysaccharides, and all the things that we talk about in functional medicine. But where I think things have been missing within the conventional neurology space and most of the other areas of medicine is that that is great information. But our colleagues do not have the skill set or the toolbox to say, Okay, there are alterations in the microbiome. That is great; we all agree. What do we do about it?

David Perlmutter, MD, FACN, ABIHM

Well, I think that is fair. I think that if somebody rejects the notion of this relationship, well, what do you do about it? I think where we are in technology and understanding as it relates to leveraging this knowledge about the microbiome is at a place where we do not necessarily know what we should be doing. It varies if we are going to jump in. One very small study recently published demonstrated improvement in motor function in Parkinson’s patients who had a fecal microbial transplant. In other words, having fecal material instilled into their colons from a non-Parkinson something is going concerning the patient; they had improvement. What is that? Do? It shows us that mechanistically, something is going on concerning the gut organisms, perhaps well beyond the bacteria that influence neurochemistry and brain function, that had a positive outcome in these individuals.

But to broaden that to a general group of individuals with Parkinson’s, I think, to be fair would be premature. But just the fact that we become aware of the relationship is important because what does that do? It lights you up and it lights me up to start thinking about, hmm, if the gut bacteria are in some way related to the brain and specifically Parkinson’s, then maybe we should be looking at some of the things that affect the gut bacteria and determining; A: Their relationship to Parkinson’s that we can see and B: Does it make sense to do as much as we can to keep the microbiome as happy and functional as we possibly can, to make sure that we are looking at gut permeability via the various metrics that we have and realizing, as you mentioned, that we should be paying attention to LPs or other markers of gut leakiness because now, we are seeing science that is relating these two things? Where does that go in terms of therapy? How do we help? People do not know the answer to that just yet. But that is something that tickles your mind and something that you think about before you fall asleep at night because novel ideas will sprout from that understanding.

Kenneth Sharlin, MD

Yes. The gut is foundational. That is something, of course, you hear over and over again about Parkinson’s, Alzheimer’s, and health in general in disease. Our folks who are looking for solutions do need to be thinking about gut health as a good stepping stone, if you will, to changing their trajectory. I am just wondering if you share the perspective because you mentioned leaky gut, but I always say that while we can certainly measure markers of gut permeability, such as or whatever, I want my patients to think of leaky gut almost philosophically, saying that it is not something we treat as an infection or you get ten days of an antibiotic, and you are good. You have to think that your gut is always susceptible to abnormal or increased permeability that drives this thing we call inflammation. How we move through our lives, how we navigate that moving forward, has to be with that leaky gut mindset all the time, essentially. 

David Perlmutter, MD, FACN, ABIHM

I would agree. But it becomes a holistic perspective we take of the entire body—not just the gut, but everything. Yes. Originally, Parkinson’s was thought of in Chinese literature. Huangdi, the Yellow Emperor in the fourth century B.C. looked upon as a liver abnormality. How intriguing it is that, in modern times, we have recognized genetic issues that predispose people to problems with how their liver can detoxify certain things related to Parkinson’s disease, either through the mechanism of toxicity, which, hopefully, we will have a chance to talk about. 

Kenneth Sharlin, MD

Yes, it is. 

David Perlmutter, MD, FACN, ABIHM

It is a holistic perspective, for sure. We know that the gut is highly influential. We know when there are leaks in the gut. Oftentimes there is permeability or weakness, if you will, of another membrane, the blood-brain barrier, which does allow certain things to get into the brain and quench the brain that otherwise should not have had that ability. These are similar entities. It is not good enough to take care of one problem and think, therefore, that the whole organism is going to be healthy. We’ve got to look at everything, and every member of the orchestra is playing a part here. 

To consider Parkinson’s as a brain disease is beyond myopic and out of date. We recognized, for example, that there is a super highway between the brain and the gut called the vagus nerve and that there is a relationship between the functionality of that vagus nerve and Parkinson’s risk, such that when the vagus nerve is compromised, the risk for Parkinson’s goes down. Well, what does that tell us? Is something being transported in this superhighway—that vagus nerve—that may relate to the risk of Parkinson’s disease? Is that alpha-synuclein or an abnormally folded protein? Who knows? But the point is that it just solidifies this notion that things are related, deliveries are related, genetics are related, detoxification pathways are related, and we need to gain a much broader understanding of our patients rather than saying, Look, part of your brain is degenerating; the part that makes a chemical will give you back that chemical. End of story. 

Well, for patients with Parkinson’s, that is exactly what I am talking about. You go to the neurologist, and that medicine, levodopa, or what mimics levodopa in the brain, is what you are getting to put it back because it is not there anymore as much as it needed to be. That is the extent of the therapy. Where is the question answered? Why is it gone in the first place? That is an important question to ask. Why did I lose those cells in the past? Act of my substance in anger that makes the dog meat. How did I lose those cells? What is going on? Why don’t we pay attention to that? Again, that is looking at that fire, not just treating the smoke. 

Kenneth Sharlin, MD

As we all say, common things are common, and we do, of course, try to take that more personalized approach in the clinic, the individualized timeline, and so forth. But from your perspective, or the three, four, or five things, what are the most common triggers that you think of that you have seen in your experience?

David Perlmutter, MD, FACN, ABIHM

Well, it is very difficult to say. We live in a very toxic world, and Parkinson’s is getting worse with time. I think it is a manifestation of toxicity. In our world, this is incredibly toxic, with things that are hidden from us, things that are in the groundwater, things that we are exposed to, and the particles in the air that we breathe. These PM2.5s that are so ubiquitous—even mild head trauma—in a repeated way are certainly a risk factor. Being male is an important risk factor. Various medications that affect our digoxin location ability are looked upon as risk factors. These things that I have mentioned are all common, and who lives a life that is free of exposure to the various things that we are now exposed to aggressively? I do not know that I can put my nickel down in terms of saying that this is the most common cause that I see in my patients because there is not one variable. People have their genetics as the background upon which environmental factors then play out, as I just mentioned. was, and there are many more that we can discuss. But I think that it is quite clear that toxicity, in one form or another, will break them down and play a central role. 

Parkinson’s is primarily, pretty clearly, a failure of mitochondrial function—a failure of the energy-producing parts of certain cells. Why specifically in that part of the substantia nigra in the brain stem that makes dopamine and therefore we have all these downstream manifestations is certainly unclear. But I think that this is an area of the brain that is very highly metabolic and very highly dependent upon tip-top mitochondrial function. We know that there is a very strong relationship between exposure to certain toxins that specifically damage the mitochondria and the risk of Parkinson’s disease. Indeed, we can create Parkinson’s in experimental animals by simply giving them some of these environmental toxins to which UDP goes, as demonstrated by what is called the AMP experience. May I go through that briefly? So here’s– 

Kenneth Sharlin, MD

Absolutely.

David Perlmutter, MD, FACN, ABIHM

A chemical that was synthesized. Interestingly, people may not know the story. We understand that it was synthesized by people wanting to get high. It was a demerol drug in California in the 80s. As soon as they injected this drug, within days they got Parkinson’s. They were Parkinsonian, developed all the clinical features of Parkinson’s, were treated with standard medication, and had a response, meaning that you pretty well emulated what was going on. This turned out to be MPTP, metabolized to AMP Plus, which is a mitochondrial toxin that damages what is called complex one of the mitochondrial electron chain activities that make up energy. 

But the interesting part of the story is that this happened for the first time in the late 1970s by a chemist, a chemistry student who synthesized chemicals when he was 23 years old and inhaled them. He injected it. He developed Parkinson’s within days and ultimately died of that disease. That said, the upside of the story, if you can imagine, is that it allowed researchers to then use that chemical to study what goes on with the chemical and how it might be damaging the brain. They studied it in rodents and primates and were able to create Parkinson’s immediately. They demonstrated back in the 80s that this is a disease characterized by problems with how the mitochondria work in that particular part of the brain.

Okay, what are we doing now? We have taken a step back from saying, Your brain is low, and do not take this pill, and I will see you next month. Now beginning to understand the fire, not just the downstream manifestations of the smoke. The fire, what is going on here is that something is threatening the mitochondria in this one particular part of the brain. Secondarily, the production of this chemical is compromised. Well, that starts to set the stage for understanding what the disease is in reality. 

Getting back to your question, what do I think it is causing? We know there are a lot of things in our environment that can similarly damage the mitochondria. Importantly, what can we do to help the mitochondria get back online? Even before the clinical manifestations have occurred? I have to tell you, that a study was published this morning. I was drinking a cup of coffee, knowing you and I would spend time together, and this was in my inbox. A study from Australia indicates a new imaging technique can predict, about 24 years ahead of time, who is likely to get it versus who is not. Can you imagine? Now we know who to target so that we can begin to develop protocols to enhance not only the function of their mitochondria but to protect them against damage as well.

Kenneth Sharlin, MD

I will have to look for that article. That is fascinating. I guess I was. I must admit, Dr. Perlmutter is leading you on just a little bit because you have touched on things that I wanted you to say. We have talked about the gut and the microbiome. We have talked about toxicity. You have talked about the mitochondria and the MPTP model that came out. I was very blessed to be at Emory at the time that Mahlon Delong, Gary Alexander, and Doug Wallace were all there working on primates at the Yerkes Research Center. I am very intimately familiar with that and if folks are interested, some videos were originally published in conjunction with The Lancet on YouTube, where you can see those cases and see the individuals coming in with Parkinsonism and then getting treated with levodopa and having some with remarkable response to levodopa. 

But what we are seeing, I think, is something like that, and I think you did use an analogy of the symphony. I would say that there are different parts of the symphony, but in the end, it is the whole symphony together. It is never just the strings, just the percussion, just the horn section, or what have you. We need to start seeing how our mitochondria work together with the gut, where it and the microbiome are affected by toxins. Then ultimately, and there are other factors, we could talk about hormones and other communicators of the alluded to dopamine. We know other neurotransmitter systems are involved, and how these ultimately work in concert, and then and then having that clinical framework to help people find solutions to what is now affecting them.

David Perlmutter, MD, FACN, ABIHM

Well, you are right. This is, I hate to belabor the point, but it is not typically the approach that we see, and as we are having this discussion in terms of what the mainstream is interested in. The main mainstream of neurology, and I am not trying to be derogatory is focused on helping people manage, and that is it. That is honorable, to give them the medications that allow them to be functional and help them with their tremor, whether it is medications, more aggressive therapy, a deep brain stimulator, or exploring things like stem cell therapy. I know that people have to be able to function. But let us be clear. If we can treat the disease earlier and not the symptoms of the disease so that people do not progress and require as much symptomatic treatment, I think there is much to be said in terms of why that is valuable.

Kenneth Sharlin, MD

All of these systems, these functional systems—you are mentioning energy and gut health assimilation. I am translating a little bit into the framework we use through AFM. Of course, they all converge on some basic processes that I think are very central to what you write about and speak about. For example, oxidative stress and chronic inflammation action, which then in turn fuel that fire, does it not?

David Perlmutter, MD, FACN, ABIHM

It does. Unfortunately, when mitochondria become dysfunctional, the local environment is more polluted, if you will, with higher levels of these damaging chemicals called free radicals. More oxidative stress occurs in and around these dysfunctional mitochondria that have now been traumatized by, whether it is DDT, Paraquat, or AMPTP that we just talked about, trichloroethylene or any number, manganese, you name it—all of these toxins that are related. Once that happens, mitochondria then function less well and increase the production of free radicals that damage the local environment, which causes more damage. It creates—we call it the feedforward process. We want to do what we can to limit that damage and, in an ideal world, enhance mitochondrial function. 

Again, to the extent that perhaps considering growing new mitochondria does not sound right. Well, it is not; we call it mitochondrial biogenesis, and we know how to do that. That is something that happens when you fast for example. It is the reason that Rapamycin, which is a drug that you and I looked at years ago in terms of being an immune suppressant used in transplant patients to keep them from rejecting their transplanted kidney or whatever it may be. But nowadays, it is looked upon as a medicine that enhances the growth of mitochondria enhances the body and brain as if they were different clearances of defective mitochondria, and specifically can enhance the function of that one part of a mitochondrial function called Complex 1, is not working well in the Parkinson’s brain. 

Again, Rapamycin has become the talk of the town about longevity. We do know that it is effective in a particular mitochondrial disease called Leigh Syndrome, which is L-E-I-G-H syndrome. It is a specific genetic defect that codes for less mitochondrial function in Complex 1. There is some preliminary animal work now being done with Rapamycin to enhance and protect mitochondrial function. I think that is going to go a long way great. That does not mean that people have to come off their levodopa treatment and suffer. No, these things can be done together. But that is a far more comprehensive approach to dealing with Parkinson’s, treating both the smoke and the fire, not just the symptoms but the underlying disease. I think that is the approach that people deserve.

Kenneth Sharlin, MD

This is a wonderful lead into something you have been a huge proponent of that supports both mitochondrial health and function overall. That is what a Ketogenic diet is. How do we use food as medicine and, in particular, maximize the ability of our mitochondria to utilize energy through burning fat for fuel? Can you update us on that? 

David Perlmutter, MD, FACN, ABIHM

Yes. One would then think that going on a ketogenic diet and enhancing mitochondrial function, which it does and enhances mitochondrial biogenesis and autophagy, would be a good idea. A national trial was carried out by Dr. Matthew Phillips in New Zealand, and he demonstrated some pretty compelling improvements in what is called the UPDRS, the Unified Parkinson’s Disease Rating Scale, a scale used by researchers who are going to do something interventional to determine if it helps Parkinson’s patients in terms of their functionality. There are three different components of the scale, and he demonstrated that by putting people on a ketogenic diet. That is mitochondrial therapy. 

Interesting story, and I found out about his research. I will tell you the story very briefly. I was on a boat in British Columbia. The guy in the boat next to me had some trouble with his freshwater pump system. I love doing those kinds of fixes. I offered to help him, and we were in his engine room. I am looking at his water pump, whatever it was. We are talking, of course, about our children. He said, My son is in New Zealand. He is a Neurologist, and he is researching something called the ketogenic area. The ketogenic diet is in respect to Parkinson’s disease. He looked at me, not knowing that you, the boat mechanic, would know much about that. I said, That is interesting. I know a little bit about that. He asked, Why? I said I think that is interesting. I loved to talk to him, and I said, If you look over the boat, you see there on the windowsill a bottle of MCT oil. If I go on a ketogenic diet, I will know. He called his son and connected us, and he was, in fact, at that time finalizing. His name is Matthew Phillips, and he is finalizing this study on interventional trials, ketogenic diets, and Parkinson’s. 

I ultimately interviewed him on my podcast and got to know him. He then published a similar study on Alzheimer’s and demonstrated not just stabilization but improvement in cognitive function, as you might expect by putting people on a ketogenic diet. Again, these approaches are dietary and nutritional and are not done to the exclusion of using pharmacotherapy. By all means, if you have a patient who seems to do well on levodopa therapy, some agonist therapy, or amantadine, whatever it may be, all means, those can be continued, but at the same time, let us target the underlying problem. Let us tie in, which we know has been established. Getting back to our understanding of this MPTP story that it is a mitochondrial issue, we know that Maneb and Mocosine, which are used to get rid of pests on our vegetables, are mitochondrial toxins. That is how they work. It is why these over-the-counter pesticides are also used in experiments on laboratory animals to create Parkinson’s, and yet you can buy them online to treat your vegetable garden.  

Kenneth Sharlin, MD

I want to ask you about uric acid because I know this is the topic of your newest book, and folks need to go out and buy that book. But uric acid is not only fascinating in general but also has a paradoxical role in Parkinson’s. I have been so looking forward to this interview, and I am wondering how you can guide me, as a neurologist, through understanding why, while we look at this as a marker of inflammation and we generally want lower uric acid, why do higher uric acid levels in Parkinson’s appear to have some protective effect? It does not make sense.

David Perlmutter, MD, FACN, ABIHM

It is that difficult when I explain this to you; I think you should get your arms around it. Years ago, with that observation, I was treating Parkinson’s patients, and this was long before our new understanding. This might have been 15 years ago by giving them Inosine, and because giving Inosine, increases uric acid, we thought that because of that observation that it seems that Parkinson’s patients had low uric acid, we can raise your gas that might be protective because we know that uric acid can be an antioxidant but also a pro-oxidant. It functions in both ways. Where it acts as an antioxidant is in the serum, and where it acts as a pro-oxidant, a damaging free radical enhancer, if you will, is in the cell where the mitochondria live. 

Why would a Parkinson’s patient have a lower uric acid level? Well, think about it. What do your Parkinson’s patients look like? They are generally pretty thin, aren’t they? They generally have pretty low body mass. Unclear why. I can speculate, but that would tend to correlate with the fact that you have lower uric acid, so, to answer the question, a study was carried out and published in the Journal of the American Medical Association in 2021, where they did exactly what I had done 18 years before. They had this observation. They said, Well, why don’t we raise the uric acid level in our patients and follow them on the unified Parkinson’s disease rating scale? Lo and behold, it did not help them worsen their situation, as you would expect. Yes, you might have increased antioxidant coverage in the blood, but you worsened free, radical-mediated stress within the cell where the mitochondria live.

As expected, uric acid is a mitochondrial toxin, and at high levels, it would be expected to worsen Parkinson’s disease. It would have been great because it is sure very simple to raise uric acid. It is exactly the wrong direction. You want to lower it, and uric acid, when elevated, not only threatens mitochondrial function but is also involved in increasing body weight, increasing blood sugar, insulin resistance, and reducing blood flow. There are a lot of downsides to having elevated uric acid. I was very, very much looking forward to that study being published. It would have been a tough thing to explain. But finally, they said, No giving people, I am saying, to raise a uric acid bad idea as it relates to Parkinson’s for the reasons I just explained.

Kenneth Sharlin, MD

Then you talked about some of those drivers of uric acid. One thing in particular that the viewers of this interview can immediately take action on is to eliminate fructose, high fructose corn syrup, or fructose from their diet. It is ubiquitous.

David Perlmutter, MD, FACN, ABIHM

We live in, I would say, a world, but at least in a country in which at least 60%, or close to 70%, of packaged foods have added sweeteners. These days, it is generally high-fructose corn syrup or a derivative thereof because it is sweet and cheap. Where does it come from? Where do you think it comes from? Corn, and corn syrup. This is yet another way that the government can support the growth of corn because it can be made into sugar that can go into all of our foods, which can be responsible for so many of our maladies from a metabolic perspective, driving up the costs of health care and making people sick. 

It is fructose, and over the years in medical education, when we were trying to figure out, well, what causes high uric acid, two things happened: first, it was always in context: gout, rising, high uric acid causes gout. all we learned about. Number two was to put people on a low-purine diet. Purines are the breakdown products of DNA and RNA that are found in various cellular foods, such as meat, yeast, certain foods, and various fish. Even certain plants can be high in appearance, for that matter. Also, when we break down our body tissues and muscles, which is the reason that Parkinson’s patients have a lower uric acid level, their muscle mass is lower, as there is an obvious observation. That is what we were told. Put people on a low-protein diet, reduce their meat, wine, cheese, etc., and that way they will not have as much uric acid. Well, the biggest player by far and away is fructose. Fructose is 50% of table sugar. Table sugar, or sucrose, is half fructose and half glucose. But we get a lot of fructose at higher levels. 

I mentioned earlier that through the use of high-fructose corn syrup, which is in the sodas and the sources of the condiments and everything, that is just what is sweetened. The point is that there is an elephant in the room in terms of the reason that Americans and the Western world, and pretty much globally now, are seeing progressive increases in uric acid. High levels of uric acid are far more dangerous, aside from just increasing a person’s risk for gout. As I mentioned, higher levels of uric acid create metabolic mayhem. They rate it as raising blood pressure, insulin resistance, blood sugar damage, and mitochondrial function. As such, you might expect that higher levels of uric acid would then be associated with bad things happening in the brain.

Kenneth Sharlin, MD

It is true.

David Perlmutter, MD, FACN, ABIHM

True. One study looked at 1600 individuals, measured their uric acid, followed them for 12 years, and found a significant increase in risk for dementia in those with the highest uric acid: about 80% increased risk, about a 55% increased risk for developing actual Alzheimer’s, and about a 165% increased risk of developing what’s called vascular dementia or mixed dementia, as you might expect when you dove deeper into what elevated uric acid does. It is a real learning process, I think, for a lot of healthcare practitioners to realize there is a heck of a lot more going on with uric acid than simply causing someone to act out in their big toe.

Kenneth Sharlin, MD

Yes, so, so important. Quick anecdote. I heard this story on NPR about how high fructose corn syrup came onto the market in the United States. You were saying that it was cheap. The reality, at least the way this story was explained, is that it was not cheap in the beginning, but it had to do with a very savvy CEO of the Archer-Daniels-Midland company who manipulated the economy of sugar in the United States by limiting the import of cheap sugar. 

David Perlmutter, MD, FACN, ABIHM

That is. Yes.

Kenneth Sharlin, MD

Fascinating. Then had this product that he saw from a business perspective as being well, if I can just level the playing field in the cost of sugar, I have something that these food manufacturers will love to use in their products, and indeed that came to be, so I do not want to blame people for Parkinson’s disease and all the ailments of the world, but certainly, that appears to be very pivotal.

David Perlmutter, MD, FACN, ABIHM

Yes, it is. I think, for your viewers who want to learn more about Parkinson’s, it is interesting that you revisited that. But, I think there is a lot more you and I can dove into that will be nuggets to take home. There you go.

Kenneth Sharlin, MD

I hope so, Dr. Perlmutter. I hope so. You have enlightened us all in these past 40 minutes, and I appreciate your time. I know the viewers do that. They have, I almost hate to say if they have not heard of you, but if they want to find out more about you, we just send them to drperlmutter.com.

David Perlmutter, MD, FACN, ABIHM

Drperlmutter.com. My podcast is called The Empowering Neurologist, and as of late, we have had several programs on Parkinson’s, especially as it relates to toxicity and exposure to toxins. The Empowering Neurologist is a podcast, but I think the clearing house is good drperlmutter.com

Kenneth Sharlin, MD

Get on his mailing list. He has got a terrific mailing list. He sends out the scientific papers, a little synthesis of what they mean, and if you want to learn more, and I certainly always do so, Dr. Perlmutter, I am on your mailing list. I encourage other people to be on that mailing list.

David Perlmutter, MD, FACN, ABIHM

Well, I have to say, Dr. Sharlin, thank you so much, and thank you for the opportunity today.

Kenneth Sharlin, MD

Thank you.