In this episode, I have the pleasure of speaking with Dr. Datis Kharrazian, an award-winning researcher, academic professor, and functional medicine provider with extensive clinical experience treating chronic fatigue syndrome.
Today, we focus on how the brain contributes to chronic fatigue. Dr. Kharrazian provides a really pragmatic viewpoint that both respects and, I believe, supersedes many of the other theories I’ve heard throughout the years.
I’m very excited for you to hear his take on this debilitating but solvable topic!
This podcast was initially released in Oct 2018
Table of Contents
In this podcast, Dr. Kharrazian and I discuss:
- The number one question Dr. Kharrazian asks when working with patients who report chronic fatigue as their primary problem
- 2 forms of chronic fatigue and how to identify which type you may be dealing with
- The first signs of neurodegeneration (that commonly occur in your 30s and 40s!) that you should be aware of to avoid Parkinson’s and dementia
- 3 major forms of brain-based fatigue and the areas of the brain they correspond to
- The shocking digestive symptom that is the first sign of early Parkinson’s disease
- An easy way to assess your metabolic—and brain—health and the most common reasons why post-meal symptoms occur
- Dr. Kharrazian’s highly practical tip for reducing blood sugar imbalances
- The link between cortisol patterns, the brain, and detection of neurological diseases like Parkinson’s and Alzheimer’s
- Why cold hands and feet might be your sign for understanding and addressing brain fatigue!
- How stress, cortisol, the vagus nerve, and the gut interact to create a healthy brain, and why dysfunction in just one of these areas can generate brain imbalances
- Dr. Kharrazian’s top 5 tips to keep your brain and cognitive function strong and healthy!
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Transcript
Ari Whitten: Hey there everyone. Welcome back to the Energy Blueprint Podcast. I’m your host Ari Whitten, and today I have with me a very special guest who is an award-winning researcher, academic professor and functional medicine healthcare provider, Dr. Datis Kharrazian.
A little bit of background on him, he specializes in developing evidence-based models to treat autoimmune, neurological and unidentified chronic diseases with nonpharmaceutical applications such as diet, nutrition, and lifestyle medicine. His academic and clinical research has been featured in numerous documentaries and his clinical models of functional medicine are used by several academic institutions and thousands of healthcare providers throughout the world.
Dr. Kharrazian has received appointments as an Associate Clinical Professor at Loma Linda University School of Medicine, a Research Fellow at Harvard Medical School, and a Research Fellow at the Department of Neurology at Massachusetts General Hospital. And this is just a very, very summarized version of a very long list of impressive accomplishments. So thank you so much Dr. Kharrazian for joining me. Such a pleasure to have you on.
Dr. Datis Kharrazian: Thanks, Ari. Nice to be here.
Ari Whitten: Yeah. So today we are going to be talking about the role of the brain in chronic fatigue. And I want to kind of give a little bit of an overview of some stuff that maybe listeners of my podcast have heard before and I’m sure that you’re pretty familiar with, and kind of give that overview and then get your take on this.
So I’ve had a number of different guests on the podcast who have talked about brain function as it relates to fatigue through a number of different angles. And from what I can tell, a lot of people have kind of their pet theories and their personal take on what they think is sort of the dominant factor.
So Ashok Gupta is very focused on limbic system dysfunction and the role of that in chronic fatigue syndrome and kind of a focus on psychological, emotional stress as being central factor that results in limbic system dysfunction. There’s another chronic fatigue syndrome researcher named Raymond Perrin out of the UK, who’s very focused on the glymphatic system of the brain and lymphatic drainage and kind of blockages of that and then toxins accumulating in the brain.
There’s also Alex Vasquez, who kind of focuses on the gut and leaky gut and dysbiosis resulting in neuroinflammation and excitotoxicity, but kind of seeing the gut as more primary and the brain as secondary. There are people who have a more of a neurotransmitter focus.
There are people who have more of a childhood trauma focus, or a belief, and sort of negative thought and belief focus. So, but there are also people who have more of a sympathetic system versus parasympathetic and vagal tone sort of approach.
So with all of that said, and kind of all of these different angles of talking about brain health as it relates to chronic fatigue or energy enhancement, I’m curious what your take is within all of that context.
Dr. Datis Kharrazian: I think, well, I’ll be honest, I don’t really, I’m not as familiar with all those areas of different theories as you are. I’m kind of in my own little world and I don’t know.
But I can just tell you if you do a complete neurological exam, and I can give an example, a complete neurological exam takes me about two, two and a half hours to do. They do comprehensive lab work. You quickly identify if it’s limbic brain or if it’s gut brain, if it’s the basal ganglia or if it’s frontal, if it’s autonomic dystonia. I mean all things are not one thing, right? So, my impression as a clinician and not knowing what anyone else is doing is you can’t even have a theory about the brain unless you first know how to evaluate it and work it up and then you actually do that.
You know, we live in a world where there are so many theories about everything. And then at the end of the day it’s kind of like the exam findings present themselves. So a limbic presentation or an autonomic dystonia presentation or a clear history of the gut-brain relationship or looking at bigger function during the exam. Those are all things you can do. So you don’t even have to have theories for it. So, but that’s one part of it. So I think, you know, at the end of the day when people have brain-related issues, it’s not that hard to figure out, you just have to work it up.
The most common sort of dysfunction in people with chronic fatigue
Ari Whitten: Okay. So, what kinds of specific dysfunction do you think are I guess the most common sorts of dysfunction that you see in people with, let’s say, chronic fatigue?
Dr. Datis Kharrazian: So I think for me as a clinician, when I see a patient that comes in, and it’s really common to see so many patients when you ask them to list their chief complaints in order of what’s bothering or impacting their life the most, fatigue, chronic fatigue is really a very common chief complaint.
But whenever I see chronic fatigue, my first question to them is, “Do you get fatigued just throughout the day or do you have fatigue when you use your brain?” So I’ll give an example. Brain-based fatigue happens when you use your brain. So they’ll say, you know, “I’m really tired after I drive. If I’m on the computer for an hour, I’m fatigued.” That’s a brain-based fatigue mechanism and depending on what part of the brain is not functioning well.
So if someone has like a frontal cortex that’s unhealthy, if they are focused on attention and concentration for a period of time, it’s very easy for them to have low endurance those pathways of fatigue.
Someone has like a cerebellar issue of the brain that’s degenerating or not healthy, standing all day or just standing for 20 or 30 minutes can really exhaust them for the whole day. It’s like a global effect in the brain. But when you look at fatigue and you kind of break it down simply just as a way to understand it from a brain model versus a metabolic model, metabolic fatigue happens all the time, happens for no reason, it’s just there.
Brain-based fatigue happens when you use your brain. So a lot of times, when patients really think about it, sometimes their fatigue really isn’t adrenal and it’s not anemia and it’s not metabolic and it’s not thyroid and it’s not hidden infection, it’s not a chemical toxicity. It’s just their brain is unhealthy and that’s one of the key symptoms.
The first sign of neurodegeneration in the way the brain works is as it starts to degenerate and fail, one of the earliest symptoms is low endurance of the brain, and then that presents as fatigue. So when your brain shuts down, everything shuts down. So you know, when your brain shuts down, you don’t want to move, you don’t want to do anything, you don’t want to stimulate, heavy stimulation for the brain.
You just want to be left alone. So that’s clearly the pattern of brain-based fatigue. Now, what I also notice as a clinician is when people come in with fatigue, how they get treated really depends on where they go. So just like we talked about different theories of the brain, I mean, it’s not as common of practitioner. Practitioners, you know, there’s a Lyme doc, there’s the adrenal doc, there is the chemical toxicity doctor there’s the…
And that’s kind of the lens they see it through. And I think one of the biggest mistakes practitioners can ever make is when they just accept one model. And you know, what’s interesting is working with practitioners and teaching and being on the road for over 20 years and getting to see all the different variations how people practice, what I’ve noticed is most practitioners kind of pick what they do because of their own experience with it. Like if I see a Lyme doc, I pretty much know in their history, they probably had Lyme.
Ari Whitten: Yeah.
Dr. Datis Kharrazian: A doctor that who like asks to treat their adrenals, they probably had a good experience treating their adrenals and they felt better and then they kind of see the world that way. So you’ve probably seen the same thing.
Ari Whitten: Yes, I also think that there’s this really unique, kind of fascinating and unfortunate psychological tendency that humans have where we tend to always try to reduce things down to the one thing. I think just, we are psychologically wired to say, you know, once we start, let’s say getting some results with an adrenal supplement, we’re like, “Oh, it’s adrenal fatigue and it’s all about the adrenals.” And then our brain just goes that way and we kind of dig our trench and say, “This is my position and this is what I think it’s all about.”
I really appreciate what you’re saying here that we need to have a much more, a much broader and more encompassing perspective that looks at all of the different pieces of the puzzle and how they fit together.
Dr. Datis Kharrazian: Right. So let me give you some further insight into that as a clinician. So you know, when you look, when you work with patients that are chronic and they’re suffering from fatigue and they’ve got a whole list of issues.
First of all, if they’re suffering from fatigue, that means at the end of the day they have lost their physiological ability to make ATP, right? So that’s the final common pathway is they can’t make ATP. Whether it’s a mitochondrial defect, whether it’s not getting enough fuel, whether it’s oxidative stress, whether it’s a hormonal issue, whether it’s a chemical issue, they’re all up for grabs, they are already in play.
Now when you have long-term mechanisms that cause fatigue, you do have insult or lack of function of the mitochondria, right? But the biggest effect of that we really see on the brain, and the brain is one of the early signs of where this happens because the brain has what’s called post-mitotic tissue.
Once you develop cells there, you don’t develop new cells. There’s some new research being done with neurogenesis and things like that, but they have very limited expressions. And we don’t really, you know, make more neurons than what we really get when we’re born.
So when people have various mechanisms causing it, there sometimes tends to be an effect in the brain and everything else gets treated besides the brain. So brain health is really a key factor I think for a lot of people to have the key. And not really focusing on how to recover their brain function is an overlooked area with chronic fatigue issues.
So I think if you’re a person searching for your cause of fatigue or if you are a clinician working with practitioners, one the easiest questions to ask is if you have fatigue, “Is it all the time?” Which is more of a metabolic type of thing.
“Does it come and go? Or is it after meals? Is it after some event?” But if it’s very specific to “If I read a chapter, I’m done, if I try to do this activity, I’m finished.” Those are pretty straightforward brain related fatigue mechanisms.
How brain fog and brain-related fatigue are related
Ari Whitten: Okay. So let’s dig into brain-related fatigue. I assume that’s very much intertwined with brain fog. Those two things kind of go together, do they not, or how do they, where do they differentiate?
Dr. Datis Kharrazian: So brain fog is… yeah, they do, they go together. Brain fog typically takes place when neurons are not synapsing properly. So, you know, neurons communicate with each other through a synapse message.
Certain things can slow that communication down. So one of the major things is inflammation. Inflammation can impact how efficiently neurons synapse the other. And as the synaptic rate slows down, people can’t find words, people can’t focus, people can’t do the tasks they normally do or it takes them longer to get there.
And many people explain that as brain fatigue. So whenever we hear brain fatigue, we tend to think that there can be an inflammatory component to it. But they don’t always overlap. So sometimes people just don’t even have that connection with brain fog. They just lose their function and get really, really tired and don’t really have that as part of the component.
Now, one of the earliest signs of brain fatigue is actually neurodegeneration. So, you know, you don’t just develop Parkinson’s, you don’t just develop dementia. So let’s talk about dementia, which is really prevalent and that’s really common, something that we’re all at risk for as we get older.
How brain fatigue is a sign of early brain degeneration
Ari Whitten: I just want to quickly interrupt. So you said one of the biggest signs of brain fatigue is nerve degeneration? Or is that in reverse? Is a sign of nerve degeneration is brain fatigue?
Dr. Datis Kharrazian: Yeah. Let me clarify that. I’m sorry. So one of the first things we see with early neurodegeneration is brain fatigue.
Ari Whitten: Got you.
Dr. Datis Kharrazian: Thank you. So I think what people don’t understand is when they start to have their brain health compromised, they start to lose their brain endurance. As they lose their brain endurance, they get tired. And when they get tired, they start to look for other things that cause, that are causing it. For example, let’s just stick with the adrenal glands. “Oh, my adrenal glands are so wiped out. I got to take adrenal support and I got to take adaptogens.” And maybe they do, maybe they don’t. Maybe they do and it gives them a little boost. Maybe they do it, It has no effect. There still could be an underlying neurodegenerative process. And supporting the adrenals may not be what they need to do.
They may need to get to get in there and aggressively support the brain health and make a difference that way. So it’s one of the most commonly overlooked things when we see patients that have fatigue, they don’t think that the brain is part of it. And then quite honestly, when you look at the field of healthcare professionals practicing, whether it’s MDs or DOs or DCs or NDs or family nurse practitioners or nutritionists or dietitians, they’re not really trained in how to find early brain degeneration.
Didn’t even consider it a possibility. They wait for a person to have tremors or they wait for a person to completely lose their way home or not, remember family member names before they even go down that clinical realm. But many, many, many people start to have early signs of neurodegeneration, especially in their thirties and forties.
And each decade their risk goes up, and that then causes their endurance and their neurological pathways to be compromised. Then they try to use their brain doing their everyday tasks. That exhausts them. Then they search from one practitioner to the next trying to find something for their fatigue. And they waste a lot of time. And at the end of the day they don’t realize that they really have a neurodegenerative process that’s being overlooked.
The root cause of brain-based fatigue – how to detect and prevent Parkinson’s disease and Alzheimer’s disease
Ari Whitten: Yeah. So once you differentiate between, let’s say brain-based fatigue versus more metabolic fatigue, how does that then influence the sort of, the sequence of how you go about looking for the underlying causes of that? So I guess to phrase this differently, what is the picture of the underlying root causes look like for brain-based fatigue versus more metabolic fatigue? And I know that’s a very complex answer that you could probably spend five hours answering, but if you could kind of summarize maybe where they differ in terms of some of the root causes.
Dr. Datis Kharrazian: Sure. So if we see, let me put it this way. So in a clinical setting, if we come to the scenario, a person walks in the door, they say, “I’m fatigued, I’m exhausted.” And then we do some further questioning and we find out their fatigue is really maybe more brain-based because it tends to happen when they use their brain. Then the next clinical question, which I think you’re asking, is what do we do and where we go from there, how do we find the causes, right?
So once we determined it’s brain-based fatigue, the next question is where in the brain is it? So different regions of the brain have different functions. So if it’s focused attention and concentration, then we know it is the frontal lobe. If it’s memory and recall, then we know it’s the medial temporal lobe. If it’s related to things like balance and coordination, exercise and movement that really fatigue them when they try to do it, then we know it’s the cerebellum.
Let’s just stick with those three for now, okay? Now if it’s as long-term memory and recall, that’s one of the early signs of dementia. If it’s more in… some dementia is frontal temporal. So if their focus, attention, concentration are also being impaired, than we know that can be an early sign of dementia, too. So that kinda helps us to see where we are.
And then certain conditions, like the two most common neurodegenerative diseases you always have to rule out when you hear people have brain-based endurance issues is, is it dementia or is it Parkinson’s? So when we see brain-based fatigue, the first thing we try to rule out is dementia. And if it is memory and recall, and if it is getting worse and they have a family history of it, the risk significantly goes up, okay? And what people don’t realize is that dementia and Alzheimer’s goes on a progressive scale.
So it doesn’t just happen overnight. So it starts with not being able to find your keys and your, you know, your phone numbers or your phone or whatever the things are that you normally recall. We don’t recall phone numbers much anymore because we have these great apps, but it could be just directions, it could be the next level of impairment.
And then it’s to the point where their function goes down in daily life. So things take longer to do. They are less, they can’t be on time as well as they used to. People around them, family members, co-workers start to notice that. That’s when their functioning gets impaired. And from there it starts to just progress. That’s a red flag. That is a serious issue. And that is something you should know, in that early, those early stages if you get a complete neurological exam, you still have a normal neurological exam. But there are no findings for dementia on an exam.
It shows up with clinical presentation. Now, if we talk about the other neurodegenerative diseases, the second most common disease is Parkinson’s. Once you start to see brain endurance issues and fatigue that is brain-based, you always throw out Parkinson’s. And the first sign of Parkinson’s disease is actually loss of gastrointestinal motility. So Parkinson’s, what you get is you get what is called protein aggregates, alpha-synuclein aggregates. They build up in the brain, but they build up in the gut nervous system first. So when people start to get brain-based fatigue patterns, we want to make sure they have healthy motility. And then from there they get slowness and stiffness. So if someone comes in and says, “I’m exhausted and I’m tired,” and you’re, “Okay.” And then we find out that the fatigue is always worse when they use their brain. Now we know it’s brain-based fatigue.
Now we see them taking 50 supplements to treat a bad gut and they don’t have normal bowel movements and their GI tract is not functioning well. And then in the clinical exam, we see they have stiffness or they complain about shoulder stiffness or hip tightness, which is the most common thing. The movements are a little bit slower.
That is early Parkinson’s. That’s the early pattern. So as soon as we hear that a person has fatigue and we find that it’s brain-based, the initial first step is to go, “Is this an urgent disease?” So we always start from worse than go down to the less aggressive. And then if it’s not a neurodegenerative pattern, many times the brain is fatigued just because it’s not getting what it needs. The brain needs oxygen and the brain needs glucose. So then we go down to the very basics, and you know, do they have a blood sugar issue. And then the next clue for us to see if they have a blood sugar issue is how do they feel after they eat.
The normal response is when you eat a meal, the only thing that should happen is you’re no longer hungry. Any change of your energy is a sign of a blood sugar problem. So if a person has low blood sugar throughout the day and they eat, they usually feel better and their function comes back. So if someone clinically states that, “Hey, I feel better after I eat.” And we go, “Wow, you probably have low blood sugar throughout the day.” Because that’s not normal. Normal is you just get hungry and then you eat and there’s no change in function. And then people that have high blood sugar, insulin resistance patterns, they usually get tired. And then, you know, so we can immediately look at that as a reason why the brain may not be functioning well because they are not getting proper glucose to the brain. So a third of the…
How certain conditions put you at risk of developing neurodegenerative diseases
Ari Whitten: If you get tired after eating.
Dr. Datis Kharrazian: Yeah. So a third of the body’s glucose is used by the brain. I mean, if there’s any shift, any slight abnormalities in your blood sugar stability, your brain will feel it. Okay, now these types of mechanisms are important, too, because they don’t, they enhance and promote neurodegeneration.
So if you have an ongoing blood sugar issue that is not part of your brain based fatigue, you are definitely dealing with a risk factor to develop a neurodegenerative disease. The other thing is sometimes people have poor brain function, like they just have poor endurance.
They have anemias or they have poor circulation, they have things that impacted them. They have underlying asthma or respiratory issue that’s never really been managed well. And sometimes we have to correct those things clinically to make a difference. Just yesterday I had a very interesting case. I had a patient that came in, she was a 36 year old female and her biggest complaint was her brain doesn’t work, she can’t focus and she can’t concentrate.
Very intelligent, but she really barely, she barely made it through college despite her intelligence. And then when we examined her, she basically had thalassemia, which is a genetic disorder where the red blood cells break down. She had mitral valve prolapse, she doesn’t have proper injection fractions and she had really bad circulation.
And she had a raging hypoglycemia pattern. She just missed meals throughout the day, like all those things have really dampened her brain function and she’s tired all the time. But those things, so now we’re trying to put, antioxidants and different things to help with the thalassemia and then trying to do things to improve her circulation naturally with things that activate endothelial nitric oxide and we’re trying to get her to stabilize her blood sugar and then we want to see if that changes her brain function and her overall energy throughout the day. And that is a case that is not uncommon, things like that.
Ari Whitten: Interesting. So you mentioned a couple factors, blood sugar regulation issues, and then getting oxygen to the brain, you know, as far as circulatory issues. Obviously, if somebody has mitral valve issues or thalassemia, that’s, those are, I would say very big issues and probably not necessarily that common I would imagine. So what are… well, I guess we can address these in a stepwise fashion. But let’s say somebody who has low blood sugar, what are some of the most common root causes of why somebody’s going to err more on the side of hypoglycemia?
Dr. Datis Kharrazian: Low blood sugar, hypoglycemia. Okay, so the most common cause someone has low blood sugar, hypoglycemia, is first of all just lifestyle. They just don’t eat. They forget to eat and then when they eat they just eat sugar. They’re not the junk food, fast food diet people. They’re the ones that will wake up and have like tea and honey and that’s about it. And then when it’s time to eat, they’ll have like fruit.
That’s the typical hypoglycemic pattern and over time their adrenal gland is exhausted. That’s one way. So whenever we see a low blood sugar pattern, the first question, is it caused by their lifestyle or is it caused by a physiological thing? But the most common cause is that it’s caused by lifestyle.
And then that type of lifestyle where they’re constantly missing meals or having high sugary foods for a meal, like they’re having a fruit smoothie for a meal that’s, very little protein or fat or fiber in their diet, that’s going to cause a functional low blood sugar pattern, hypoglycemia.
And then that eventually taxes the adrenal glands. Other times people may have their adrenal glands completely depleted from infections, from stress, from other things, and then their adrenal glands really lose the ability to make adequate cortisol.
So they have a hard time getting their blood sugar stable. Now there’s a really easy way to tell the difference clinically. Patients that have adrenal gland exhaustion that end up with low blood sugar, they usually come in and they say, “Man, I have to eat protein every two or three hours or I don’t function.” They’re just trying to survive and they have to eat that way to get through the day.
People that have reactive hypoglycemia pattern from lifestyle, they’re like, “I just don’t know why I’m so tired. I don’t know why I feel bad. I don’t know why I’ve lost my menstrual cycle. I don’t know what’s going on.” It’s like, “well, tell me what you eat.” “Well, I eat really healthy, like great,” and then they go through the organic list of fruits and lack of, and all the things they do throughout the day and they don’t understand that that’s not healthy for them. Those are the two typical patterns we see with low blood sugar.
Ari Whitten: Now. Are those really that different or have they just found, one type of people have found the sort of way of coping with it by eating protein every two to three hours.
Dr. Datis Kharrazian: Well, let me explain. If you choose to eat protein every two or three hours, that’s different than having to eat protein every two to three hours to make it through the day. The people who have really got to the point where their physiology is so compromised where they have to eat every two to three hours are the ones that really have a physiological mechanism why they are hypoglycemic.
The person that chooses to for various reasons, that’s different. But the person that has to do it to get through the day is usually, it’s low adrenal, a person who has low adrenal function causing hypoglycemia. The most common thing though is a person whose lifestyle is causing low blood sugar.
How to treat brain fog when you are hypoglycemic
Ari Whitten: Okay. I would like to dig into that a little bit more. What do you do in that scenario? Let’s say somebody has low cortisol levels and they are one of these people, that’s eating every two to three hours a high protein snack. They need to in order to function. What do you do to try to help that person?
Dr. Datis Kharrazian: Okay, so let’s say we run an adrenal profile. We have a baseline cortisol output throughout the day. So we want to get a baseline and then go from there, right? They have to stick with their diet because it helps their adrenal glands have a chance to recover and that’s the only way they can function anyways. Then you can give them adrenal support, but there’s something driving that.
So the things that drive… that could be infections, they can be immune challenges, they could be… immune challenges means they can have a reaction to the chemicals and environment around them or food proteins they are still consuming. They could have an underlying disease that no one has diagnosed yet. They could have things where even traumatic brain injuries have been shown to sometimes dysregulate the feedback loop systems. So you’re kind of going the route of what’s the trigger and sometimes it’s just chronic stress.
Maybe we can only handle so much stress for a period of time. That’s not as common, but sometimes it is for some people. So we’re trying to look for sources of it and you can’t really supplement your way out of that with adrenal gland support. They can help aid the patient so they can function better. But you can kind of go there.
The easiest way to figure out those things just does a comprehensive blood test. If you see low white blood cells or high white blood cells, you know, you’ve got kind of an immune component. You can look at different T and B cell profiles and see if there’s some type of subtle immune temperature that’s not showing up the total white blood cell count. You can see if there are any things going on with the liver, diseases or infections or viruses.
You can look at the thyroid, you can look at basically the entire physiology with a comprehensive blood test and then that really, most times it helps narrow it down and then you kind of go from there.
How Dr. K analyzes cortisol patterns
Ari Whitten: Got you. So one of the other strategies… actually, you know what, before I get there, real specific question on the cortisol pattern that you’re talking about. Are you talking about a very, very overt sort of low cortisol pattern or are you talking about a subtle dysregulation, maybe a slightly lower morning cortisol awakening response and then slightly higher evening levels like a flattened diurnal cortisol curve that’s slightly off what’s average. Or are you talking about like an overt pattern that’s maybe closer to something like Addison’s disease?
Dr. Datis Kharrazian: Well, with Addison’s disease, the adrenal salivary cortisol, it’s not a good test for that because it’s not… with Addison’s disease, you have to lose at least 60 to 70 percent of your adrenal gland reserves and tissue to show up, and you have to do a 24 hour urine cortisone test to find that. That’s better diagnosed with adrenal antibodies, 21-hydroxylase antibodies specifically. But in this case, we’re not talking about Addison’s, it’s pretty rare. But you know, whenever you look at an adrenal cortisol profile, there are different components to it. The output of cortisol throughout the day is a function of the factory which is, the cortisol factory is the adrenal glands. The rhythm itself has nothing to do with the gland. The rhythm is all hippocampus. So when you look at the feedback loop, there are feedback loops within the brain, specifically the medial temporal lobe and in the hippocampus.
The hippocampus communicates with an area of the hypothalamic area called the periventricular nucleus. And integration through supraoptic pathways through serotonin projections modulate the effect of these supraoptic areas. They activate the periventricular nucleus area of the hypothalamus that controls pathways with the circadian rhythm through the hippocampus that controls the cortisol rhythm.
So when we see a rhythm problem, it’s a brain problem. And many things can impact that. And when we see an adrenal gland itself that’s an issue, that’s when we see the cortisol output throughout the day that’s off. So they’ve actually done multiple studies now where they look at cortisol rhythms and they use it as a way to determine the progression of dementia and Alzheimer’s.
Because the first area in the brain that dementia hits is the hippocampus which controls this rhythm. So that’s another thing. A lot of times when you see just dysfunctional rhythms, but they’re able to make cortisol throughout the day and they have brain fatigue issues, that’s another early sign of Alzheimer’s or some type of dementia pattern that hits the medial temporal lobe.
So people that have the hypoglycemia issues, though, we’re really more concerned about their cortisol output throughout the day. Now the problem is when their cortisol output course is so low throughout the day, they appear like a flat liner, like all the way through. It’s just simply because they don’t even have the factory to respond to a rhythm. They don’t even have the outputs to respond to a rhythm. So the ones we see totally exhausted have that. Now the ones we see to have rhythm issues, you know, those are really more of a brain-based pattern. They don’t do, they don’t respond as well to things like B vitamins in general, adrenal gland glandulars or things like that. They need to be supported at the hypothalamic areas with things more like adaptogens and things like acetylcholine support, like huperzine, they have a better effect.
Ari Whitten: Got you. So just, real quick, the reason that I asked is I’ve reviewed the literature pretty extensively. I’ve got actually a very long article, almost like a short book reviewing literally every study that’s ever been done on HPA axis function and adrenal function and cortisol levels in relationship to stress related to exhaustion and burnout syndrome and all the different fatigue syndromes, chronic fatigue syndrome, fibromyalgia.
And actually adrenal dysfunction seems to be extraordinarily rare in any of those populations. It seems like the vast majority of people with any of those fatigue syndromes have normal cortisol or very close to normal cortisol levels. So the kind of overt adrenal abnormality that you’re describing, I’m sure that it actually exists. I’m not skeptical about that.
I’m just saying it seems to be extremely uncommon at least, or it seems to be just… I guess the only way that it could be there is that it’s uncommon enough to be completely sort of removed from the picture when you take the averages of those populations of people with fatigue syndromes.
Dr. Datis Kharrazian: Well in the scientific literature arena, in endocrinology journals, the whole concept of adrenal exhaustion, fatigue is controversial.
Ari Whitten: Correct, yeah.
Dr. Datis Kharrazian: Absolutely. So that’s true. But you have to understand when you look at the scientific literature and those things as well, you have to understand what are they using as the biomarker to assess them. So if they’re looking at serum CRH, cortisol and cortisone, you’re not going to find anything.
So if that’s their study design, that study design is good for what it is, but it’s not going to find somebody who is more of subtle type reactions. Simply because the ranges with them are very, very broad and that really makes the fact of there’s bias into their study and confounding because of the type of method of measurement they are using,
Ari Whitten: Yeah, I think 90 plus percent of them use salivary cortisol measurement, you know…
Dr. Datis Kharrazian: Well yeah, again, let me get through this. So if they’re using salivary cortisol profiles, they’re using salivary cortisol profiles with various things and some research, and there really hasn’t been a good list of research on these subtle functional hypo, what we call functional adrenal type patterns that are there. But there was definitely lots of good studies on rhythms.
But to be quite honest, you have to look at what the study design and the interest was. You don’t have a lot of people looking at low chronic fatigue issues and trying to look at general low salivary cortisol profiles that are publishing on it. That’s just the fact. So I’ve spent a lot of time looking at the literature, too. Related to stress response in HPA axises. I haven’t read all of it because there’s, I don’t know how many now, 50,000 papers or something. So if you put in stress, there’s an enormous amount of papers.
Ari Whitten: Yeah, certainly on stress. On stress-related exhaustion and burnout specifically…
Dr. Datis Kharrazian: Yeah. Stress-related exhaustion and burnout are going to be something where you find limited amounts of information for sure. But, I think part of it is because we actually don’t have like the best study designs done or even actually the actual studies are done. But it’s still an area that needs to be researched and investigated. I don’t disagree with you.
Why isn’t my brain working – how circulation plays a role in brain fog and fatigue
Ari Whitten: Sure. Got you. So one of the other factors that you mentioned is a big factor in brain health is circulation and oxygen delivery to the brain. So what are some of the underlying causes that might impair that aspect of things?
Dr. Datis Kharrazian: Well, we know… well some people do have subtle anemia so we’d want to look at a CBC. And then one of the key factors is poor circulation. So you know, a lot of times people complain of cold hands, cold feet, so you can just palpate it, you can see it. And you know, one of the key things, people that have poor circulation is they’ll notice their best brain function if they exercise and move and their blood flow and circulation comeback and then the energy’s there.
So typical thing you see with patients that gots like chronic fatigue issues related to lack of blood flow to the brain is when they actually move they notice that their circulation changes for the next few hours, they have the best amount of energy. And then as the hands and feet get cold again, their energy goes down. So sometimes we’ll have patients kind of track their fatigue levels and their brain function symptoms based on how they feel the temperature on their hands and feet. And they can actually get a surface thermometer and just kind of measure their hands and feet and they can kind of compare the temperature on the wrist or pay attention to fingertips.
They seem like a 10-degree difference. That’s usually a sign of poor circulation. And then if you can start to correlate their energy level, like they notice their brain functions great and their energy levels are great and then they measure their temperature and it’s somewhat normal. And then they notice when their function is down, that really helps us in a clinical window to determine like, “Well, we have to improve your circulation.”
So then we’ll maybe consider strategies to improve their circulation, which may be things like bepotastine which activates endothelial nitric oxide synthase. That’s a really fantastic way to get improved circulation, but just from different types of compounds. Just in the fact that they can just do some physical exercise and decrease things that impact the adrenaline levels, that could be an issue there. So those are all things that they should do.
Ari Whitten: Excuse me. So I’m sure that there are a number of different, like overt genetic conditions that might impair circulation, like mitral valve prolapse or something like that. How much of this, the circulatory issues do you think are more a direct function of nutrition and lifestyle inadequacies? Like somebody is just like mostly sedentary and maybe their heart muscle itself is just not that strong.
Dr. Datis Kharrazian: Well, yeah, so that’s a good point. So some would say very few cases are related to things like heart disease or things like mitral valve prolapse or pulmonary issues or Lyme disease. Those are more significant and those are usually associated secondary disease.
Now the other things are there’s some genetic susceptibility for some people. I mean one of the things we know with the whole, with all of the studies being done, the human genome project and just the genotype is that there’s so much variation between them. We don’t know what all the gene SNPs mean and we don’t know what the gene SNPs mean in combination.
And I think at this point the scientific community is at the point where they have to use machine learning to try to interpret all this because it’s just too many variables to do it. So in a clinical setting though, behind the science where the genes really fit in, we know that there’s a genotype and then all you can really do in a clinical setting is try to modulate the phenotype, the genes plus environment, nutrition and the lifestyle.
So when you see someone come in and they tell you, “Everyone, their sisters, their mom, their grandmother, they all have really cold hands and feet. Then they always get cold.” There’s probably some type of genetic uniqueness that impacts various receptor pathways. But at the end of the day those things can be one of the reasons why they’re not functioning as well as they can. If they can change those things, that can be a factor.
Sedentary lifestyle is for sure one of the most common ones for poor circulation. And some people are prone to things like hypothyroidism and various things. But I think as a clinician and as a patient suffering through it, you just kind of have to go through and figure all those things out and find the best way you can change the expression of your genes to make a difference, right?
Ari Whitten: Yeah, absolutely. A couple of specific questions on that one. One, are you aware of any other sort of common lifestyle factor other than exercise that can, that has a strong effect on the circulatory function?
Dr. Datis Kharrazian: Say that again. Besides exercise, what can affect circulation?
Ari Whitten: Besides exercise, is there any other common lifestyle factor that has a big impact on circulation?
Dr. Datis Kharrazian: Lifestyle factor, sedentary lifestyle and physically active is the single most common factor.
Ari Whitten: Okay.
Dr. Datis Kharrazian: That is without question. The other part of it could be like we just talked about. Some of the genetic variations we don’t totally understand why some people have issues. They’re like, we see people who work out all the time, but everyone in their family has cold hands and cold feet and the circulation is poor. And if we can do things to change the expression of that, then they do better, but they always have that vulnerability. Outside of basic sedentary lifestyle and movement and genes, I’m not really sure of anything that comes to mind that is a key factor there.
Ari Whitten: Okay. Got you. You know, I always wondered, you know, just the fact that we’re living such indoor lives now and we have so much less exposure to infrared rays from sunlight, from spending time outdoors. I was, I always just kind of thought that that might have a big impact on things. Because, you know, I might in the middle of my house, I might feel cold in the winter and, you know, it might be as simple as going outdoors and just getting some rays of sun on my skin and all of a sudden I no longer have cold hands and feet. Do you know what I mean?
Dr. Datis Kharrazian: Yeah, absolutely. And every person is unique to themselves and you have to kind of dig through all that and figure out the best strategy.
How to treat brain fog and prevent Parkinson’s disease and Alzheimer’s disease – how stress and sleep affect your brain and health
Ari Whitten: So, stress. I know that a couple of the big factors, I have your Save Your Brain program and have gone through that extensively. So stress and sleep are a couple of the other big factors that you go into, in that program.
Dr. Datis Kharrazian: Yes.
Ari Whitten: How does stress affect the brain? And I know that’s very broad and there are lots of different factors, but just kind of a broad overview of what stress does to our brains.
Dr. Datis Kharrazian: So to make it very simple long-term chronic stress has several effects. One of them is the, and this is really related to, it would be specific to the cortisol shift, okay? So if cortisol goes up is the key factor.
So some people can adapt to stress, some can’t adapt to stress, but if we’re really talking about it, let’s just be specific. We’re talking about the effects of elevated cortisol on the brain. And cortisol, either it could be exogenous because someone’s taking cortisone or someone has just high production of cortisol. But cortisol itself can thin the blood-brain barrier, it can break down the gut barrier. That’s one key thing. Extensive cortisol use and high cortisol levels can atrophy the brain. And when you look at the brain, the hippocampus, which we talked about earlier, which controls the circadian rhythms, it is loaded with cortisol receptor sites. And because of that, it’s most sensitive to cortisol. So high chronic exposure to cortisol tends to have a degenerative effect there.
And so those are the key things that we know about the brain. So it can impair and promote degeneration overall throughout the brain. But the most sensitive area is the hippocampus, the medial temporal lobe for long-term memory recall, and the blood-brain barrier being breached and just global atrophy to the brain are all associated with high cortisol.
The vagus nerve and how it links to fatigue
Ari Whitten: Got you. So that’s sort of the primary thing that stress is doing to our brains. Is it, is there any issue of, sort of, I guess over time, decreasing vagal tone or rewiring the limbic system into hypersensitivity. Kind of like the limbic triune theory and kind of hyper excitatory state of the limbic system.
Dr. Datis Kharrazian: Sure. Okay. So the limbic system and the medial temporal lobe are different and have different responses. So the adrenal glands make cortisol, aldosterone and epinephrine, right? Different types of pathways. The effects of cortisol on the brain are different than the effects of epinephrine or norepinephrine. So the adrenal cortex releases cortisol.
But the dura mandela releases epinephrine, norepinephrine. The epinephrine and norepinephrine are what hits the limbic system. So when you look at the amygdala and you look at different areas of the limbic system that are involved with anger and stress and pain and heart rate and autonomic responses, those are real catecholamine based receptors.
So the effects with stress, I mean for some people they have stress and they release catecholamines, and for some people they have stress and they release cortisone. Then for some people who have stress and they have an opioid response and they have beneficial effects from it. So, and this could be some of the things that I think are conflicting with some of the research findings, stress and looking at cortisol because there are all these other variable factors.
That’s the way I was answering you this time. I was using not the word stress as a broad term. I used the actual chemical pathways itself, which I think is more precise, anyway. But, yeah, adrenaline and norepinephrine over-activate the limbic system.
So some people can have… so there’s a concept called negative plasticity. And we think of plasticity is how neurons communicate with each other and as they branch into each other more efficiently, that’s plasticity, right? But if you have pathways activated that have an adverse effect on your health, that’s called negative plasticity. So for example, phantom pain is negative plasticity.
You get such a severe injury, your arm is cut off, but you still feel your right thumb that’s no longer there. It’s still burning. And autonomic responses with the limbic system is also PTSD. Those are all considered negative plasticity. So you know, there are different theories about this from what I understand about it. And if you bombard a region of the brain with a high load of stress, whether it’s pain, whether it’s injury, whether it’s psychological and you continue catecholamine elevations that can auto-activate those centers.
Now I think with the limbic pattern, they are describing what I think a lot of people use in the literature called dysautonomia, where their sympathetic system is kind of firing at their own rate and their resting heart rate’s higher and then they have dilated pupils and they start sweating for no reason and trivial things like sound or light can increase their heart rate. Those are limbic phenomenon.
So that could be due to several things. It could be due that they have negative plasticity developing in their limbic system. It can be that they have some gene uniqueness where they’re extremely sensitive to catecholamines, so they react that way. The limbic area is shut down by an area of the brain called the basal ganglia indirect pathway that just shuts that system down.
Like I just had a consult and worked up a patient on Monday. He had an infection in his brain. He injured his basal ganglia, and now he can dampen his thalamus and his heart rate’s up all the time and he can’t handle sensory input. And he has to focus and concentrate on an iPad just to not be sensory bombarded.
So that’s a basal ganglia pathway. So if we see someone who’s got autonomic dystonia… like we’ll see it with some of these soldiers that have been in combat or they’ve had some serious traumatic events. We’ll see it with some people that have developed negative plasticity through some kind of sensory bombardment that’s been very adverse for them.
Other times we’ll see it because the basal ganglia have degenerated or they had injury to certain parts of the brain. I’m not really sure if I’ve answered your question, but the autonomic dysfunctions are all different.
Ari Whitten: Yeah, got you. So where does vagal nerve under-activity fit in all of this?
Dr. Datis Kharrazian: Sure. So sorry. Alright. So the vagus nerve in the brainstem, we have the vagal motor nuclei and we have an area called nucleus ambiguous and they fire into the gut and then we have motility and blood flow to our gut and all those things.
So the majority of the brain’s output… so the brain is constantly getting input from all the different receptors we have like sound, smell, taste, and whatever. Gravity’s pulling our muscle spindles. They all fire to the brain than the brain fires most of its output to the brainstem, which then has respiratory centers and our digestive centers, and that’s how we stay alive. So in the lower parts of the brainstem, we have the vagus nerve and the vagus nerve is constantly getting bombarded by the cortex. So when brain function starts to go down, we get decreased output, many times at the vagus and people start to have their digestion motility impacted.
So we know, for example, when kids are born their brains are not fully developed. They can’t digest. And as their brains develop they move and they function they start to be able to digest food and they’re getting neurological activities to the vagus and the gut now starts to develop.
But when people start to degenerate at the brain, not just the gut because the gut has a nervous system too, but the brain starts to degenerate, you get decreased output just like how movement and cognitive function slows down. You also can get slow down function in your output to the brainstem from the brain.
And then, too, from the cortex to the brainstem and then from the vagus nerve to the gut. So we sit all the time with people that have neurodegenerative changes.
Ari Whitten: Excellent. And I know you focus quite a bit, at least with a significant segment of the people you work with on vagal nerve activation.
Dr. Datis Kharrazian: Sure.
Ari Whitten: Can you describe what the benefits of that are and what are some of the techniques that you use to accomplish that?
Dr. Datis Kharrazian: Well, we only do that with people that actually have impairments. So let me kind of take a step back. So in a clinical workup… so if I see a patient that comes in and they tell me, “So it’s like I can’t swallow well,” or even more subtly, “Please don’t recommend supplements to me. Pills because I can’t really swallow them well, if you can give me liquids.” That’s a hint, that’s a red flag that their vagus nerve function is not doing well.
So the vagus nerve not only controls gastrointestinal motility, but it controls the palatine muscles in the back of the throat so you can swallow, right? So swallowing is primarily vagal activity.
So one of our red flags that someone may have an impaired vagus is that they come in with that type of history. Then on an exam, we actually evaluate vagus function. One of the things we do is just have him say, “Ahh” and look at their palatine muscles. And the Palatine muscles should move and they should be robust and have great activity when they say, “Ahhhhh.” Those things should move.
Sometimes we don’t see much movement there. Then we check their gag reflex, make sure their gag reflex is working. And if those things are not functioning, then we consider the vagus is a problem, but we wouldn’t jump to a clinical approach to the vagus until, unless those things were impaired.
Ari Whitten: Okay. What are some of the other kind of key signs or symptoms that indicate an impaired vagus activation?
Dr. Datis Kharrazian: Another vagal issue concern is when you look at gastrointestinal problems and the gastrointestinal problems are specific to motility, to movement. So a chronic inflamed gut or distention is different than just not having bowel movements.
To people that, there are people that have vagal dysfunctions like they have to have magnesium or soften their stool to have a movement. They have to take some type of botanicals to enhance the mobility to be able to have a bowel movement. Those are the ones that we’re worried about the vagus.
But also remember that those are the first signs of Parkinson’s disease. Parkinson’s disease starts with gastrointestinal motility and then loss of smell, especially to coffee and peppermint and peanut butter. Those are the three known sensitive loss of smells first. And this goes into stiffness of joints and then rigidity.
So we always rule out vagal issues. And now there’s some research showing that the buildup of alpha-synuclein related to Parkinson’s starts in the gut and goes actually up the vagus nerve to the dopaminergic centers in the brain.
Ari Whitten: Oh, wow.
Dr. Datis Kharrazian: So, vagal issues are always important for us. But when we see them, especially with low motility in the gut, again, we rule out Parkinson’s as we talked about. And the thing with Parkinson’s, too, is there is early onset Parkinson’s. People under the age of 30 develop Parkinson’s and it takes decades before they even have any signs of tremor.
Why chronic exposure to chemicals can cause Parkinson’s
Ari Whitten: I have a very specific kind of personal question on the topic of Parkinson’s. This is a bit of a digression, but I’m just curious because you have so much clinical expertise here. My uncle who’s now in his mid-seventies has Parkinson’s.
He was a highly competitive swimmer growing up for decades, actually well into old age. He has continued to compete, but he was a very, very high-level competitive swimmer at Harvard and then, you know, in various games, athletic games. But I always thought that the chlorine toxicity could have played a role in the neurodegeneration. And I’m just curious if you’ve seen any relationship with swimming and chlorine exposure.
Dr. Datis Kharrazian: I don’t have any experience with that, but I can tell you some research, we’ve been doing with that related to chemicals. So a paper that’ll be published a couple of years ago in the Journal of Applied Toxicology, we found that chemicals bind to proteins. So when chemicals bind to proteins they become new antigens.
And even though you may not be able to measure chlorine levels in them that are high, if you measure chlorine bound to proteins, like albumin is the most common of the proteins, you can find very, very high levels. So first of all, when we published that paper, we were saying the way we are looking at toxic insults may not be the only way of just measuring the level of the chemical.
These chemicals bind to proteins that become new structures and the only way you can find them is with antibodies. We published that a couple of years ago. And subsequent to that we then took those patients that had antibodies to chemicals, and we listed a host of chemicals, and we saw which of them had antibodies and we saw if there was an effect with that.
Right now we’re finishing the manuscript to submit to the Journal of Parkinson’s Disease where we measured BPA bound to protein antibodies because BPA exposure is common, but not everyone gets Parkinson’s. So what we found is that people who had BPA bound to protein, BPA bound to albumin, which is a protein antibody, there was a correlation rate of like point nine, which is almost one to one. So we’re trying… with the theory of like maybe the way we’re looking at how chemicals impact Parkinson’s is more than just what’s in the bloodstream.
Because you can do a study and measure chlorine levels in the blood of patients and then find nothing.
Ari Whitten: Right. I mean, I think even also just a basic epidemiological study to see if rates are higher in competitive swimmers versus nonswimmers would be interesting even though it’s not mechanistic and direct causation.
Dr. Datis Kharrazian: Yeah, I mean epidemiology studies would be interesting. You know, obviously they are always going to get criticized because they don’t have a causative role. And then so what? We have our problems with our correlation study, too. But you know, you did the best you can. I wouldn’t be surprised if chlorine was the factor. Certainly there are publications between people who work around chemicals, especially oxidized manganese and industrial chemicals have higher rates of Parkinson’s disease development. That’s definitely in the literature. Yeah.
How to treat brain fog – heal your gut
Ari Whitten: Interesting. Good to know. Well, thank you for that. So I want to be respectful of your time here. My last question to you is brain and gut health. Can you kind of quickly describe the relationship of gut health to the brain and how that might play a role, like how somebody’s gut health disturbances might manifest as brain fog or brain related fatigue?
Dr. Datis Kharrazian: Sure. So, you know, it’s interesting… is like back in the 1990s, 2000s, it was the decade of the brain. The decade of the brain lasted for like 30 years. And now we have this new big decade, the decade of the gut-brain axis, whereas there’s all this funding and research being done to look at these relationships and a lot of departments are studying it.
So lots of new information is coming in all the time. But it’s pretty clear now that the gut microbiome has a direct effect on the brain. And there are two types of effects on the brain, what are called canalized pathways and non canalized pathways. So canalized pathways are actual neurological tracks. So the thing to understand is that the brain is intimately connected anatomically to the gut through the vagus nerve.
I used to teach human brain dissection at Bastyr. One of the things we would do is we would do this extraction of the brain. But in order to extract the brain properly, you cut around it and pull the brain out, but you have to go behind the neck and do a laminectomy, cut the spinal canal out and then you can cut it there and preserve the brainstem and the vagus.
And if you do that, you can see the vagus go all the way from the brain stem all the way into the gut, all over the gut. And the vagus is a wandering nerve. It’s huge. You can literally take your hands on the gut, follow it all the way up to the brain stem into the brain. Like it’s anatomically connected. So those are canalized pathways. So there’s a lot of research and these pathways are bidirectional.
So there are actual chemical signals that go back and forth through the vagus, through the brain and down. Okay? Then there’s this whole field of non canalized connections. Non canalized means not an anatomical pathway, just chemicals. So there’s a bunch of chemicals that are released that pass the blood-brain barrier unrelated to the vagus and get effects in the brain. These are like neuropeptides and cytokines and proteins. But this constant feedback loop between both those systems is happening all the time.
So there’s no separation between these two. And what they’re finding is that that the microbiome, these bacteria produce different substances and different peptides and different polysaccharides, and these things have a direct effect on the brain. And the interesting thing that… what we know with the microbiome research is they don’t really know which bacteria species are bad, but the different bacteria species have different effects on different neurochemical pathways and the function in the brain. But there is a common agreement that the more diverse the microbiome is, the healthier you are. The more bacteria species you have, the more enzymes you have from these bacterial species to do various things. The more potential you have to be balanced out and attain homeostasis.
So to make it very simple, the more diverse your gut is, the healthier you are. And the more diverse your gut depends on how diverse your plant fiber foods are in your diet. So eating a highly diverse list of plant fiber foods, you have a healthy microbiome and you have the best potential for your brain/gut axis to function.
Ari Whitten: Which is a big problem, I think, when you consider the… I think the numbers are something like the average American has no more than three types of vegetables in their diet, if I remember correctly.
Dr. Datis Kharrazian: Yeah, that makes sense.
Ari Whitten: They eat iceberg lettuce and, you know, maybe potatoes, they count potatoes and French fries and potato chips as one category, and maybe tomatoes, tomatoes are technically a fruit, but yeah. It’s very, very limited in terms of…
Dr. Datis Kharrazian: Yeah. And even people that are healthy they, or people that are sick, they’ll just plan like three things to eat every day and have the same salad every day, and then eat the same things and they don’t get the diversity they need, you know?
Ari Whitten: Yeah. I’m sure you saw the Hadza gut study where they looked at, you know, they were kind of expecting to find in the Hadza tribe in Africa. They analyzed the gut microbiome of these people and they were kind of expecting to gain this deep insight into what are the true good types of bacteria and the bad types because these people don’t seem to have really any of the gut issues and the IBS and the Crohn’s and all these things that we have.
So they analyzed this and they were actually shocked to discover that there was an amazing diversity of different microbes, and included lots of different microbes that actually were previously thought to be pathogenic. But they weren’t manifesting in any pathogenic way in these Hadza people because of the overall context of their lifestyle, their diet and just the context of those pathogenic organisms in balance with all the other organisms in there.
Dr. Datis Kharrazian: Exactly. In the, I haven’t read that study that you pointed out to, but this is a similar thing that they’re finding is that there is this whole version of bad versus good bacteria is really questionable. And, how one bacteria species works in combination with other species is another variable onto itself, and…
Ari Whitten: Yeah. It’s endlessly complex, I think.
Dr. Datis Kharrazian: It’s exciting and also kind of defeats your excitement, too, at the same when you hear how complex it is, you know?
Ari Whitten: Yeah, absolutely. I think the same thing is going on with the whole, the gene SNPs and that whole area of research. But, Dr. Kharrazian, thank you so much. This has been an absolute pleasure. I have one final request for you. I know that you often work with a selection of the population that, you’re working with very complex cases. If people are ending up in your office, it’s because they’re kind of, they’ve probably have been to 50 other people and haven’t had results so they’re finally ending up in your office.
Dr. Datis Kharrazian: Right.
Dr. K’s top three tips to protect your brain health
Ari Whitten: And you’re dealing with a lot of complex stuff. But for those people who are listening to this interview who are maybe on the healthier side of the spectrum, maybe have some mild brain fog, maybe some low energy, but who don’t have really serious symptoms or complex illness in any way. What would be your top three tips for those people to protect and preserve their brain function and create the healthiest brain possible, that is the most resistant to neurodegeneration and neurodegenerative diseases.
Dr. Datis Kharrazian: Okay, I’ll try. The first key thing is healthy relationships. I mean we tend to focus on nutrition and diet and all that stuff, but healthy relationships are the most important. So not having toxic relationships, having an environment where healthy in your work, in your home, those are critical. That is absolutely a key factor in any chronic illness or just to be healthy. It has to be addressed.
Sleep is completely overlooked. You have to have sleep. More and more studies show if you’re not getting proper sleep, your brain’s in trouble. And so healthy relationships. Sleep is a great one.
Finding something that makes you happy every day, gives you joy, makes you smile. It’s important to have an opioid release throughout the day.
And you know, just things like you’re saying, get out there and get some sun, eat a diverse plant-based… diverse series of plant food in your diet. You can still eat other food, meat and other things if you want. But it’s not being vegetarian, but having a diversity of fibers in your diet. It seems to be critical of what we’re learning. And those are like very basic things that we all know. It’s just a matter of when we get stuck out of the routine of doing those things or having those things being part of our everyday life. Then we get in trouble and sometimes the answer is so obvious. Yeah.
Ari Whitten: Yeah, absolutely. You have just reminded me as you were speaking there with you… you know, earlier in this interview, you went into such amazing complexity and then I love how you brought it back to a few simple things. But you reminded me of one quote that you had in the human longevity project film that you and I were both featured in. You said something that was so great. I’m trying to remember exactly what it was, but it was like something like, “You know, most people have this chronic stress. You know what? Most people just need to get outside and go for a fricking walk for 10 minutes.” You know?
Dr. Datis Kharrazian: Yeah, that’s true.
Ari Whitten: Yeah, absolutely. So thank you again so much for doing this interview. It was such a pleasure. I’ve enjoyed it immensely and I’m sure that people are going to love it and learn a lot from it. Where can people find out more about your work? And also, I know that you have a new product or maybe a few new products coming out in the near future. If you want to let people know about anything that you have coming out in the near future.
Dr. Datis Kharrazian: Well, everything is in drknews, d – r – k – n – e – w – s.com. And the one thing we have is, I just wrote a couple of books. One on the brain. We have an online brain program. Then I have an office in San Diego. So those are actually the things I have to offer to people. But it’s all there at that website if you want to check it out.
Ari Whitten: Excellent. So drknews.com. And then you have this, you have a book on Amazon, what’s it called? “Why is My Brain Not Working?”
Dr. Datis Kharrazian: “Why Isn’t My Brain Working?”
Ari Whitten: “Why Isn’t My Brain Working?” That’s a great book.
Dr. Datis Kharrazian: Autobiography.
Ari Whitten: Yes. And your course, your six-week course, “Save Your Brain” which is on your website, which I have as well and I highly recommend. So Dr. K, thank you. It’s been an absolute pleasure and enjoy the rest of your day.
Dr. Datis Kharrazian: Thanks, Ari, pleasure.
Show Notes
00:00 – Intro
00:18 – Guest Intro – Dr. Datis Kharrazian
04:38 – The most common sort of dysfunction in people with chronic fatigue
10:08 – How brain fog and brain-related fatigue are related
11:25 – How brain fatigue is a sign of early brain degeneration
13:27 – The root cause of brain-based fatigue – how to detect and prevent Parkinson’s disease and Alzheimer’s disease
18:39 – How certain conditions put you at risk of developing neurodegenerative diseases
23:51 – How to treat brain fog when you are hypoglycemic
25:46 – How Dr. K analyzes cortisol patterns
32:02 – Why isn’t my brain working – how circulation plays a role in brain fog and fatigue
37:22 – How to treat brain fog and prevent Parkinson’s disease and Alzheimer’s disease – how stress and sleep affect your brain and health
39:01 – The vagus nerve and how it links to fatigue
47:28 – Why chronic exposure to chemicals can cause Parkinson’s
50:20 – How to treat brain fog – heal your gut
56:02 – Dr. K’s top three tips to protect your brain health
Links
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