Brain health is critical for our energy, mood and focus.
Today, I had the honor and privilege to discuss brain inflammation with one of the leading experts in the field, Dr. Datis Kharrazian. Combining his observations in his clinical practice with his background as a research scientist and academic professor, Dr. Kharrazian tackles some of the most challenging brain related health challenges, including autoimmune, neurological, and chronic diseases.
Brain inflammation symptoms: Slowed mental speed. As the brain gets inflamed, you lose brain endurance. You can’t focus, you can’t concentrate, it’s called brain fog. Because inflammation reduces nerve conductivity. A typical patient that has brain inflammation is just fatigued, depressed, can’t focus, can’t concentrate, and can’t do activities they used to do for as long as they used to do them. Like reading or driving or things like that. That’s the neuro inflamed patient.
Brain Cells Primed for Inflammation: Brain cells are glial cells that are activated by trauma, infections, toxins and stress and then more susceptible to inflammation, triggering an inflammatory cascade in the brain.
What Happens When Glial Cells are Activated? When glial cells become activated, they begin an inflammatory response. As neurons become inflamed, they first lose their nerve conduction, nerve speed. The biggest symptom of this is brain fog. It is the feeling of slowness, disconnection, or when one cannot get their thoughts together. Neurons are connecting more slowly. Eventually, these inflamed neurons can cause atrophy in the brain. Depending upon which area of the brain are involved, different symptoms will occur.
Increased Susceptibility to Other Triggers: Once glial cells have been activated, inflammation is more easily triggered by other things. Once glial cells get primed, they’re forever changed.
Depression: In the literature what’s really popular now in the clinical research with depression is the inflammatory model of depression. They call it the cytokine model of depression. It’s unresponsive to anti-depressants. You have some of those patients suffering out there. You have a lot of patients that have chronic fatigue syndrome that are just tired and exhausted all the time. But they’re tired and exhausted because the brain doesn’t have endurance.
Sleep: If you don’t sleep and you have brain inflammation, you can’t recover. Stress response, that being kept under control, blood sugar spikes and surges, turn those things on. Those are the basic lifestyle factors. Exercise has been shown to dampen it, but too much exercise has been shown to inflame. You can work with finding balance between those things, that’s critical.
Vagal functions: How to assess if your vagal function and ability to drop into the parasympathetic state is off, so they can’t get the gut function to work, and they can’t get blood flow to the gut, they can’t heal the gut, and that’s causing brain inflammation.
CLICK HERE to Register for the Kharrazian Institute Treating Neuroinflammation Course
Dr. Datis Kharrazian – Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal
Dr. Datis Kharrazian – Why Isn’t My Brain Working
Jodi Cohen: I am so honored to be here with one of my biggest idols, who I think is unbelievably brilliant. Dr. Datis Kharrazian. He is an award-winning researcher, clinician, author, educator, with more than 20 years of experience using functional medicine to treat highly complex patient cases.
Dr. Kharrazian is a faculty member for the Institute of Functional Medicine and associate clinical professor at Loma Linda University School of Medicine, and on the scientific editorial board for the Journal of Functional Neurology, Rehabilitation and Ergonomics and alternative medicine therapies and health and medicine.
He specializes in developing evidence-based models to treat autoimmune, neurological, and unidentified chronic diseases using non-pharmaceutical 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.
He also has written two amazing best-selling books. One about the thyroid that I think really revolutionized how people looked at the thyroid and looked at autoimmunity, and also one on the brain. He’s both a clinician and a researcher, so he’s actually treating clients and seeing what is moving the needle for inflammation. Welcome.
Dr. Datis Kharrazian: Thank you so much.
Jodi Cohen: Thank you. If you could just talk a little bit about how your path towards functional neurology and the brain, how you started that focus.
Dr. Datis Kharrazian: Well, I was growing up and I had a sick family member, and I remember going to all the different medical appointments with them. I didn’t know anything about healthcare, because I was just a kid in elementary school, and then middle school, and then high school, and then the only person that ever made a difference for her was a chiropractor in a small little office with a nutrition focus.
At that time, functional medicine wasn’t even around. But just to see what an impact clinical nutrition can do with the chronic disease was mind blowing for everyone in our family, including myself. Then over the years just to see how supporting the brain came in, and then autoimmunity was a factor, so I think just when it came to the point in your life like, “What do you want to do?”
I thought, “Well, maybe I want to do that,” because that seemed pretty cool. That’s kind of what got me there, is just to see the impact and how powerful, how therapies can be that are looking at lifestyle and nutrition, and then eventually this translating to something we call functional medicine now, and I’ve been with that community since it started, and I’m really loving it. I think it was just like most people, they had something in their life that dramatically impacts them, and they get interested and excited about it.
Jodi Cohen: I’m so glad. I’m sorry that you had to go through that as a child, but I’m so glad you chose this, because you’re making such an impact. One of the things I wanted to talk about, you really focus on inflammation, which needs to be talked about more, because so many people, some of the symptoms, people just say like, “Oh, you’re fine. Oh, you’re just getting old. Oh, you need anti-depressants.” Can you talk about how some of the symptoms of inflammation might present?
Dr. Datis Kharrazian: Sure. Brain inflammation is really very common. We know we’re all used to inflammations around our body, but inflammation of brain is first of all, very unique than the rest of the body. But the main symptoms of brain inflammation are really slowed mental speed.
You can’t focus, you can’t concentrate, what we call brain fog. Because inflammation reduces nerve conductivity. Then the other key thing is just depression. We see people that have lots of depression. Can’t focus, can’t concentrate, and as their brain gets inflamed, they also lose their brain endurance.
Their energy level, the capacity to handle doing things for longer periods of time, has all become a factor. The typical patient that has brain inflammation is just fatigued, depressed, can’t focus, can’t concentrate, and can’t do activities they used to do for as long as they used to do them. Like reading or driving or things like that. That’s the neuro inflamed patient.
Jodi Cohen: One of the terms that you use is glial cell priming, and glial cells are brain cells. What are some of the things that you believe lead to brain inflammation or set people up to tip into illness in the brain?
Dr. Datis Kharrazian: There’s four different pathways that we know about that cause brain inflammation when the blood-brain barrier is intact, so you can say there’s five pathways if the blood-brain barrier breaks down.
We’re getting information constantly from our gut to our brain through the vagus nerve, this is called brain-gut axis. There’s been an explosion of research in that in the past few years, and they’re finding that diseases like Parkinson’s Disease and even dementia may actually start in the gut from an inflammatory cascade and then cause brain inflammation. Which is very fascinating.
There’s just a bit of pathway through what they call active and passive diffusion, where different inflammatory chemicals can cross the brain. But then the worst scenario is if the blood-brain barrier, which is the barrier we have to keep things out of our brain, breaks. Then we know about leaky guy, that there’s now leaky blood-brain barriers. When the blood-brain barrier breaks, the brain’s really in trouble.
Jodi Cohen: That’s why brain injuries are so damaging, because that’s one of, trauma, can damage.
Dr. Datis Kharrazian: Yeah. When the brain has this traumatic impact on it, several things happen. One of them is that the blood-brain barrier breaks down. Some studies have shown within the first two hours, the blood-brain barrier’s broken down, and then the gut barrier breaks down, and then you have this inflammatory cascade.
When the blood-brain barrier breaks down and severe inflammation in the brain, because it allows T cells to activate inflammation. The blood-brain barrier breakdown isn’t all from injury. It’s actually a cellular response. If somebody already has pre-existing inflammation or pre-existing immune dysregulation of autoimmunity, and then they get a head injury, it’s a completely different response. Because now that the blood-brain barrier’s become open is a protective mechanism to bring T cells into the brain that don’t usually exist there.
You’ll see, sometimes someone has a traumatic brain injury, and they feel fine, and then five or ten years later, they’re not the same. They don’t associate that that initial traumatic brain injury was the cause. There’s been a lot of research now, they call it CTE, Chronic Traumatic Encephalopathy, Encephalopathy being brain inflammation.
They get a brain injury and what they realize is that the major effects of it are not after the injury. You recover, you get dizzy and you feel off for a few days, but then it causes a cascade in the brain that can be permanent, and this is what they call priming. That these cells in the brain called glial cells, which are immune cells, they actually change in the structure. Just like a hard-boiled egg can never go back, these glial cells, once they get primed, can never go back.
Jodi Cohen: I see.
Dr. Datis Kharrazian: There’s an ongoing inflammatory state, and then the brain starts to degenerate. Then during that process, the inflammation keeps adding up and adding up and adding up like a forest fire. A year later, two years later, three years later, four years later, they have this progressive inflammatory state, and now they get into the point where the inflammation is so great they can’t think, they can’t focus, they can’t concentrate.
They’re really puzzled, because they’re not linking that initial head trauma may have caused it, because it was so many years ago. But that’s what we’re seeing. That’s what we’re seeing with the NFL players now reporting it, this is what we’re seeing with the soldiers that have been to Iraq that have had blast injuries, they’re having these effects, and because of those high profile groups of people, soldiers and football players, there’s been an explosion of research. Our entire model of brain inflammation has changed because of these new understandings.
Jodi Cohen: Do you believe there’s a negative synergy between toxins or infections or stress and brain inflammation? That if your cells are primed and then you add another stressor, it makes it harder to navigate?
Dr. Datis Kharrazian: Sure. For me as a clinician and the way I teach at the practitioners is so they can use the clinical model that we’re using for their own practices. When a patient comes in and you suspect they have brain inflammation, if they come in, they have focus issues, concentration issues, depression, brain fog, you have to put them on a scale of where they are.
One type of inflammation, this is the less concerned, the subtle one, is just the transient. Inflammation comes and goes. They may have a reaction to a food protein, and that causes stomach inflammation and the brain gets inflamed from that. Maybe they’re sensitive to gluten, they exposed to gluten, and now they got brain fog for a few days, and then they are fine. Or they may be exposed to an environmental chemical, and then they get exposed to that chemical, and then it causes the brain fog for a few hours or a day, and then they go, that’s transient. That’s one thing.
Jodi Cohen: Right. It’s acute, and it happens and then it passes.
Dr. Datis Kharrazian: Yeah. Okay. Right. That’s not too big of a deal, it’s something I think most people have experienced at some point in their life. The next level is chronic, where people just have chronic brain fog, depression, and that’s, there’s then it’s the clinically it’s is an ongoing inflammatory mechanism that’s causing it.
Someone has celiac disease and they continue to eat gluten, for example. Or someone has an autoimmune disease, a chronic autoimmune disease, or the Inflammatory Bowel Disease, and Inflammatory Bowel Disease keeps causing brain inflammation.
That’s a chronic pattern. Then the third level of progression into the neuro inflammatory scale is someone who has primed glial cells. Primed glial cells means the inflammatory reaction against the brain was so intense that these cells called glia have now changed their structure.
Now they’re active constant soldiers for the rest of the person’s life. The most common cause of that is traumatic brain injury. But any type of infection can do it. You can have a viral infection that gets at the brain, for example, that can cause glial cell priming.
Jodi Cohen: Right. Like Lyme.
Dr. Datis Kharrazian: Right, like Lyme Disease, and even certain viruses can cross the blood-brain barrier. Sometimes people getting bacterial infections and they do have meningitis, it still exists sometimes. Things like that can prime glial cells.
But once these glial cells get primed, they’re forever changed, but that’s the third level of the intensity. The fourth level of this scale in neuro inflammatory intensities is now they turn into brain autoimmunity. Now the immune system has made antibodies against the brain itself, and then there’s an active destructive response against the brain when there’s an inflammatory cascade.
In a clinical setting, we see a patient come in, and they report, “I have fatigue, I have depression, I can’t focus, I can’t concentrate.” We’re trying to figure out where on the scale that they’re at. Is it just transient, is it chronic, or is it primed, or is this really neurological autoimmunity?
The key difference between primed glial cells, let’s say, than someone that has a chronic or transient inflammation, is if people have primed glial cells, their brain function completely shuts down. Meaning a stress response can impact all of us, we get stressed, we have not the best sleep, we may have our blood pressure go up, might have anxiety throughout the day, and that’s pretty normal for everyone if they’re stressed.
But if you have primed glial cells, you may completely lose your brain function. You might not be able to get to bed when you’re under a stressful response. Because the stress response activates these glial cells. People that have primed glial cells that they get exposed to chemical, they could be in bed for days. Whereas someone who doesn’t have primed glial cells, they get exposed, they get a little bit of brain fog.
Jodi Cohen: Right. It destroys their resilience.
Dr. Datis Kharrazian: Right. These glial cells prime, and you can autoimmunity in the brain even without glial cell priming. You see a mixture of those variations. But there a lot of chronic patients out there that have neuro inflammation that no one’s looking at, and let’s say they have chronic depression, and they’re trying every anti-depressant, it doesn’t work.
In the literature what’s really popular now in the clinical research with depression is the inflammatory model of depression. They call it the cytokine model of depression. It’s unresponsive to anti-depressants. You have some of those patients suffering out there. You have a lot of patients that have chronic fatigue syndrome that are just tired and exhausted all the time. But they’re tired and exhausted because the brain doesn’t have endurance.
Jodi Cohen: Right. Or multi-chemical sensitivity or fibromyalgia.
Dr. Datis Kharrazian: Exactly.
Jodi Cohen: Here’s the exciting turning point. What do you do? How do you help these people?
Dr. Datis Kharrazian: You have to create a clinical model, and then ….
Jodi Cohen: Which you’ve done.
Dr. Datis Kharrazian: Which we’ve worked through. But it’s a personal lifestyle model, because it’s not the same for everyone. At the end of the day, there’s only so many interventions we can do. Where we start with lifestyle, diet, nutrition, there’s lots of triggers for people that have these things, we want to identify those triggers first. Starting with lifestyle, the most obvious one’s you have to sleep.
If you don’t sleep and you have brain inflammation, you can’t recover. Stress response, that being kept under control, blood sugar spikes and surges, turn those things on. Those are the basic lifestyle factors. Exercise has been shown to dampen it, but too much exercise has been shown to inflame. You can work with finding balance between those things, that’s critical. Someone could have chronic depression, and until they do that, the depression won’t go away despite any anti-depressants they take.
Jodi Cohen: Right. Exercise moves oxygen to the brain, which is good. Blood sugar gives you the optimal amount of glucose in the brain. Sleep helps the glymphatic system so you can detoxify. All these things are just doing what you can to balance. Is there any way to turn off inflammation once it starts in the brain?
Dr. Datis Kharrazian: Yeah. Of course. There’s also a nutraceutical. Once you go through lifestyle, then you can go into diet and nutrition, and there’s dietary protocols that have been published on neuro inflammation. Some as simple as maybe just being gluten free, and more complex too, things like ketosis or fasting. Those things can have an impact on neuro inflammation.
Some new papers have just come out that shows actually ketones dampen brain inflammation, that it’s not just another fuel source. You take a patient to the spectrum of how intense of the inflammation is, what type of dietary changes is. Some people, it’s just getting off inflammatory foods. For some people, they have to get off and be gluten free.
For other people, they have to completely go into ketosis and do even fasting. It really depends on the scale of the inflammatory response and what they need to make that change. That’s where diet comes in. Then as far as nutraceuticals that have been shown to dampen brain inflammation. Different types of flavonoids. Flavonoids only work if they can cross the blood-brain barrier.
There’s about 20 flavonoids that have been published that can cross the blood-brain barrier path through passive diffusion. There’s also some research that’s been shown that various nutraceuticals, things like short chain fatty acids, butyrate, turn on pathways in the gut that then reduce inflammation in the brain.
They’ve been using animal models of autoimmune disease and inflammatory reactions. Then you can put a person on a cocktail of different, once you go through lifestyle and you go through dietary changes and you go in through a list of nutraceuticals, you try to dampen their inflammation.
That’s what I call still all level one care. It’s very basic. Level two care is you dig deeper as a clinician and go, “What are the triggers?” This is where a systems biology approach comes in. This is where we do blood work. Are their compliment proteins high? C3, C4, C5. That means there’s an active immune infection or immune response.
Do they have high HBA1C? Do they have high reaction? Do they have S100B protein markers? Is the blood-brain barrier broken down? This is the model that I teach, and it’s hard to summarize here, but that’s the next level. There’s some patients that just need a very basic lifestyle change.
Jodi Cohen: Right, I think your first level helps everyone. Maybe for 50% of your people, it’s enough. Then the next 50% need to go to the next level.
Dr. Datis Kharrazian: Right. I formed the Kharrazian Institute recently, and the first course we’re putting together is on neuro inflammation. The reason I want to do this course first was because it’s such an overlooked area in healthcare.
People that are practitioners really need to understand the scale of it and the management of it, and where level one care gets you and level two care gets you, and understand what’s been published on it, because there’s a tremendous amount of information published on this topic.
With dietician lifestyle. That’s one of my initial goals, is to get that information out, and then where I wrote a book on the brain, and we talk about neuro inflammation has a chapter, some subtle things in there people can try. That’s one option to help people.
Jodi Cohen: Right. One of the things that I do, I have an oil that helps to trigger the vagus nerve to turn on the parasympathetic response, because parasympathetic is related to inflammation. I know you pioneered that, you were really the first one to start talking about vagal tone and vagal activation. Is that something that you integrate into your protocol?
Dr. Datis Kharrazian: It really depends on the …. That’s where the level two comes in, and the individualized approach. We always suspect vagal issues if we see a loss of vagal functions, we can see in an exam.
If we have someone with a palette. When you go into your doctor, they go, and then the palette should move. If those palettes aren’t moving, we know the parasympathetic systems are firing, they don’t have a gag reflex, the gag reflex is abnormal. We know that’s there. We listen to the gut, if the gut’s not moving, we know your motility, we know that whole vagus system is down.
If we see those exam findings with symptoms of constipation and poor digestion, then we know that whole vagus pattern is down. That’s when I’ve always taught activating the vagus with things like gargling and trying to improve that pathway.
But for some people that could be a factor for them. Their vagal response is down, so they can’t get the gut function to work, and they can’t get blood flow to the gut, they can’t heal the gut, and that’s causing brain inflammation.
For one patient, you may have to go through the whole vagal response pathway, improve that integrate to help with their brain inflammation. But for someone else, that’s totally fine. They’re pre-diabetic, and their HBA1C is really, really high, and they’ve had a past head injury.
Those two combinations can now cause chronic depression for them. Now you got to control their diabetes and repair their blood-brain barrier, and then put them on a bunch of anti-inflammatory things and get their insulin under control, and also the brain inflammation goes away.
Jodi Cohen: For the clinicians that are listening, Dr. Kharrazian is offering an amazing neuro inflammation deep dive. It’s May 18th and 19th and San Diego, where he’s really going to go into this. One of the things, I heard you in a seminar, and someone asked you, “This person has this theory. What’s your theory?” You said, “Well, it really depends on the patient.” I think you’re right. They’re maybe 15 things that could be wrong with different people, and they’re going to present differently, and you really need to address what’s going on with the individual person. One of the other questions that I’ve wondered about, sleep. You’ve talked about how sleep is critical. Which, that’s when the lymphatic system turns on. One of the things that I’ve noticed in a lot of clients is [inaudible] glial cells, and they’re related to the lymphatic system. Sometimes the Aquaporin-4 channels are turned off. Have you found a way to turn that back on, or to balance that?
Dr. Datis Kharrazian: The Aquaporin water channel proteins, and they’re involved in blood-brain barrier. There isn’t a lot of various research other than blood-brain integrity in them that’s studied to that specifically. There’s some research on neuromyelitis optica, which is an autoimmune target site.
We published some research on cross activity with food proteins with the Aquaporin-4 receptors, and I think the Journal of Autoimmune Disease, where we published it. [inaudible] cross react with it, so we do see people that have Aquaporin-4 antibodies, we do get them off the cross-reactive foods.
Jodi Cohen: What are those cross reactor foods?
Dr. Datis Kharrazian: It’s corn, soy, spinach, tomato. They have the most amino acids [inaudible] similarity. If you have antibodies through those and you eat them, you get specific targeting binding of those food proteins with the Aquaporin-4, which can cause blood-brain permeability.
We did a study where we did the cross-reactivity, and then we took a group of patients that had neuromyelitis optica and a control group, and we looked at the levels between them, and we found a huge, huge difference. I think if you google my name with autoimmune disease or neuromyelitis optica, that paper will come up. But we summarized the whole concept there.
Jodi Cohen: That’s great.
Dr. Datis Kharrazian: But that’s one thing. But for the most part, yeah, you can get really specific with things. But sleep has a major impact in lots of different ways, and we do have a circadian rhythm even within our neurons. Astroglial cells have their own circadian rhythm, and they have different types of growth factors and hormones that only get released when we’re sleeping.
It’s a key factor. If a person can’t sleep well, it’s going to be very difficult to bring down brain inflammation. No matter what supplements a person takes or what else, other strategies they use. That actually is one of our top priorities and we work with the patient. We wouldn’t put someone on a cocktail of flavonoids if they’re not sleeping. We have to figure out how to get them to sleep before we’d expect any of those things to work.
Jodi Cohen: That’s another thing that I love about you, is I think there is a sequencing to things, and I really appreciate that you’re very thoughtful in the way you sequence and flow people through. We’re going to have a link where people can sign up for your webinar, and then they can also do it online, if you can’t make it to San Diego. Your books are both amazing. I don’t know, is the thyroid book still in print? It’s very hard to get.
Dr. Datis Kharrazian: No, it’s still in print. It’s still on Amazon, you can find it HERE. https://amzn.to/2GXIkke
With the neuro inflammation course, even if, it’s going to be on demand after the course. People can go and take it whenever they like. All the courses will be that way. Once we go through the brain inflammation course, then we have an entire module on the gut.
We’re going to teach people how to assess the different gut issues and then the third module this year will be on autoimmunity. We’re going to break down all the newest research on autoimmunity.
Because I think what we have right now, I think the feedback I’m getting, for myself, I’ve always worked on trying to develop my own clinical model when I see a patient. I rewrite my new patient exam and workup every three months.
Jodi Cohen: I know, I love that about you.
Dr. Datis Kharrazian: I’m always reading papers, because I practice one day a week, and I do research one day a week, so I go back and forth. I’m constantly going through material, I like to try it, and then eventually create a clinical model for myself, and then after I feel comfortable with the clinical model, then I try to share it with people.
Then that becomes what I basically teach on. With the neuro inflammation, I think we have a very effective clinical model. But what we face right now is not lack of information, we have too much information. It’s how to use the information, and then what are priorities.
Jodi Cohen: Yes. Priorities are huge.
Dr. Datis Kharrazian: There’s no way you would, I think, be able to know what priorities are unless you were actually in clinical practice. That’s the difficult ….
Jodi Cohen: I agree.
Dr. Datis Kharrazian: That’s what I’m saying. For example, sleep. I know as a clinician, if I can’t get my patient to sleep, there’s nothing that’s going to happen with anything else I do [inaudible] information. But how would you know that unless you were in practice?
Because you would see 20 other things and you would just go wonder what priority is. Having this environment of constantly failing with patients and seeing what works and doesn’t work, and being able to put the literature together is, I think, the key thing that can create and affect a clinical model.
Jodi Cohen: I think there are a lot of bright shiny objects, and I think a lot of people that have been sick for a long time have spent a lot of time, energy, and money, and it’s, they question themselves. It’s hard for them. Having someone who’s been doing this for so long and also is researching at the same time and can just tell them step one, step two, step three, I think that’s incredibly valuable.
Dr. Datis Kharrazian: Yeah. Thank you.
Jodi Cohen: But I really appreciate that.
Dr. Datis Kharrazian: In crossing these two courses, we’re actually bringing on my own patients that want to share their clinical case. For this first one, we have two patients suffering from glial priming. There’s ups and downs with them at a roller coaster ride, and I want practitioners to really understand that.
Because some patients will have an ongoing challenge because of their physiology. I don’t think some practitioners realize that. I think they feel like, “Well, I should give them this, this, and this, and I should fix them.”
This mindset of fixing them is the model for failure when you work with certain chronic pathophysiology responses. Sometimes it’s not about fixing, it’s about improving quality of life and maintaining more good days than bad days.
I see a lot of burnout also in people who like to do functional medicine and nutrition. Because they think that if a patient doesn’t immediately respond with something that they’ve failed and didn’t realize for that patient it may be life-changing.
Jodi Cohen: Yeah. Our expectations are maybe, yeah.
Dr. Datis Kharrazian: Also sometimes some patients have unrealistic expectations. They may have had a head injury that they completely injured their brain and they’re like, “Well, I want to function like I was when I was 20.” You’re like, “That’s probably not a real clinical outcome.”
Jodi Cohen: Even for non-practitioners, like moms who are practitioners in their own homes who have, a lot of my daughter’s friends play competitive sports, and they’ve had four concussions in a row. They’re still functioning, but I worry about them, and I want those moms to know what they can do now to unravel, you can’t unscramble the egg, but you can maybe set them up for greater success.
Dr. Datis Kharrazian: Right. Another major area breakthrough of head injuries has been, it’s not how hard you hit your head, it’s how active those microglial cells were before the head injury. For example, if someone was a smoker and was anemic and they had a little bit of hypoxia, lack of oxygen, going to their brain before their head injury, they would have a significant different impact after the head injury than someone who didn’t have anemia and was a smoker.
Jodi Cohen: Correct. I think the earlier that you can address the issue so that you’re addressing it when it’s still acute, before it becomes chronic, that’s, in my experience, the better the outcome.
Dr. Datis Kharrazian: Right. These inflammatory responses are like a forest fire. They just spread. Once they start converting cells to prime cells, they don’t go back, just like hard boiled eggs. The sooner people intervene, the better. It’s just sometimes hard for people to make that connection. We didn’t know about that. We didn’t really know ten years ago that a head injury would really catch up with someone and years later, 20 years later, and that they should …. You didn’t even think about those things.
Jodi Cohen: That’s a great analogy, by the way. I just want to thank you for your time and for sharing your knowledge. How can people get in touch with you? What’s the best way for them to find you, find out more about the course, about your work?
Dr. Datis Kharrazian: Sure. The Kharrazian Institute. K-H-A-R-R-A-Z-I-A-N Institute is where I teach my courses for healthcare professionals. Then I have a website called Dr. K News. Drknews.com, Dr. K News, and that’s where I put articles on there. I also put together a six week program for patients, consumers, people that aren’t health professionals to guide them through how to improve their own brain health where each week we’d be teaching different concepts, things to do in their life.
Jodi Cohen: Which is good, because you’ve got what, a two year waiting list to see you in person?
Dr. Datis Kharrazian: We have quite a bit, yeah.
That’s something that’s available. Then what do I still have? Why Isn’t My Brain Working is a book and Why Do I Still Have Thyroid Symptoms is a thyroid book that’s available on Amazon. Those are all my things.
Jodi Cohen: Yes. I highly encourage everyone to dive deep into Dr. K’s work. It’s amazing. Whether you’re a clinician or someone who’s just tired and has brain fog, or a mom who wants to help her kids with concussions, I really think that what you’re doing is just groundbreaking and very preventative. I love, maybe if your relative had known you early on, they wouldn’t have had to go for a lifetime of suffering. Thank you so much.
Dr. Datis Kharrazian: A pleasure. Thank you. Thanks.
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