In this episode, I speak with Justin Harris, a certified functional genomics practitioner, who explains how understanding your genetic blueprint can unlock personalized strategies for managing thyroid health. We dive into how genetics influences key factors like oxidative stress, detox pathways, and autoimmune conditions such as Hashimoto’s and Graves’ disease. If you would prefer to listen to the interview you can access it by Clicking Here [1].
Dr. Eric Osansky:
I want you to expand on your background. It always fascinates me as to why my guests started doing what they do now. How did you start working with The DNA Company, becoming an FDN practitioner, a certified functional genomics practitioner?
Justin Harris:
It’s quite the story, Dr. Eric, honestly. I think most of us have some sort of a wounded healer journey that we started with. I’m no exception.
When I was a teenager, I had acne. Many teenagers have that. Unfortunately, my doctor put me on antibiotics really early on. It was literally my 13th birthday. I started on this cycle of antibiotics. When I say “cycle,” this was meant to be a couple of week treatment. I stayed on it for a really long time, from age 13 to age 18 straight. I was on tetracycline. You all know, you’re not supposed to be killing your flora for that length of time. I wasn’t put on probiotics at the same time. It ended up really wreaking havoc on my health.
You start to dive down the rabbit hole. I’ll follow the Canada food guy. You get this generic health advice. When it doesn’t work, which it inevitably doesn’t work, you dig deeper and deeper. I started messing around, taking different supplements. I worked in the supplement industry because I had a passion for ingredients.
I became a personal trainer. I became a nutritionist. Then I got really interested in evolutionary biology. I asked myself where does the human genome start? What are the lifestyle behaviors that got us to this point? I ended up becoming the primal health coach. The whole thing is stemming from that evolution biology and ancestral lifestyle behavior component.
It was just a natural transition from there to want to personalize what I was doing. I think the primal blueprint is something that really applies to all of us. Within that is the more personalized genetics.
I heard about The DNA Company, and I learned that they have a certification called Functional Genomics and DNA University. If I take my already existing health coaching certification and utilize this to filter it down and figure out the more nuanced components to what people’s health is looking like. I did that. As soon as I started adding in the genetic considerations, my actual results with clients started going way better.
I knew hundreds of things about my clients before I met them by understanding their genetic report. I could see what their genetic insulin response would look like. I could see what their dopamine response would look like. I could see their detoxification pathways, micronutrient pathways, red flags, different ways I could personalize.
FDN came in because I recognized that genes are extremely upstream. They are way up in the rapids. Genes encode enzymes, and enzymes tell the cells how to behave. That’s great as an upstream indicator. I recognized I wanted a way to have windows into the downstream.
That’s where FDN came in because I could really look and have a high-quality set of labs. The genes are suggesting this; it’s showing up this way that I can see with the lab. Everything in between is lifestyle behavior.
I call it alignment with your assignment. Your genes are your assignment. The better we can pull you into alignment with your assignment, the more your physiology starts to heal itself.
Now I am doing this full-time. Functional genomics, really analyzing lab work markers. Being that primal health coach that I already was but with way more tools at my disposal for personalization.
I think functional health is moving in a direction where people don’t want blanket answers anymore. They want real personalized strategies and approaches. That’s what we’ve been building out at The DNA Company. It’s going great so far.
Dr. Eric:
Awesome. How long have you been doing this? When did you get your certification in genomics?
Justin:
It’s been about three years now.
Dr. Eric:
Very cool. It’s definitely evolving. When it comes to genetics, I don’t know if you want to say there is a love/hate relationship. A lot of people find it fascinating and interesting. Some people wonder is it really something- You could change the expression of genes, but you can’t change your genes themselves. Some people feel stuck. “Do I want to look at my genes if I can’t change what’s on a genetic report?” What would your response be to that?
Justin:
Absolutely. We encounter that constantly. This hesitance. People don’t necessarily want to know what some of their genetic red flags are because it’s scary.
The reason why we do functional genomics as opposed to just genomics is I’m a “what do we do about it” guy. The devil you know is certainly better than the devil you don’t know. Once we know the devil, we can start to put strategies in place to work yourself out of it.
Genes really represent hardware. It’s the hardware of your system. They’re static. You can’t change what they are. Epigenetics represent software. You can change that. You can download new apps, and you can upgrade the software.
Our lifestyle behaviors, energy, thoughts, actions is what we have control over. Understanding what that baseline blueprint looks like in the first place allows you to know where you need to put your priorities. It can guide your epigenetic behavior.
For example, we look at genes that are associated with oxidative stress clearance. I have clients with poor oxidative stress, and they are marathon runners. Their epigenetic output and lifestyle behaviors are such that they are creating massive amounts of free radicals and oxidative stress. Now that we know that, we can put some interventions in place to help clear that oxidative stress further. We may actually alter what your lifestyle behaviors are. Maybe we will favor weight training and less high cardio.
We can look at the same thing with regard to macronutrient intake or blood sugar regulation and insulin response. We can tailor your diet, the way you work out, the way you supplement. There are genes associated with sleep. It goes on and on. That’s why we zoom out and take that functional, 360-degree view.
It’s more of an empowering thing than anything. None of the conversations I have with clients are doom and gloom. This is good. We know what’s wrong. We know indicators as to what’s wrong, so we can do something about it. It eliminates that throwing spaghetti at a wall aspect. Now I know the areas of your physiology that need to be reinforced.
A lot of my job is connecting the cellular pathway to the genomic pathway. People show up with symptoms, and it’s important to recognize that symptoms are not the problem; they are the result of the problem.
If I could look at your genes and your genotype and say, “Okay, at a baseline, your cells are being told this, and they’re being told to do this job in a suboptimal manner,” now I know an area that absolutely needs intervention and reinforcement, be that from supplements, lifestyle tactics, etc. We have seen incredible healing as practitioners because we know what that upstream balance really looks like in the genes.
Dr. Eric:
Well said. One of the most well-known genetic SNPs, MTHFR, I have personal experience as a lot of people do. When I saw years ago that I had elevated homocysteine, sure enough, I did some genetic testing and had the MTHFR homozygous CC77T variation. At one end, it’s like you can’t change it. There’s nothing I could do. But knowing I could support it and do things to lower homocysteine, which when you have an elevated homocysteine, there is cardiovascular risk and some other roles, which I’m sure you’re familiar with. You’re the expert, so you’re going to be doing most of the talking.
Let’s jump to the nitty gritty and talk about some of the more key genes influencing thyroid, immunity. You mentioned oxidative stress, which is huge when it comes to autoimmune conditions such as Graves’ and Hashimoto’s.
Justin:
We have whole panels that are associated with various ways your body detoxifies itself. For example, the oxidative stress pathway. There are a couple of genes. The first one is SOD2, superoxide dismutase.
Just to zoom out for a second, within the mitochondria, every second that the mitochondria are creating the ATP that fuels every cell in your body, it’s also creating a byproduct to that ATP. It’s just like when you light a fire, you have to have smoke. Energy creation is the fire, and smoke would be the oxidative stress, reactive oxygen species.
The universe, the good lord, whatever you believe in, also blessed us with a HEPA filter in the mitochondria to clear those ROS. That HEPA filter is SOD2.
The second mover there is glutathione peroxidase. This is also genetically encoded, so there is a gene called GPX. The way that it works is that SOD2 soaps and scrubs the dishes, and GPX rinses them and clears them away.
Understand that what I said there is genes encode these enzymes, and when we know the genotype, we can see what the speed of these clearance enzymes actually are. If you have a CT or TT genotype for SOD2, it represents a reduced clearance. That SOD2 could be slow.
Mine actually is slow myself. I have the TT genotype. That can reduce SOD2 function by up to 70%. Very significant. I’m also an athlete. I’m always creating these free radicals that I know I genetically don’t clear particularly well. This guides the therapy because now I know that oxidative stress is among the things that I have to prioritize.
If I had fast SOD2 and GPX, it would be less of a priority because that job is being done on its own quite well. Every gene represents a job that needs to be done. My genes are not doing that job well. Okay, I am going to add in some clearance factors. I will make sure I’m in the infrared sauna. Maybe I’ll use some peptides like carbon 60. Maybe it’s hydrogen water, added antioxidants. It could be intermittent fasting, anything that improves that clearance rate.
Knowing there is a problem is a good call. Understanding the lab markers, there is one called 8-OHdG, which is a pretty direct marker of oxidative stress and how it’s impacting the DNA. I can also measure it. Know the red flag in the genes, understand markers that you can look at to see how it’s going, and control that middle ground, the energy, thoughts, and actions associated with it.
Dr. Eric:
For example, you said you could measure it. I don’t know if you do the DUTCH test. There are a few different tests that look at that oxidative stress marker, the 8-OHdG. It doesn’t say why you have that oxidative stress. If you have genetic testing, and you mentioned SOD2 and GPX genes, if you have genetic variations in those, depending on the variations, that could mean that you need to do more for the oxidative stress to reduce it, if I’m understanding you correctly.
Justin:
Yeah. At The DNA Company, the panel we landed on, we are only really testing for a couple hundred genes, which is a very small segment of the actual genome. Understand here that genome sequencing, the more SNPs that you look for, the more expensive the test is. The more you look, the more you have to pay.
Also, many of these genes are not fully hashed out, and they are not necessarily actionable. We use something called the DNA 360, which was really wound down to the main genes associated with the main systems of the body that deal with inflammation and detoxification, sex hormones, executive function (dopamine, serotonin, etc.). We whittled it down into systems that are meant to be applicable to the general public. We’re not zooming in on really specific genes associated with conditions, but the genes we do look at when you zoom out are applicable to all of it.
If you have a thyroid condition or MS or whatever, it still matters the way your body detoxes. It matters the way your body deals with inflammation. It matters how you methylate, MTHFR, etc. it’s applicable to the general pop because health problems can be manifestations of upstream issues. We’re looking as far upstream as it gets to understand baseline encoding processes that suck or don’t suck in your body. That’s what we do. We like to work forward from the genes as opposed to working backward from the symptomology.
Dr. Eric:
I do have a question. I’m not sure if you can answer this. With relation to estrogen metabolism, two of the bigger genes here are MTHFR and COMT. I don’t know if there are others related to estrogen metabolism that are important.
Justin:
We have a whole sex hormone pathway, the steroidogenesis pathway. A lot of the genes in there come from a family of enzymes called CYP450. It’s a step-by-step process as you know.
What we do is we look at the initial step of progesterone converting to testosterone. That’s done by a gene called CYP17A1. The speed of that enzyme really dictates what’s called dominance. If you have a heck of a lot of that initial testosterone conversion right off the bat because of this CYP17A1 enzyme, that creates what we call dominance. You get that bigger pulse as soon as you hit puberty. That is the first step there that we look at.
From there, we can actually see if the testosterone is androgenizing, which means it’s converting to DHT from a gene called SRD5A2. How much of that testosterone is aromatizing via a gene called CYP19A1? We determine if you are more dominant in the first place. Once we establish that, are you more androgen or estrogen dominant?
From there, the pathway goes even further. Now we start looking at metabolites of the estrogen. We can actually see genetically based on the enzyme pathway what the conversion rate is to things like 2-hydroxyestrogen, which is quite protective to the body, or the inflammatory 4- or 16 alpha-hydroxyestrogen. We can see how that pathway looks.
Let me say if there are any practitioners in the audience who do HRT, endocrinologists, etc., it’s a really good idea to understand these enzyme pathways before you prescribe hormones. Whether your body made the hormone or you took it in exogenously, the enzyme pathway is still going to steer what that ultimately looks like. If you add in estradiol or something like that, you will want to know how much 4-hydroxyestrogen is taking place. You may need to add in an intervention, some DIM or sulforaphane to protect from the estrogen toxicity.
Dr. Eric:
If you do a DUTCH, it will show those metabolites that you just mentioned. Again, it’s not necessarily telling you why you might have excess 4-hydroxy or 16 alpha-hydroxy.
I don’t know if you use the DUTCH test or how familiar you are with it. It gives an indication of low methylation. If you have low methylation, and I have seen this before, and your homocysteine looks fine. I know it’s not perfect. There are other ways to determine methylation.
If you look at a DUTCH test and see low methylation, elevated 4-hydroxy or 16 alpha-hydroxy, and again, homocysteine looks good, does that mean that there might be something else causing problems with methylation? Or is the test not accurate in saying there is low methylation when it says that?
Justin:
We actually also have a full panel for methylation. I always preface the hormone conversation with the methylation conversation to make sure we are supporting that cycle to the best of our ability.
The DNA Company differs a little bit from these genetic testing companies because MTHFR is just one gene in the panel that we look at. There are actually several genes in the panel. You mentioned COMT; that would be one of them. There is SHMT1, methionine synthase, methionine synthase reductase. It’s a whole step by step pathway.
What we do is look at the different enzyme speeds within the methylation cascade. We look at how we support it. Some people don’t do well with methylated vitamins as you know. A lot of that has to do with if you’re kind of at risk of overmethylating. Some people under, and some people over.
We always make sure that we’re supporting that cycle with our targeted therapies, different types of B vitamins. Some people need sublingual formats; some don’t. Some people need the support of the methyl group; some people don’t. We make sure that the methylation cycle in and of itself is being supported prior to talking about things that are being methylated, like hormones. Again, we zoom out. It’s a whole 360-degree viewpoint. We get the detoxification working as well.
Let’s say you have liver congestion. That’s going to impact your body’s ability to convert hormones. There’s some liver dependence with thyroid as well. If your liver is all messed up, and you won’t get proper T4 to T3 conversion because so much of that happens in the liver as you know, we look at it all. We are treating the whole body instead of treating one thing at a time, if that makes sense.
Dr. Eric:
Yes, it does. I have a newsletter, Healthy Gut, Healthy Thyroid. Are there any panels that The DNA Company offers that relates to optimal gut health?
Justin:
Yes, we work with a company called Jona. They get our Gut 360 Premium test. That would be like the stool test that we look at.
Within the genes, there is a really important one that has some correlation to things like Hashimoto’s, Graves’, etc. We have a panel that is glutathionization.
One of the things that’s really cool about what we do is we don’t just test for SNPs. Most genetic companies do what’s called SNP testing, single nucleotide polymorphism. It’s like a spelling mistake within the gene. We look at other stuff as well like copy number variations (CNVs), indels, and deletions. There are different types of genes as well besides SNPs. Some of the most important genes we look at are CNVs. How many copies did you get from your parents? You can have zero, one, or two copies.
There is a particular gene that I look at in relation to autoimmunity called GSTM1. It’s associated with glutathione at the level of the gut microbiome. If you’re not familiar, glutathione is a very important part of phase two detoxification.
What we’ve found clinically is there is a sweet spot genotype for GSTM1. If you have zero copies, like yours truly, it means you don’t detoxify well at all at the level of the gut. You’re literally missing one of the primary detox genes.
One copy is actually appropriate. If you have one, you’re detoxing well, but you won’t overdo it.
Two copies, we have found significant clinical correlation with autoimmunity. It’s almost like your gut is too good at recognizing things as enemies. It incites that immune response when you take in something that it doesn’t look like. That could be glyphosate. That could be a food sensitivity, gluten, if you’re sensitive there.
A whole lifetime of that immune response being kicked off, that’s what tends to wear away that mucosal barrier. You end up with a mucosal injury, so-called leaky gut. You and I both know that leaky gut is a major factor when it comes to all things immune system related. 80% of your immune system lives in the gut.
Once that starts, that’s the beginning of Hashimoto’s. It could be RA, eczema. A lot of people with two copies of GSTM1 end up having that as an issue. There is some pretty strong connective tissue there between Hashimoto’s, Graves’, etc.
Dr. Eric:
How about caffeine? To determine if you are a slow and fast metabolizer of caffeine?
Justin:
I mentioned the CYP450 family of enzymes. There is one called CYP1A2. It’s actually a phase one detox enzyme as well. That’s one of its main jobs. Phase one detox being taking fat soluble toxins, changing them around to make them water soluble, so your body can get rid of them with phases two and three.
It also metabolizes stimulants being caffeine, ephedrine, kratom, whatever you people are doing. That’s one of the main things that it does. If you have a faster genotype there, it means your body rapidly works through the caffeine.
There are pluses and minuses. Genes are never good or evil; it’s a context-specific thing. I have a fast CYP182. If I have caffeine, I can have it later in the day without it disrupting sleep. It takes a while for other people to work through it. It can be disruptive of circadian rhythm and things like that.
It’s an interesting thing that we look at. I usually get people to do caffeine cycling if they are slower for CYP182 to make sure they are not messing with their sleep.
Dr. Eric:
I am a fast metabolizer as well. Unfortunately, I don’t drink coffee. I do drink green tea. I can’t say I take advantage of drinking coffee late at night.
Justin:
It’s not necessary, but it’s one of those things that a lot of people are into, myself included.
Dr. Eric:
How about some of the genes tying into weight loss? There is a lot of interest there with GLP1s. How do genetics and testing tie into that?
Justin:
There are quite a few genes of relevance there. It’s almost like what gene doesn’t matter when it comes to things like weight loss and ideal body composition?
We have a whole executive function panel as well that looks at the dopamine pathways. If you have a high binding of dopamine, you’re a lot more likely to have binging or addictive behaviors.
We also have a whole diet and nutrition panel that looks at things like satiety signaling, ideal macro and micronutrient synthesis. We can see genetically speaking if you will do well metabolizing starches versus lipids. We have a great gene called TCF7L2 that is a tremendous indicator for insulin response. Some people are genetically dysregulated for insulin, and they can have 1.5 greater times insulin response when they take in an energy dense meal. That matters for blood sugar management.
With regard to the GLP1s, it’s interesting. There is a gene called fucosyltransferase, FUT2. We include it in our methylation panel because it has a secondary job of being a transporter gene for Vitamin B12. Cobalamin is unique in that it’s the only micronutrient that does not get passably absorbed into the gut. it requires the secretion of an Uber to get through the gut lumen. FUT2 does that.
It also has a significant impact over the microbiome. It influences short chain fatty acids, which influence GLP1 production in the first place.
If you’re what we call a nonsecreter, which means you have an AA genotype of the FUT2 gene, it means that you’re not creating a heck of a lot of those GLP1s in the first place. These are the people who tend to respond a little bit better to taking GLP1s because you’re overriding the mechanism by taking a peptide and injecting it.
GLP1 response is determined by other stuff as well. I typically don’t recommend stuff like that. If so, or if a client comes to me who is already taking it, I will also look at things like their glutathione profiles. If you’re suboptimal for glutathione, you may be the one who gets nausea and an upset stomach.
Understanding your detox pathways, your insulin response, your macronutrient response, then your satiety pathways. We look at a gene called FTO, which works on the gut-brain axis, that bidirectional circuit of your gut communicating with your brain.
When you start chewing food down, there is a signal that is supposed to go from your gut to your brain, saying, “We’re all set, mate. You don’t need to keep eating calories.” For people who have dysregulation in this FTO gene, it’s a much slower signal. By the time it hits your brain, you’ve already gone back and had the second or third portion.
We look at it from several different angles as you can imagine. It helps to guide therapies, how we do it. For some people, you need to prioritize detox. For some people, it’s more of a cognitive binging problem. For some people, it’s gut health related, insulin response related. Just knowing the genes, it helps you to guide what that therapy looks like. It helps you be more detailed with your intervention.
Dr. Eric:
In that example, if you have a genetic variation of FTO, as far as intervention, it sounds like you have to look at some of the other genes as well to determine which direction to go.
Justin:
Yeah. Being a health coach, I’ll recommend everything from an appetite suppressant, like a ketone ester, to a gratitude practice before your meal to help you get in that receptive, parasympathetic state, all the way to chewing your food properly. That will help speed the signal up.
How many people are not chewing their food down? Their saliva isn’t changing the pH and aren’t getting that signal moving quickly. There are many tactics that you can use to health coach them out of it. This is why this person has difficulty not going back for the second and third servings. There is a genetic element. We just coach them out of that as you would with anything else.
Dr. Eric:
Does the panel also look at markers related to histamine?
Justin:
We have a bunch of new genes being created in there. Among them are the DAO enzyme. There are a few genes relative to that. We will be looking at histamine genes in the near future, like in 2026. It hasn’t completely rolled out yet. That’s a sneak peek for you guys.
I do consider histamine as well with any genes that impact the HPA axis. Some people for example, even if you have a really bad anxiety response, which we do look at genetically within our adrenaline pathway, you are a more cortisol dominant person more likely. We know when the HPA axis gets kicked off, the mast cells will release proinflammatory cytokines, histamine, and tumor necrosis factor alpha, etc. We look at it a little bit more indirectly, but it will be more direct shortly here with the DAO enzyme genes.
Dr. Eric:
I’m sure there are many other genes you could talk about. Let’s talk about any health condition, whether it’s thyroid-related, autoimmune thyroid-related. You look at all the different systems. All these are relevant in some shape or form.
How about bone health? Are there any genetics that relate to bone health with The DNA Company?
Justin:
I would say the most relevant ones would be the Vitamin D pathway, Vitamin D being quite important for such a thing. Practitioners even now are a little bit too linear in their recommendations for Vitamin D. They give an IU dosage and maybe base it on body weight.
We have a whole pathway associated with Vitamin D. As you know, it’s more of a hormone than a micronutrient. You’re not getting so much of it from a dietary pathway as you are a hormonic pathway.
There are three genes involved. We have just added a fourth. When you get sunshine on your skin, your body doesn’t make active Vitamin D, D3. It makes a precursor to D3 called D2. D2 is inactive and has to be converted to D3 in order to exert its influence over the cells.
There is an enzyme encoded by a gene called CYP2R1. There is that CYP family as well. That’s what does the initial conversion.
Once it’s active in its D3 useful format, the second gene takes over, GCVDBP, Vitamin D binding protein. VDBP is the Uber that takes the now active D3 to the receptor site. You can be suboptimal for both of these genes, none of these genes. That guides dosing protocols.
The third gene that we look at is the receptor itself. It’s simply called VDR, the Vitamin D receptor. I look at that being like the bouncer at the nightclub. He is letting the Vitamin D in. Some people’s bouncer is a hardass. He’s not letting people in very well. The other people have a bouncer who is texting and is like, “Yeah, get in there, whatever.”
That guides how you go about your dosing. Some people don’t do well with a large Vitamin D dose in one go. You can take 5,000-10,000 IUs. If you have suboptimal delivery, you’re not going to get it into the receptor, and it won’t do its job until it’s in that receptor. That would mean that you need to take smaller doses, but you better space it out by a couple hours because you’re effectively putting more people in the line to get into the nightclub.
Dr. Eric:
Very interesting. If someone is taking 10,000 IUs of Vitamin D, which is a decent dose, not that practitioners haven’t recommended higher doses, but you wouldn’t want to continue taking 10,000 IUs of Vitamin D indefinitely. Someone takes 10,000 IUs for a couple of months, and they do a 35 hydroxy Vitamin D, and it’s still not optimal.
Even taking into consideration genetics. I have thought about that, too. I am not familiar with all the genes you mentioned, but the VDR, I am. Logically, you would think, “Well, maybe you have that genetic polymorphism, so you’re one of the people who need more. Maybe you need 15,000 IUs.”
What you’re saying is that may backfire because you don’t want to give that all at once. Maybe the problem is that they’re just taking it all at once when you should space it out. Don’t even need 10,000. Maybe you can get away with 6,000. Make the math easy. 2,000 IUs three times a day.
Justin:
It’s a protocol problem, not a volume of Vitamin D problem. You’re right. The first place any practitioner would go makes sense. You need more; let’s up the dose. A delivery problem is what’s actually going on there.
There are risk factors as well with taking massive amounts of Vitamin D that is not being absorbed. Especially if you are doing it in the absence of K2, we know there is such a thing as Vitamin D toxicity, and it can calcify in the arteries.
One thing I look at when I go about this Vitamin D dosing protocol is I look at their APOE gene. Everyone knows about this, just like MTHFR. If you have a 4 allele in APOE, which by the way I have a 4 allele, it makes it so there is a stronger likelihood of calcification of your cholesterol that will go on within the endothelium of the body.
If you have a 4 allele, and you think it’s a good idea to take massive amounts of Vitamin D3 without any K2, you could create a cardiovascular issue just like that, or amplify a cardiovascular issue, which proper Vitamin D can help the cardiovascular issue. It’s anti-inflammatory. You’re boosting your immune system.
This is where the genes are valuable. It can allow you to guide interventions and protocols and avoid mistakes. I’ll tell ya, even with the glutathione pathway, if you’re suboptimal for all of your glutathione genetics, understand that genes are like little instruction manuals. If you’re not detoxing well, a lot of well-informed practitioners will give you a big dose of glutathione, thinking it’s ideal to raise that up.
If you’re missing the instruction manual internally for what we do with the glutathione, now we have given major amounts of a substrate that the body has no instruction for what to do with. Instead of binding to toxins, it might just go bind to something else, like minerals. We have seen that. People deplete their mineral reserves because they are taking IV glutathione and are missing the genes for what to do with it.
Functional genomics in my opinion is a layer of personalization. I recommend it for absolutely anybody. If you’re a personal trainer, a nutritionist, why wouldn’t you want to know your client’s insulin response? It only makes sense if you’re a cardiologist and don’t understand the APOE gene, the nitric oxide genes.
There is a gene called 9P21 that translates to the density and toughness of your endothelium. Some people genetically are a lot thinner and weaker there. When you have inflammation, there are these micro tears that happen along the lining of that endothelium, and you will want to know that as a practitioner. Do they have rhino lining, as the endothelium? Is it plastic, saran wrap? You want to know these kinds of things.
Any practitioners in the audience, you can take what your already existing practice is, utilize functional genomics as a filter to know “I better not prescribe that, so I should go this route.” It’s a way of dialing it in that much further. I have seen significant results with many people.
Dr. Eric:
If I asked a question which you just answered, who should consider getting genetic testing? The answer probably would be everybody. If I reworded it to say is there anybody who should not consider genetic testing, would you say the answer would probably be no?
Justin:
I’d say anybody who doesn’t want to be healthy, you can avoid it. I hate to be this guy and be so adamant about it because not everything is for everyone.
In the case of genes, especially the way we do it, because we really highly prioritize cybersecurity, we won’t sell your stuff to Bill Gates. The day that happens is the day I’m no longer associated. The samples are destroyed. Everything is protected. It will give you a 360-degree view of what your genes are. We are not testing nine million SNPs. We are testing 200 things that are clinically relevant for what your health picture will look like.
I will say there is something called subclinical. That means before the problem shows up. I try to get people in that subclinical zone, before they’re actually having a disease manifesting. If you’re a child, or you’re a young person or someone who is interested in health, you really should know what your blueprint looks like. You can establish the highest quality epigenetic environment that way, by knowing what the weak points are.
If you give your body the best quality information, understanding what that blueprint looks like, you can establish high quality methylation patterns early on. Your body is going to be strengthened in any number of ways.
We even look at a gene called brain derived neurotropic factor, BDNF, which is a Miracle Gro for your brain. We know if you have genetically suboptimal BDNF, or your kid does, you may not want to put them into football or something where they may be taking a lot of shots to the head. They may do better on the golf course. We know that concussions require BDNF to help recover. It can even guide different lifestyle stuff early on.
If you know that your kid doesn’t process Vitamin C very well, there is a gene for that, SLC23A1. This is the kid that is going to do better if we incorporate more of that into their diet. Just that guidance and providing the ideal epigenetic environment, you will know what to do once you know what the blueprint looks like.
Dr. Eric:
This has been awesome. Anything else you’d like to discuss before we wrap up? Anything I should have asked you that I didn’t ask you?
Justin:
I think this was great. I think you asked all the right questions. I believe it was Reed Davis who said, “The general principles of health building always outweigh specific treatments.” As a health coach, I operate in that realm. I try to treat the whole body holistically as opposed to zooming in on one symptom over another.
There is this concept in personal training called moving from general to specific. You start with general exercises. If you’re a golfer or something, you get more into rotational exercises. You get into the specified zone once you have covered all of your basics. Provide your body with high quality epigenetic signals. That’s all your body understands: how to take in information, methylate it. You end up with what’s called an acquired phenotype based on your lifestyle behaviors.
Living a healthy lifestyle is a great start, but then you can use the genes to personalize that healthy lifestyle. It’s not the same for everyone. We’re all beautiful, unique snowflakes, including yourself, Dr. Eric. I don’t mean to call you a snowflake; you’re not a snowflake, but you know what I mean.
That’s what functional genomics offers. It’s an exciting area that will help revolutionize functional health.
Dr. Eric:
Thank you for this. Where can people find out more about you and The DNA Company?
Justin:
The DNA Company is at TheDNACompany.com. We also have a YouTube page where we upload the DNA Talks podcast as well as weekly webinars. I actually did all three of them this week, which was a lot of public speaking. We cover different topics, and we also plug it through that filter of functional genomics.
I have Instagram, @JustinHarrisOfficial. That’s where you can find me.
I hope we maybe do a round two sometime. This was great.
Dr. Eric:
I agree. In the future for sure. They are always adding genes to the panel, so I’m sure we will have more to talk about in the future. This was awesome. Thank you so much, Justin.