In this episode, I am speaking with Joe Cohen – who is the founder of SelfHacked, SelfDecode, an author, and speaker and has specialized in genes and biohacking. We will talk about the science on COVID-19, genes, supplements, and biohacking.
Joe has compiled a free ebook with his tips on how to fight COVID.19, you can get it here.
Table of Contents
In this podcast, Joe will cover:
- What the research on COVID-19 has taught us so far
- The best supplements for preventing infections
- Does melatonin help prevent viral infection?
- The most common causes that can trigger a severe infection (and the best action to eliminate these)
- How to use biohacking to prevent infections
Listen or download on iTunes
Listen outside iTunes
Ari: Hi everyone. Welcome back to The Energy Blueprint Podcast. I’m your host, Ari Whitten, and today I have with me my friend, Joe Cohen, who has a very funny bio. I’m going to read it to you right now. It says, “Joe Cohen won the genetic lottery of bad genes.” [laughs] That’s quite a way to start off. He said as a kid, he suffered from inflammation, brain fog, fatigue, digestive problems, anxiety, depression, and other issues that were poorly understood in both conventional and alternative medicine.
Frustrated by the lack of good information and tools, Joe decided to embark on a journey to explore the information contained within his own DNA and lab results to improve his symptoms and optimize his health.
With thousands of experiments and PubMed articles under his belt, Joe founded SelfHacked, the content resource that was missing when he needed it. He also founded SelfDecode and Lab Test Analyzer to help decode his genetics and lab tests.
Now Joe is a thriving entrepreneur, author and speaker continuing to live out his mission of helping people optimize their health with the most up-to-date, unbiased and science-based content and tools. Welcome to the show for the second time. Nice to have you back.
Joe: Thank you for having me, Ari.
What the science on COVID-19 has taught us so far
Ari: Obviously, you’ve got a background in– You started off for several years with SelfHacked, which was about bio-hacking. You then got into SelfDecode, which is a massive resource that I know you had a giant team of employees put together to put together all this research on genetics, and basically created this analyzer to analyze people’s genetics, paired that with trying to piece together this full body of research on, whether you’re at increased or decreased risk for all kinds of conditions in relationship to these genetic markers. You formed over the last several years, a lot of expertise around genetics as a result of that.
In this podcast, we’re going to talk about COVID-19. We’re going to talk about your take on the situation in a more general sense. We’re also going to talk about genes, we’re going to talk about supplements and your protocol as far as what you’re doing.
To start off with, let me get your take on the big picture of what’s going on with COVID-19, this pandemic, and your sense of the severity of it. We can talk some specifics from there.
Joe: Okay, definitely. There’s obviously a lot of disagreement on what is the fatality rate, so how likely someone to die. I think there’s people that are very scared, and then there’s people who are saying that it’s like the flu. There’s a lot of experts that have different opinions as well. I’ve done my own analysis just out of curiosity, because I want to see if it’s something– I’m not a person who freaks out about things. I look at the data and I say, “How concerned should I be about this based on the data?”
Obviously, there’s nothing set in stone right now, because they haven’t done high quality studies, looking at how many people actually have it in the population. You don’t know that because you don’t know how many people are asymptomatic. You only really know how many people are going to the hospital or going to the doctor and most of the time, the doctor won’t even check you.
We know that a lot of people are not being checked and we see fatality rates at 12% in Italy, right? [chuckles] They’re obviously not checking a ton of people. We don’t see that many low fatality rates, because a lot of countries are really not checking a lot of people.
There was one study that really interested me, that they looked at just the number of people who were on the Diamond Princess cruise ship. Since they tested everyone on the Diamond Princess cruise ship, it’s very interesting, because now we know what the denominator is, as they call it. We know the total number of people who had it on that ship. They didn’t miss anyone. The tests are pretty accurate to detect people and so they know-
Ari: Just real quickly explain the numerator and the denominator issue to people, what those numbers actually are.
Joe: Okay, definitely. The numerator is the number of people who die from COVID-19. If we’re looking at fatality, let’s say it’s one out of 100. The numerator is one, out of 100 is the denominator. That’s 100 people, the denominator, who got COVID-19 or got the Coronavirus and then the numerator one. If it’s one who died out of 100, that is a 1% fatality rate. If it’s 200 people that got it, all of a sudden it’s a half a percent fatality rate. If it’s 1,000 people, it’s 0.1%.
Ari: Assuming again, you still have that one person who’s died.
Joe: Yes. Right. Of course. You have the one person. It’s just a fraction, so I’m just using the simplest numbers. One out of 1,000 is basically how many people are dying from the flu. Initially, it seemed like one out of 100 were how many people were dying from this thing. There was an interesting study that came out, because I didn’t– I was like, “I don’t really trust any of the numbers, because there’s not enough information.” I still don’t trust any numbers, but the best number that we have-
Ari: Just to be clear, it’s not that I don’t trust the numbers, it’s that I just think the data is very limited right now. I’m not suggesting there’s a conspiracy or anything like that.
Joe: That’s a good qualification. [laughs] As in trust the estimates of what people are saying it is.
Joe: Yes, but essentially, what I wanted to do is, I looked at– The best data I saw was the Diamond Princess cruise ship, because that happened early on and it was a fixed number of people. We’re talking about 712 people on that cruise ship. It was around 20%. They tested everyone. That’s how many people had it. It was around 20% that didn’t feel any symptoms when they tested them, because they tested them early on. It was around 50% but then, I think eventually, it was around 20% that didn’t feel any symptoms. As of now, there was 12 fatalities and there’s 10 people in serious condition. Critical serious condition, that usually means ICU and it could be 50% of them are not going to make it. It’s hard to say.
Ari: Quickly recap those numbers. How many people were on the cruise ship in total?
Joe: Around 3,700. Yes, something like that.
Ari: Okay, and about 700 were positive for COVID-19?
Joe: 712. Yes.
Ari: Okay. What’s the percentage of-
Joe: 12 people died. If you do 12 divided by 712, right now that’s a 1.7% fatality rate. You’re assuming that, let’s say, this is an unknown, maybe two more people are going to die, we’re at 2% fatality rate.
The reason why these numbers are a little problematic is because this is an older population who’s also spewing male and both of those groups are at risk or at higher risk of complications and dying from Coronavirus. You don’t really know.
There is a study who adjusted for certain things and they also looked at the number of people who were repatriated. That means that they went to their host country, and so a lot of countries were testing people who came back, if they came from, let’s say, Wuhan, China. That’s also a good number because they were testing everyone, even if you didn’t have symptoms. They looked at basically everyone who they were testing, whether they had symptoms or not. This was published in The Lancet on March 30th. They adjusted for things and they found that the fatality rate in a normal population would probably be around 0.66%, which is around six and a half times more dangerous than the flu. Even the CDC says that the fatality rate is somewhere between 0.25% and 3% and it’s probably on the lower end.
Ari: I think that that matches up well with a lot of what I’ve seen the infectious disease experts saying.
Joe: Yes. I think we just need to get that out in terms of, how dangerous is this thing? Six and a half times as dangerous as the flu is not something you should freak out about, but it’s also not nothing. It’s not just the flu, but okay. That’s done. I think the next thing we want to think about, and this is something that was really fascinating is, who’s at risk?
Ari: Actually, before we get there, just a couple of points. I don’t know if you saw the Iceland data, but I found that really interesting. They seem to be the only country that’s done widespread testing of the general population and not just symptomatic patients. Just for clarity, The Diamond Princess cruise ship is a great piece of data and I agree with you on that point. So much of the other data is, I don’t want to say nonsense, because it’s too strong of a word, but it’s extremely limited in terms of how we can extrapolate it to form predictions or how well we can draw the mortality rate figures from it. The reason why is selection bias, that the testing kits, speaking specifically about the US, the amount of testing that’s going on is not being applied to the general population, it’s being applied only to, in general, the most symptomatic people. Even people who are showing up at the hospital sick and saying, “Please test me,” in many cases are being turned away. They’re only using the tests on the people with the most severe symptoms.
As you said, the numerator is the number of deaths. Even that’s somewhat of a question because of reporting. There’s some questions of reporting there. It’s maybe too much of a digression to get in all the details of how that number is limited, but let’s just say it’s 100% accurate. The denominator number now has this huge selection bias issue because it’s saying the deaths from the portion of people that have the most severe symptoms, instead of the deaths from the general population. When we know that this condition seems to manifest in a mild or asymptomatic way for about 50% of people, and then moderate symptoms or below for something like 85% of people. There’s just this huge issue of what you’re comparing the number of deaths to in terms of that denominator.
Iceland has done a really good set of systematic tests of the general population, and what they determined is that– I think the numbers were, at the time of testing, which was maybe a week ago or something like that, it was something like 1,300 cases of their entire population, and maybe less than 10 deaths, if I’m remembering correctly. 10 deaths in that proportion of people would be– I think it might have been less than 10.
Joe: Six people?
Joe: The problem with that is, you have to give it time because this obviously goes up a lot.
Ari: It can, but there’s a number of people that have already had this and recovered from it. It’s spreading. It’s unclear where at the point we are in the curve of growth of this, but anyway, I think they found that something like 0.5% of the entire population had this. There were five or six deaths as of the time of when we’re recording this. If you extrapolate similar numbers to the United States, that would mean that instead of the reported number of cases, which is something like 180,000 I believe, or 200,000-ish. The actual number of cases is something like– If that 0.5% of the entire population holds, it might even be much higher than that, because there’s probably a lot more travel between China and the US than there is between China and Iceland. Let’s say it’s 0.5%. That would mean it’s not 200,000 cases of this, it’s more like 1.5 or 3 million cases in the United States.
Joe: That would be reasonable.
Ari: That number as the denominator obviously changes the fatality rate by orders of magnitude. That’s really the question of why the state is so limited right now.
Joe: Yes. That sounds reasonable. There’s definitely a lot of people they’re not testing. I heard the Iceland statistic on the talk that you sent me, but I wasn’t able to find the study. The other thing is that, since it’s early on, people are dying basically two, three weeks later, so that’s also a little bit unclear. What is going to be the end fatality rate? They’re doing more studies, but we’re going to get an understanding later on.
Ari: You want to shift now into who’s at risk, and what’s your analysis of the data as far as who’s very likely to experience severe symptoms or death from this? I know you alluded to a couple of points as far as age, male gender and so on, but what’s your analysis of that situation?
Joe: I’ve been reading a lot about this in order to understand what are the supplements or things we could do to prevent risk from it, to decrease risk from it. What it comes out, what I’m able to see is that one of the biggest risk factors is cardiovascular disease. I have friends who are doctors in the hospital and they told me the cardiovascular disease patients were really getting hit hard.
There’s one study that shows that out of the people who are hospitalized, so these are already serious people, out of people who are hospitalized in China, 15– It was a study done on something like 100 and some odd people. There were 15 of them cardiovascular, 13 of them didn’t make it.
There’s cardiovascular disease, there’s hypertension, there’s high blood pressure, there’s diabetes, there’s obesity, and then there’s lung diseases, respiratory diseases, COPD, asthma. These are not really controversial. There’s smoking. Like you said, there’s age and being male. They think being male’s a risk factor because males drink a lot more and smoke a lot more.
Ari: Is that the only reason? I was under the impression they were almost suggesting something to the effect that estrogen might be a protective factor for cytokine storms or something to that effect.
Joe: Yes, of course. There’s other reasons as well, but some of the biggest reasons have to do with alcohol and smoking. It’s unclear. It hasn’t been–
Ari: Because we’re men and we like to get drunk.
Joe: It’s a fact that men, I think, they drink five times more than women. Yes, it’s something to that effect, and they’re more likely to smoke, and if they do smoke, I think they smoke more. This is another unknown, it hasn’t been teased apart.
There’s some people saying estrogen is probably a combination of factors, but when you’re looking at things like alcoholism or smoking, these are obviously huge risk factors for COPD. That’s a lung disease, a respiratory disease. COPD is a huge risk factor for having complications, so you’re up to five times more likely to have complications if you have COPD. They think that the age has to do with the immunity, because the older you get the worse your immune system works, generally speaking.
The role of melatonin in inflammation
Ari: There’s some suggestion of melatonin being a factor there, related to age, that melatonin might be this extremely powerful anti-inflammatory agent. I forget the specific name of the inflammasome. It’s a bunch of letters and numbers mixed together.
Joe: NL something. Starts with an N.
Ari: Yes. Melatonin apparently acts on this inflammasome and helps suppress cytokine storms. There are some people also suggesting that supplementary melatonin may help prevent cytokine storm in severe cases.
Joe: I read what you were talking about, and it turns out that that inflammasome is pretty much inhibited by any natural supplement. Not that it’s not true, it’s just that there’s a lot of things that can inhibit that inflammasome.
Ari: To focus specifically on melatonin, you think is misguided?
Joe: I think it’s an important thing if you’re not getting enough of it. If you’re sleeping with the lights on or if you have light at night and you don’t wear blue blockers or things like that, then it’s an important thing because you’re not getting enough melatonin.
I don’t want to say it’s not important, but I think saying that it’s particularly important for this, just based on that inflammasome research, I wouldn’t say that’s the case. A lot of things are going to inhibit that inflammasome. There’s a lot of natural supplements and herbs that have pretty anti-inflammatory profiles, and they also act on that inflammasome. I’m not saying it’s not good or whatever, it’s just I haven’t seen research that’s specifically good for this.
Getting into what we were talking about, the risk factors, when you look at all these risk factors, besides being male, you can pretty much counteract– Having diabetes is a disease that– I don’t know any healthy people with diabetes. Hypertension, it’s something that if you’re living a healthy and optimal life, you should not have hypertension. You should not be obese unless you’re– If you’re obese and you’re trying to be healthy, you’re doing the wrong thing.
The most common underlying causes of severe COVID-19 infection
Ari: All of those diseases you mentioned up until you mentioned COPD and asthma and some of the lung specific conditions and smoking and things like that, but hypertension insulin resistance diabetes, cardiovascular disease, this is all part of a cluster of really the same cardio metabolic dysfunction that comes from the same nutrition and lifestyle factors. They can even manifest slightly differently for different people, but we know it’s very, very much nutrition and lifestyle related.
Joe: COPD is also a lifestyle disease. Asthma, I believe, is also to some extent, less than the others, but it is also to some extent, a lifestyle disease more than certain other things. More than cancer, I would say. Everything to some extent, you could reduce your risk. I’m not saying [unintelligible] I’m just saying there is a spectrum of things that– Diabetes is going to be something that you’re not getting unless you are living pretty unhealthy.
When I look at these things, what’s clear is that the cardiovascular system is really important. The immune system is really important and the respiratory system is really important. These are fundamental systems in the body and it’s really like almost a general health thing. How generally healthy are you? If you’re generally healthy, you’re not overweight, you’re not obese, you don’t have COPD, again, that’s a lifestyle disease pretty much, and you don’t have cardiovascular disease, high blood pressure, your risk is dramatically lower. In that case, you really should not be that worried.
Ari: Just to add one layer of data, going back to the data we were speaking about before, but on the mortality rate. I believe there’s some data out of Italy showing that 99% of the deaths have been over the age of 60 or 65 and have at least one comorbidity like diabetes or hypertension or heart disease.
Joe: Yes, I’ve seen that as well. Exactly. There are young people dying as well, and sometimes you read new stories that somebody was healthy. What they mean is that they weren’t outwardly unhealthy. They weren’t obese, they didn’t have cardiovascular disease. When you’re young, you’re much less likely to have– It’s very rare to have a heart attack when you’re young or have some cardiovascular disease when you’re in your 20s, even if you are doing things that are harming it. It’s very hard to detect your overall immune system, so they’re not able to detect actually how healthy these people are.
Ari: Right. One anecdote on that front. I was having a conversation with a friend of mine, and speaking about the same thing that we’re talking about now. She said, “I know a 17 year old in my daughter’s high school who’s on a ventilator right now. Young, healthy.” A few days later, she let me know he actually has a big vapor, so he likes to vape a lot. Just like smoking, that seems to be another potential risk factor here.
I do think that one other element here which is scary and really unfortunate is the viral load issue, and I’m starting to see more articles talking about that. This is especially relevant, I think, to the people on the front lines. The doctors, the nurses that are treating patients who have this are potentially being exposed to a much larger load of this virus. In those scenarios it has a much higher potential to take down somebody who is young and healthy.
Joe: Yes. That gets to another point which is, how are people actually dying from this thing? It turns out that if you look at what’s going on, even with conditions, what are people actually dying from? Usually, it’s from something called ARDS. It’s acute respiratory distress syndrome. Also, it’s a related thing called cytokine storm.
What’s happening is that if the virus overwhelms your system and then you have– Your body and your immune system is not good, so now your virus has just taken over your whole system. The viral load is increasing a lot because your first response of the immune system, which is less damaging–
If you want to think about it like this, you have two big responses in the immune system. You have the first response that is not so damaging. It doesn’t do a lot of damage and your body prefers to use it. If that works, then it doesn’t have to resort to secondary emergency measures.
What’s happening with old people is, if the immune system is not good enough, the viral load gets too high and then they have the emergency system come in. This is stuff that the top experts are saying. It’s not something that I’m just putting it together.
Then you have the cytokine storm. The cytokines are basically these inflammatory proteins that are very damaging. They are good at taking down infections, but they’re very, very damaging as well. If you have too much of it, it can basically shut down the system. Since the virus really hits the lungs very hard, if it replicates too much in the lungs, the cytokine storm will cause acute respiratory distress. There’ll be so much inflammation, there’ll be fluid that comes into the lungs. It just shuts down the lungs, then you need to be put on a ventilator. That’s also why people die from the flu as well.
Once I started reading about it, it was like, “Why didn’t I pay more attention to this before?” because it’s actually something that is pretty serious. Once you get that, the mortality rate, the chance of dying is up to 50%. There’s not much you could do once you already get that. It’s like at that point–
They did a study on vitamin C. A very, very high dosage vitamin C, intravenous, and that did have some positive effects. There is limited things you can do once you get there. What we’re doing is, we’re looking at genetics that are basically increasing your risk of this ARDS, the cytokine storm.
Ari: Real quick, Joe, before we move to the genetics piece, I’m curious if you saw this video from an ICU doc in New York that just came out, I think in the last two days. It’s about a five minute video. I’m forgetting the guy’s name offhand, but basically, he’s saying he’s operating in an ICU unit, treating COVID-19 patients and he believes that they actually have it wrong and that this is not quite the same ARDS that they see with, for example, severe cases of the flu, true ARDS in that scenario. I’m curious, have you seen the video that I’m referring to?
Joe: I’ve heard things that it’s not the same, it’s much more severe.
Ari: What he’s saying specifically is that, this is not a failure of the respiratory muscles, that in true ARDS, the patient gets so exhausted that their muscles of breathing basically become wiped out and so they put them on ventilation to do the breathing for them. He’s saying in these patients that he’s seeing, the muscles of respiration work fine and that it’s more akin to altitude sickness. The analogy he gave was like, if you just pulled these patients off the top of Mount Everest. This is what they-
Joe: I’ve seen that.
Ari: This is what they would look like. He’s saying that he believes the whole ventilation approach is actually not the correct approach. Which is also interesting because I’ve talked about the survival rates on mechanical ventilation in some of my previous podcasts and that the rates of survival are extremely low and disheartening, much lower than they are from treating ARDS in the context of severe flu cases. It’s potentially lending support to this theory that maybe ventilation is not the correct avenue of treatment, but I definitely– I’m not an ICU doc on the front line, so I don’t want to be in a position where I’m even thought to be giving advice. I’m just conveying what this guy is saying.
Joe: Yes. What this guy is saying could be true, but in any case, what we are seeing is situations like ARDS. Whether you call it a ARDS or whether you call it– It looks like something different maybe because something’s different with the muscles. What is clear is that people are getting a cytokine storm. That’s what many experts on the frontlines are saying.
This is a cytokine storm, and they are getting ARDS. It could be some variation of it that’s slightly different than how it’s working with the flu. I’m not an expert to comment about who should be on a ventilator and who should not be on a ventilator. What we’re doing is, we’re looking at the genetics of this thing, and we’re seeing, like, what are the genes that are increasing your risk of complications from cytokine storms and the Acute Respiratory Distress and complications from respiratory infections in general? What we’re seeing is, actually the genes that are cytokines are– Let’s say, for example, have you ever you heard of TNF Alpha?
Joe: It’s a popular cytokine. There’s Interleukin 6, IL-6, TNF Alpha. There’s basically all these cytokines that I’ve been studying for a while and it turns out that right now, they’re implicated in people who have variations, who produce high levels of these cytokines. You’ll produce high levels of IL-6 or TNF Alpha and IL-17, which is another–
Basically, a lot of these cytokines, they’re associated with autoimmune disorders as well because they can cause autoimmune issues. What we’re seeing is that a lot of these cytokines, for example, when people have variants that are increased, they could increase the risk for Acute Respiratory Distress.
Ari: Got it. Interestingly, I got an email just a few hours ago this morning from Chris Masterjohn who’s been a guest on the podcast four times. He’s a friend of mine. He mentioned two new studies that just came out showing that there’s two lab markers that they found to be highly predictive of whether someone will develop severe symptoms from COVID-19. One is low leukocyte count and the other one is high IL-6.
Joe: CRP? IL-6. CRP as well.
Ari: He didn’t mention that in the email this morning. I haven’t seen any studies on that, but it’s possible.
Joe: They go together because IL-6 increases CRP.
The ACE2 Gene and how it is involved in Corona infection
Ari: Yes. I don’t doubt that it’s possible. It could be a predictive factor, but as far as the studies that have come out so far, those are the two lab markers that seem to have predictive value.
Joe: If we look at the things, let’s say, for example, that will decrease TNF Alpha, we see things like moderate exercise, weight management, quitting smoking, sun exposure. For example, vitamin D is associated– Vitamin D within a healthy range was associated with lower complications of this Acute Respiratory Distress Syndrome. What’s coming out is that, even if you look at the genetics, living a healthy life is really important.
For me, I personally find it very interesting because it motivates me and also sometimes, there is unique genes. For example, when it comes to Coronavirus, there’s two interesting genes. One is ACE-2.
ACE-2 is a receptor that is found in the lungs predominantly. It’s very heavily found in the lungs and it’s basically the portal to how the virus gets inside the cells. Variants, for example, that have more of these receptors are more likely to get COVID-19. Knowing which variants you have in that, could also be very interesting and then there’s–
Ari: Is that speculative or is there actually any data showing that people with certain variants of the ACE-2 gene actually have greater risk of severe symptoms?
Joe: It’s greater risk of getting COVID-19 actually, but it’s research. It’s not speculative. I don’t know if it’s the most rigorous research, but it is published in a scientific paper. Meaning these things are generally pretty new. It’s a lot of things. Better data is coming out, but it’s not just some armchair hypothesis.
Ari: Got it. is there any usefulness of that information on a practical level? Let’s say somebody goes to get their genes analyzed because they want to know their ACE-2 variants and therefore help predict if they’re more likely to get this thing. Let’s say they find out that they are at higher risk based on their genetic variants. Other than panicking or freaking out [chuckles] that you’ve got bad news, is there any good news you can take from that, of how you can use it for anything practical?
Joe: Yes. There definitely is. When it comes to genetics, our philosophy is always to make sure that you’re doing things that are generally helpful for whatever you’re trying to do. Number one is, we only give recommendations that we think are the top recommendations that you want to do. We’re not going to recommend some very random supplement that barely anyone has heard of and that you can find in the middle of the Amazon rainforest.
In general, what we’re doing is we’re connecting healthy lifestyles, because, for example, it is a fact that if you moderately exercise, you’re going to be at lower risk for pretty much every disease you could think about. The chronic diseases. Rather than if you just never exercise. Obviously, exercise interacts with a ton of your genes. Exercise will come up a lot when it comes to genetic variants. What we’re doing is, we’re showing you exactly how these healthy behaviors that we– We first start off with the top list of healthy behaviors that, for example, what can be good for the immune system? What’s good for the respiratory system? What’s good for the cardiovascular system? Then we say, “Okay, here’s about 100 healthy things that we would recommend. Let’s narrow this down to the things that will also help this gene.” If we’re talking about the ACE-2, it turns out that something like zinc which is helpful for all the things that I mentioned and is a really good supplement in my opinion, it turns out that in animals, increase zinc concentration reduce the binding power of ACE-2 enzyme. That would be an example of– I’m reading this and–
Ari: Just to translate that into Coronavirus language, you’re saying zinc decreases the ability of this virus to dock on the ACE-2 receptor.
Joe: We don’t know that for sure but it’s– Basically, we can’t say anything that hasn’t been directly tested. Since this novel virus is so new, we can’t say anything about zinc and Coronavirus for sure. What we can say is zinc is great for the immune system. We can say it’s great for the– It really is amazing for the immune system and it reduces inflammation. We can also say that if it reduces the binding power of ACE-2, you could theorize that it could, let’s say, counteract some negative effects of the gene. There’s doctors using zinc to great effect. There’s one doctor who is on Fox News. [chuckles] He’s a really big fan of zinc, hydroxychloroquine and an antibiotic that he gives as well for secondary infections.
Joe: Yes, Azithromycin. Basically, he says that the hydroxychloroquine opens up the channels and allows the zinc to go in more. It allows the cells to absorb more zinc. In general, like I was saying, what I’m trying to do for myself is prepare my immune system before. What I like to do, it’s half hobby and half– This can help me a bit by tweaking my regimen, that this– Understanding that, let’s say, if I have this negative variant– I actually don’t have the ACE-2 variant, but let’s say I did. I know that zinc could be more important for me, based on my genetics. There’s other things as well, like Aloe vera for example. Aloe vera, and Japanese knotweed, which is basically in resveratrol supplements. Let’s see. We have it as a recommendation if you have the variant. We see that it binds to the ACE-2 receptor and it blocks it, so this-
Ari: [unintelligible ] resveratrol?
Joe: It’s Japanese knotweed. I’ve also read a paper from Nature. They listed about 50 promising substances that can be good for COVID and they actually listed resveratrol. That’s why resveratrol–
If resveratrol had nothing to do, it’s possibly we would exclude the recommendations. Since we felt like it has some potential and then it also has some potential to counteract some of the negative effects of this receptor and it is also good in some other ways, we included it as a recommendation if you have the variant.
Ari: Okay. You’ve got zinc, Japanese knotweed/resveratrol. You mentioned one other one. Are there any others to mention here?
Joe: For the ACE-2, those are the only ones.
Ari: Was there one other one? It was Japanese knotweed, zinc, and I think you mentioned one other one.
Joe: There’s Japanese knotweeds, zinc, and Aloe vera, which contains Emodin. It’s Emodin, which is found in Japanese knotweed and Aloe vera and there’s zinc. It also turns out, let’s say, Emodin and Aloe vera can lower blood pressure. There’s benefits of Aloe vera, and for example, if you have hypertension, that could be a beneficial thing to lower your blood pressure and also potentially counteract some negative variant that you have.
Ari: Got it. Are there any other genes that are relevant to this discussion of COVID-19 or ACE-2 is the big one?
Joe: Right now, we have about five to 10 genes that are published and we’re going to be publishing 30 genes and creating a report out of it. What you’re able to do is, you’re actually just able to browse and see which genes you have a variant for that is increasing your risk. Maybe out of 30 genes, you might look at four or five posts that might have something increasing your risk and/or that has some associations with higher complications or something like that. Then you look at the recommendations, you see which ones would be interesting for you, that maybe you even were looking at anyway. Maybe you read something about zinc that was good and now you see it again.
Basically, you’ll look at that and then you have to create a regimen, which we do once we– In our report, we’re going to– By the time this is released, it’s probably going to be published. We take into account all the recommendations and we give you the top ones. Whereas in the blog, the SelfDecode blog, which is a personalized blog, you can scan through and look at the genes individually.
I’ll give you one example for me, that has susceptibility and that’s a gene that– It’s called Mx1 and it has to do with interferon. My initial response based on this Mx1 is not as good as it could be. This is the initial immune response. What that means is potentially, the virus does have more of a chance to replicate more. Again, I’m very healthy, so that obviously counteracts any negative variants. Things like moderate exercise, which even though I know it’s really important for me, I haven’t done it in a week because I’m locked up in here, whatever. You see what I’m saying? Now I see that for example, moderate exercise actually is able to counteract this variant. It’s even more important for me if I want to strengthen my immune system with regard to this virus.
Ari: Got it. Have you seen any information on how vitamin D might interact with the ACE-2?
Joe: Yes, that’s a good question. Vitamin D is something that, in this case, I don’t recommend to take a lot of it in pill form, if you don’t know what’s going on. Making sure you’re not deficient in vitamin D is a good idea. You don’t want to be deficient, but then there are some people who go overboard. They want to lift a 300 and they’re like, “I’m going to have my vitamin D at some very high level.”
Not having a deficiency is important for respiratory infections. Whether it’s COVID or something else, it’s important for immunity, so getting enough sun, for example, would be a good idea.
When it comes to vitamin D, it actually could increase the expression of these ACE-2 receptors, especially if you had that ACE-2 variant. It’s just something that I wouldn’t go overboard with. If you’re not deficient, then don’t take it.
Ari: Got it. Any other things worth mentioning as far as genes?
Joe: In general, there’s genes that for example, are important for the initial immune response, there’s the ACE-2 receptors, and then there’s also this– What’s really amazing is all these genes related to cytokine storm. Keeping inflammation low is one of the best things you could do. There are specific
Ari: Okay, are there any other things worth mentioning when it comes to genetics and COVID-19?
Joe: Yes, mainly what we’re looking at is a lot of genes that are related to that cytokine storm that we spoke about, there’s a lot of cytokines and immune genes, and then there’s genes that are involved in antiviral function. Then there’s some genes that are specific to COVID-19, like the ACE2. Then there’s some genes as well that are related to cardiovascular function, which is really interesting, like nitric oxide production, that’s the NOS3 gene. The reason that’s very interesting is because, it also is related to cardiovascular health, blood pressure.
For example, if somebody does have high blood pressure, they do have that gene, sorry. They want to really focus on ways to counteract the negative effects of that variant which, again, it’s going to be healthy lifestyle and supplements but it’s going to be specific for that gene.
Joe’s personal immune boosting protocol
Ari: Got it. Do you want to talk about your personal protocol? I’m very curious to hear what you are specifically doing to prep your immune system and take care of yourself. I don’t know how much this is tailored to your specific genes or how much of it is easily applicable to pretty much everyone, but maybe you can talk about your protocol.
Joe: My protocol is half-based on my genes and half-applicable to everyone. Meaning, you could look at the protocol and there’s generally beneficial things that you can get from it. I do make sure to look at my genes and also my lab tests as well, making sure that my CRP is low and things like that. In terms of my protocol, one thing I do is I do take zinc. I find that is good for my immune system and I am less likely to get sick, and when I stopped taking it for a while, I got more infections than I have in a long time.
I did have some variants in the gene that was not producing a good antiviral response, that MX1 gene. It could be something like zinc was helping with that, it could be for a different reason, but zinc does seem to help me. There is a lot of information, it seems like zinc is good for the immune system and respiratory factions, that is something that I am make making sure I’m taking. I do combine–
Ari: Two questions on that.
Joe: Okay, go for it.
Ari: Yes, we’ll come back to what you’re about to say there as far as what you combine with it, but two questions on zinc. One is, how much do you take? Two, what form of it? There’s some discussion of people talking about the zinc lozenges that ionize and coat the mouth and the throat with zinc ions, versus just taking it internally. I’m curious your thoughts on that.
Joe: I do take it internally, historically. I am taking the lozenges now, because of the reasons that you mentioned. In a normal setting, if I was less concerned about an infection, then I would just take a supplement and even just taking it as a supplement is good. Now I’m starting to take the lozenges more and ideally zinc acetate is better, but right now I’m just taking zinc gluconate because all the zinc is sold out. Zinc gluconate is good enough. Yes, I’m taking zinc gluconate and I do have copper as well. For every 15 milligrams of zinc, you want to take 1 milligram of copper. Copper also has some immune benefits. There is some theoretical benefits toward COVID-19, for example, I think it’s a good protocol of copper and zinc.
Ari: What total dosage of zinc do you take? There’s a proper ratio of zinc to copper, but are you taking 15 milligrams a day, 30, 60, how much?
Joe: Normally, I would probably recommend 30 milligrams a day, but since I’ve been taking it for a while now and I get a lot of zinc in my diet, I’m just taking 15 milligrams a day.
Ari: Got it.
Joe: 15 milligrams, 1 milligram of zinc I think is a good dose for me. Now, again, I eat a lot of meat and so I’m getting a fair amount of zinc. I’ll also go to 30 milligrams sometimes I kind of waiver, but in general like a maintenance is 15. Then if I want to go a little higher, I might take 15 and then also take some lozenges as well.
Ari: Got it. Do you know what the upper range is as far as concerns of toxicity?
Joe: In general, they’ll say do not go above a 100 milligrams. There is a margin of error, there was like one person taking 2,000 milligrams for a really long time which is a huge dosage.
Ari: 2,000 milligrams a day?
Joe: Yes, I don’t recommend it to anyone.
Ari: Quick anecdote, I remember one time I mixed my own zinc, magnesium, B6 formula with the raw powders. I was trying to save money. This was many years ago, my early twenties. I was trying to save money instead of buying ZMA, which was a popular supplement at the time, to make my own with raw powders. When I was doing all my measurements, I got the measurement of zinc off by one decimal point, I was one order of magnitude off.
Joe: Oh my gosh.
Ari: Which means I took 10 times the amount of zinc that I thought I was taking. I had-
Joe: You got nauseous.
Ari: -not only nausea, but I had like the most intense abdominal pain that I’ve ever had in my life from basically zinc poisoning. I think I was even, it’s a little graphic, but I had diarrhea that was even a little bloody. As with everything, you can overdose on it and things become toxic.
Joe: I don’t recommend going over 30 milligrams a day.
Ari: Got it.
Joe: That’s my recommendation that you should not go over. Maybe one day is okay or maybe if it’s– This doctor was giving 200 milligrams a day for five days, but in general, not in a medical setting or whatever, I would not– At 100 milligrams you could start feeling nauseous, 50 milligrams you could start getting copper deficiency and it also competes with iron, so you might start getting iron deficiency.
Something that I would like to point out, and this is again a personalized health approach, that you do want to measure your iron levels. You want to measure it with ferritin, you can look at your haemoglobin. There’s a lot of different iron measures and you want to make sure that you’re not deficient in iron, it is very common in women. Taking a high level of zinc can also compete with iron, that’s another reason you don’t want to take too much, but again, something like 15 milligrams is really safe. It could be pretty much good for everyone, whereas 30 milligrams, maybe if you’re a larger guy and you have something you want to do and you’re also taking copper, 15 milligrams you could get away without taking copper because we get a fair amount in our diet, especially if you’re eating like a lot of vegetables and plants.
Ari: Got it. What other supplements, are you taking and would you recommend to people?
Joe: My team is doing a lot of research right now on supplements and how they relate to coronavirus and COVID-19. We’re publishing all that for free on SelfHacked, by the way. We’re also going to create an ebook out of it. Some of the basic stuff that I saw is that like, for example, if you have an inadequacy of a lot of nutrients, it could really impair your immune system. Things like vitamin C, selenium, vitamin E, B vitamins and iron. If you’re inadequate in any of those, your immune system could be impaired and that could have a very big difference. Something came up for vitamin E on one of my genes.
I looked at my diet to make sure I was getting enough vitamin E, and I was getting like half of the recommended value because I am on a– I mean, you have to eat like a lot of nuts to get vitamin E or there’s certain vegetable oils or whatever. It’s not that you don’t have that much in olive oil and that’s my main oil. I’m eating a lot of meat and things like that. I was not getting enough vitamin E and I started supplementing with vitamin E. Making sure you’re adequate. B2, B6 and B9 is very important for the immune system. Then there’s things like NAC that increased glutathione, and they’re also good for the respiratory system.
That’s something that I’ve also been taking but I kind of fluctuate with that. Right now, I’m taking it because of COVID-19. I want to make sure that my immune system is up to par. The other thing is medicinal mushrooms, there’s a lot of them. I generally find that I like them and they are good immune boosters. There’s different ways to get them actually like there’s a maitake mushroom snack that was really tasty. Right now, I cannot get a hold of them because they’re sold out on Amazon.
Also supplements. Right now, I’m doing supplements. Black cumin oil is another one. These are the basic ones that I’m taking. Again, some of them are there. I’m a little push towards doing them because of my genes but also, I think these are generally good things to take as well.
Ari: Got it. Do you have any thoughts on medicinal mushrooms as far as how to take them? Just for context, there are certain compounds which you might want to take, which might have some specific antiviral effects, which maybe you’d take after you get an infection and while you’re sick, in other words, and you could take certain antimicrobial or antiviral compounds, let’s say, olive leaf, or let’s say, oregano oil, or something like that, but you wouldn’t necessarily want to use antimicrobials prior to getting sickness.
Do you have any thoughts on like medicinal mushrooms? Should they be used on an ongoing basis? Do they help ramp up the immune system only when you take them consistently over a period of time or do they act instantly within hours or a couple days to– Do you get what I mean? Should you take it like for months leading up to an infection to prevent it or take it only in the context of after you get sick?
Joe: That’s a really good question. I think it actually gets to a bigger question where I do think you need to do things before you get sick. The reason is, because it takes around five to seven days to notice symptoms. If your immune system is not up to par, if it is or isn’t, it’s still going to take a certain amount of time, you’re not going to notice symptoms for some time. It’s a little stealthy like that, the virus. It’s replicating while you don’t know what’s going on. Then, finally, you start to feel some symptoms and depending on how much it’s replicated, you might get side effects or complications.
Basically, by that time, it theoretically could be too late. For example, if somebody were asking me, all the things I’m recommending is not to take, if you already have ARDS. That’s a minefield. There are some things that they studied for that is limited. Anything I would recommend is going to be limited, they haven’t really studied much for that. At that point, it’s already this– Things can act in weird ways. Supplements might act in weird ways. You don’t know for a fact, what is going to [crosstalk]
Ari: What you’re saying is potentially supplements which can help prevent an infection or combat replication early on might in the context of once it’s already severe, in the context of ARDS, or in a cytokine storm, potentially could be counterproductive?
Joe: Yes. I’ll give you one very specific example. Remember that gene that, for me, MX1, didn’t have a good initial response. What this gene does is it increases the interferon response. My interferon response based on this gene is lacking. I want to strengthen this before the virus hits because this is part of the early response system. Now, once it hits, the virus replicates and it takes over your interferon system. Theoretically, if you increase interferon at that point, theoretically, you could make it worse so taking immune stimulators. Doing something that would be great for you before the virus hit would be incredible.
You get your immune system up to shape the virus hits, you beat it down, it’s already beaten down, it doesn’t cause that much effect. If, a week or two later, you’re like, “All right, I’m going to start taking some immune stimulants here.” Theoretically, the virus has already hijacked your interferon system, and it gets more complex. In truth, I would have more of a limited regimen if I already had the virus.
I probably would not be taking medicinal mushrooms, two weeks in, let’s say, because, again, we don’t really know what’s going on, what I do know is that before it could be helpful in beating down the virus, let’s say or infections, in general, we don’t know for sure if this one, but it is good for the immune system and we already see that having a strong immune system seems like it’s a great thing to have before you get the virus.
Now, once you have it, again, this thing is hijacking the interferon system, it could be like putting fuel on a fire and then causing the cytokine storm maybe to even get worse. Now, I’m not saying that it’ll happen. It’s just that it’s unclear. Let’s say, I did recommend, let’s say, three, four days, five days and it could be that you only have symptoms two weeks in. It’s something that, in this case, I would take a preventative approach. If you have any of the risk factors on that list, if you have a poor immune system, you have an autoimmune condition, which can create a poor immune system.
For example, you mentioned the low white blood cells, that is a risk factor. People with autoimmune issues also can have low white blood cells because the white blood cells are basically attacking your own body, and they get out of circulation more. That’s one theory as to why white blood cells could be lower in certain autoimmune issues. When I had some autoimmune issues, my white blood cells were lower, and since they resolved, they actually went up.
You want to make sure that you could check your labs, your CRP, your white blood cells, if you could get an IL-6 test, that could also be good. You want to make sure you don’t have any risk factors. You want to check may be certain variants to see if you have a receptor that maybe is increased and the coronavirus can latch on to more easily. One thing is clear is that the healthier that your immune system is, in general, before this virus hits the better. After that, things get way more complex.
Ari: Got it. Do you have any final words that you want to leave people with? I know you’re putting together an ebook which by the time we release this episode, hopefully, will be available and we’ll have a link to it at the podcast page for this episode which will be theenergyblueprint.com/coronagenes, so theenergyblueprint.com/coronagenes.
Joe: And that’s G-E-N-E-S, not the jeans that you put on.
Ari: Any final thoughts you want leave people with?
Joe: Yes. Just like I was saying, I think that you just need to make sure that your immune system, your general health. Look for any variance. Things like that. We are going to be putting a report together. We do have a free resource on SelfHacked that you could look at the information on supplements and coronavirus. I think people are going to make it. That’s it. I think the people listening to your podcast are probably health-conscious. They’re listening to you. They want to know about health. I think these are the types of people that are going to do well.
Joe: They shouldn’t freak out.
Ari: Yes. I agree with you. Joe, thank you so much for coming on and sharing your knowledge. I appreciate it. I think there’s some great takeaways for people here. I definitely would encourage all the listeners to go to theenergyblueprint.com/coronagenes. Go to SelfHacked. You can check out the previous articles there but definitely go to theenergyblueprint.com/coronagenes and download the ebook that Joe and his team are putting together. Joe, thank you again. Pleasure chatting with you as always and I look forward to the next time.
Joe: Awesome. Thanks for having me.
What the science on COVID-19has taught us so far (01:22)
The role of melatonin in inflammation (17:27)
The most common underlying causes of severe COVID-19 infection (20:08)
The ACE2 Gene and how it is involved in Corona infection (32:40)
Joe’s personal immune boosting protocol (47:05)