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Weitz Sports Chiropractic and Nutrition
Healthy Biological Aging with Dr. Daniel Stickler: Rational Wellness Podcast 184
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Dr. Daniel Stickler speaks about Healthy Biological Aging with Dr. Ben Weitz.

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Podcast Highlights

4:10  The difference between biological age and chronological age is that biological age or epigenetic age reflects the overall health of the system.  We are talking about health span as compared with life span. One way to think about biological age is that lower biological age is associated with greater levels of function–physiological, physical, and cognitive. 

9:50  We know that as we age, we tend to accumulate damage to our DNA. The telomere test is one way to measure damage to our DNA as a measure of biological age.  Telomeres are the ends of our chromosomes that tend to shorten with age, though we are not sure if telomere length is a result of aging or a cause of aging. Another marker of aging is GlycanAge, which measures glycans that build up in your bloodstream. 

12:25  Dr. Stickler said that when he is looking at markers of aging he will do DEXA scans of patients to look at lean body mass and bone density testing.  EEG studies can be helpful, since certain brain wave patterns are indicative of aging. He will perform skin glycation scanning with immunofluoresence. He will also measure senescent T-cell levels to look at naive (young) vs aged T cells in the blood.

13:05  Dr. Stickler looks at functional mobility and balance. He will look at a bunch of blood metrics like albumin and uric acid levels.  He also looks at hormone levels. They are trying to figure out a way to test intracellular NAD levels.

15:02  The methylation clock was first developed by Dr. Steve Horvath of UCLA and it looks at specific methylation patterns on our DNA.  The Horvath Clock was developed in 2013 by looking at a constellation of epigenetic marks on the DNA that correspond to chronological or physiological age.  Dr. Horvath now has the GrimAge Clock, which is an updated version, which looks at a couple of hundred methylation points on the DNA.  Last September we saw the first study published that showed an epigenetic age reversal, the TRIIM Trial by Fahy, et al, which stands for the Thymus Regeneration, Immunorestoration, and Insulin Mitigation trial.  [Reversal of epigenetic aging and immunosenescent trends in Humans]  Gregory Fahy, Steve Horvath and the other authors showed that their intervention resulted in a reversal of aging of 2.5 years, the first time this has ever been proven. The intervention used a combination of growth hormone, DHEA, metformin, 50 milligrams of zinc, and 3000 milligrams of vitamin D.

24:32  There are a lot of products on the market now that have anti-aging benefits, including Rejuvant, which was developed by Stanford’s Buck Institute on Aging that contains calcium AKG.  Also, there is NMN (nicotinamide mononucleotide), an NAD precursor, and there are also senolytics like quercetin and fisetin.  Disatinib is a prescription medication that induces apoptosis in senescent cells. 

45:03  Dr. Stickler does recommend resveratrol for anti-aging, though it is probably not a powerful stimulator of NAD. He recommends a multivitamin, 5000 IU vitamin D, 2 gm of fish oil, and sublingual or injections of B12.

 



 

Dr. Daniel Stickler is the co-founder and Chief Medical Officer at Apeiron ZOH, Inc.  He is a physician for high-performing executives, entrepreneurs, and elite athletes. He consults with Google for wearable technology, epigenetics, and AI in healthcare. He is on the faculty of the Age Management Medical Group and is also a guest lecturer for Stanford University on Epigenetics in Clinical Practice. He is on the board of TruDiagnostic, who he is representing on this podcast today. TruDiagnostic offers the TruAge, which measures your rate of biological aging based on measuring 900,000 CpG sites on our DNA to see if they are methylated or not. Their website is TruDiagnostic.com.

Dr. Ben Weitz is available for nutrition consultations, including remote consults via video or phone, specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111 or go to www.drweitz.com. Phone or video consulting with Dr. Weitz is available.

 



 

Podcast Transcript

Dr. Weitz:                            Hey, this is Dr. Ben Weitz, host of the Rational Wellness podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to the Rational Wellness podcast for weekly updates and to learn more, check out my website, drweitz.com. Thanks for joining me and let’s jump into the podcast.  Hello, Rational Wellness podcasters. Thank you so much for joining me again today.

Today our topic is methylation, epigenetic methylation time clocks. So this is a way to measure biological aging and so we’re going to discuss that and then some of the things that we can do to try to reverse aging. We want to know why in hell we age and what we can do about it and there have been a number of attempts to develop a method to measure biological aging as distinct from chronological aging. In other words, does our health correspond to someone younger or older than our chronological age and what can we do to slow down or even reverse aging and how can we know that our methods are working if we’re engaged in an anti-aging program?   We do know that as we lead our lives, our DNA tends to get damaged and develops various types of defects and perhaps we can measure this in some way. One of the methods that has been around for awhile is measuring the length of the ends of our chromosomes, known as telomere length. Shorter telomeres corresponds to increased biological aging. Recently there’s been a lot of research devoted to developing epigenetic DNA methylation clocks, which measure the extent to which parts of our genes are methylated. Meaning are they over-methylated, under-methylated, et cetera.

                                                We know that methylation can turn on or turn off genes and there are some genes you want turned on and there are some genes you don’t want turned on. So these clocks measure whether specific locations on the DNA, known as CPG sites are methylated or not and Dr. Steve Horvath and Dr. Gregory Hannum are two of the most important researchers in this area who have each developed a different version of the methylation clock.  Now, the practical application of these clocks is starting to become available for use by clinicians and for patients to measure this biological aging and True Diagnostics is a company that’s offering the True Age test, which measures your rate of biological aging based on measuring 900,000 CPG sites on our DNA to see the extent of their methylation.

                                                Today we have Dr. Daniel Stickler joining us today and he’s the co-founder and chief medical officer at Apeiron ZOH Incorporated. He’s a physician for high performing executives, entrepreneurs, elite athletes. He’s also a consultant to Google for wearable technology, epigenetics and in healthcare. He speaks regularly and is on the faculty of the Age Management Medical Group. He’s also a guest lecturer for Stanford on epigenetics. He sits on multiple advisor boards, including the board of True Diagnostics, who I just mentioned, who he’s representing on this podcast today.  So Dr. Stickler, thank you so much for joining me today.

Dr. Stickler:                         Thanks, Doc. A pleasure to be here and look forward to the conversation.

Dr. Weitz:                            Sure. So let’s start with what is the difference between chronological age and biological age?

Dr. Stickler:                         Well, that’s a good question, because we don’t even have a consensus that aging is a true condition. I mean, we see it and we recognize that aging occurs, but some of the more recent literature coming out from the Aging Researchers is that we really don’t have a definition of age. It’s just a … It’s a constellation of markers that we allocate to it, meaning there’s no question, we gradually deteriorate and die and there’s a question is that a programmed response? Is it a gradual breakdown of the physiologic machinery or is it a combination of the two? So it’s a vague area right now, but essentially, chronologic age is just a core marker of anything.

                                                You see 70 year olds that function like a healthy 50-year-old and you can’t say that they’re 70 years old relative to a comparison of the average of that age group, so people have shifted more towards this biologic age. But again, that’s not something … I don’t like the actual metric of age as a metric, whether biologic or chronologic, because it’s really the health of the human system that we’re looking at. What we are gathering right now is all these biomarkers that indicate the health of the human system. I mean, it’s not pleasant to be necessarily told if you’re 70 years old, that you look good for your age. Well, what does that actually mean?   You’re compared to the average of people of that age. So I tend to really kind of shift away from aging as a general statement and like to look at it as more of these are markers of the youthfulness in the system or health in the system.

Dr. Weitz:                            I’ve always liked to think of it in terms of function and I think the goal for myself and a lot of us is how can we have a high level of function ’til close to the end? Instead of expecting that once you hit your 40s or 50s, you just get this gradual decline in your ability to function, in your mental capacity, in your physical capacity, so that as you go through your 60s and 70s and if you’re lucky enough to get into your 80s, you can barely move. You barely have any level of function and the idea of simply living a long time doesn’t sound all that attractive if you don’t have a high level of function.  In the past, we’ve talked about taking that curve where you gradually go downhill once you reach a certain point and trying to rectangularize it so you have a relatively high level of function until you get to the end. I think of biological aging as corresponding to having a higher level of function.

Dr. Stickler:                         Yeah and we’re seeing that. I mean, the markers that we’re gathering together, although none of them are perfect, the constellation of those markers really indicate what you’re talking about is what we refer to as health span. We want to extend health span, not only life span. People don’t have quality of life if their level of functioning is more of an invalid type of aspect or I always look at it as when I get to the point where my body can’t respond to what my brain is asking me to do. That’s a pretty broad spectrum, but it’s when it’s just basic functional aspects that get deteriorated.

Dr. Weitz:                            Right and in terms of function … Over the years, there have been a number of markers of physical function that seem to have a correspondence with healthier aging and there’s been grip strength. I saw a study where just being able to get up from the floor without using your hands and so it appears as though having a certain level of strength and mobility is important for healthy aging.

Dr. Stickler:                         Yeah, I mean, everybody’s looking for the perfect marker right now and, like I said, I think it’s going to be a constellation. I mean, in our longevity program, we call it the Rejuvenation Program, we’re looking at a bunch of metrics right now and we get varying degrees of somebody who’s really good in one area and weak in another, what does that mean? We don’t know. That’s why the more data we gather on that, and we get probably 20 or 30 markers that we use right now and we’re hoping to create kind of a health grade. Not necessarily a biologic age, but a health grade according to how you score in all these areas and it’s going to take some time and some data before we really establish what are the best markers and what grouping of markers is going to be the most telling.

Dr. Weitz:                            So we’re going to get into the epigenetic clock in a few minutes, but what are some of the other methods that can be used to calculate biological age right now?

Dr. Stickler:                         Well, like you said, the telomere testing is one.

Dr. Weitz:                            And what is the status of telomere testing?

Dr. Stickler:                         That’s a good question, because even the people in the aging industry are torn on this, because question is, is telomere shortening a result of aging such as getting gray hair or is it a cause of aging? And that question has come up recently without a good, solid answer. So telomere testing, because of such high variability in the outcomes related to other markers, it’s kind of been pushed aside a little bit. It’s an expensive test. We get it and we get it about every five years. Not frequently. And it’s not the best guide, because it takes so long to change something on that and generally you’re looking at diminishing the rate of loss on those as opposed to trying to extend them, although some of the research now is really focused on doing a genetic insertion or a plasmid that can actually add length to the telomeres versus supplements or peptides that can stimulate the telomerase themselves to add more length to it.   We use another one called GlycanAge. So glycans are substances that build up in the blood over a lifetime and we’re testing this. They have pretty good data based on some preliminary studies they did.

Dr. Weitz:                            Is that like glycation? Like glycosylated hemoglobin?

Dr. Stickler:                         Not exactly. I mean, glycation is a component, but these are glycan products that are found in the blood and they do accumulate over time. It’s a fairly new area. We’ve just started testing with it in the last year and we see huge differences in the epigenetic age and the glycan age, but they have some pretty good data from the…

Dr. Weitz:                            What’s an example of a glycan product?

Dr. Stickler:                         I don’t know the specifics on those.

Dr. Weitz:                            Okay.

Dr. Stickler:                         I mean, there’s several hundred of them that they’re measuring.

Dr. Weitz:                            Okay.

Dr. Stickler:                         We do DEXA scans, so we look at lean body mass. We look at bone density. We do EEG studies, because there’s certain brainwave patterns that are indicative of the aging process. We do skin glycation scanning with immunofluorescence. We do senescent T-cell levels from UCLA to look at the naïve versus aged T-cells in the blood.

Dr. Weitz:                            So these are young versus old T-cells?

Dr. Stickler:                         Correct and we look at functional mobility. We look at balance. We look at stress response in the system. We look at a bunch of blood metrics, so like albumin, we look at uric acid levels. We look at hormone levels and right now, like I said, it’s just a matter of collecting as much of these as we possibly can. NAD levels, if we can figure out a good way to test intracellular NAD levels is a hot topic right now as well.

Dr. Weitz:                            Right. So as a step to get into the biological clocks, what is epigenetics as different from genetics for, especially for the layperson who happens to be listening in?

Dr. Stickler:                         The best way I can put that is that genetics is the hardware whereas epigenetics is the software. What I mean by that is that the hardware doesn’t change. It is … You only need your genetic stem one time, but epigenetics is something that controls the expressions of the genes that you have. That’s why you can have one cell that creates a neuron and another stem cell that creates a lung. This is using the exact same code, so every cell has the exact same genetic code, but the expression of that code is controlled to create the outcome. We have kind of trans-generational and generational epigenetics, which are usually the epigenetics that are written in pen on our DNA so that they’re there and it’s really tough to make any changes in that and then you have the epigenetics that are written in pencil.   Those include not only the DNA methylation, but also histone methylation, which is one of the ways that we know that lifestyle, that supplementation, that medications, all of those things can actually impact and change the expression of genes and this is the area that really people focus on when it comes to the epigenetics.

Dr. Weitz:                            Okay. So what is the methylation clock? This epigenetic methylation clock?

Dr. Stickler:                         So Steve Horvath developed this methylation clock where he started looking at specific methylation patterns. So he took groupings of aged people and looked at a constellation of epigenetic marks on the DNA and what he noted is there were a bunch of these that accumulated over time that corresponded to their chronologic or physiologic age. He developed the Horvath Clock, I think back in 2013. He now has the GrimAge Clock, which is a more updated edition of it. But again, they’re only looking at a couple hundred methylation points on the DNA, so it’s rough right now, although we had the pleasure of seeing the study that came out in September of last year that showed an epigenetic age reversal.  So the prevailing theory at the time, and you even hear David Sinclair had stated it prior, was that epigenetic aging is a one way linear process where you gradually accumulate these over time and it’s not a process that we have any control over, because mostly it was thought that these were the marks that were written in pen that were accumulating.

Dr. Weitz:                            So let me just stop you for a second. So the study you’re referring to is the TRIIM Trial by Fahy and it was published in September of 2019 and TRIM stands for Thymus Regeneration, Immunorestoration, and Insulin Mitigation trial.

Dr. Stickler:                         Yes and they showed a 2.5 year gain or loss of age after a one year period on this trial and they only had nine participants, but still, it was the first time that something showed that age reversal, in a sense, if we’re using this as a marker, is theoretically possible and it excited people. So a lot of the kind of world view of aging began to shift, which was dramatic. In the same month, Sinclair releases his book, so we had the perfect storm of shifting mindset, which was great. And what they used in the trial, I mean, for those of us that do age rejuvenation medicine in practice, what they did in the trial was baby steps. I mean, we have such in depth treatments right now, not only over the counter treatments, but research chemicals, peptides and prescription medications that can be used that are amazing. Even technology. I mean, we use brain stimulation technology and we’re seeing rejuvenation of aging patterns on the brain waves with that.

 



Dr. Weitz:            This podcast episode is sponsored by Quicksilver Scientific. Quicksilver Scientific is a leading manufacturer of nutritional supplements, featuring enhanced nanoparticle delivery systems, specializing in detoxification protocols, fast acting immune formulas, and next generation longevity products. To learn more or to sign up for a professional account, visit quicksilverscientific.com. Listeners of this podcast can receive 15% off their order by using the promo code Weitz, WEITZ2020 at checkout. And I definitely utilize Quicksilver products in our office and some of their products are just absolutely amazing and there’s nothing like it on the market, so thank you to Quicksilver.

 



 

Dr. Weitz:                            Interestingly, as I have sort of been watching the anti-aging research, the predominant, as I see it, in my limited understanding of it, is a predominant theory maybe 15, 20 years ago is our cells die. They don’t get replaced. We lose muscle cells. Our bones degenerate. Our brain cells don’t get replaced. So a lot of the focus was on trying to stimulate growth. So things like growth hormone and testosterone and DHEA and these are really common strategies.  Recently, in the last five or 10 years, the focus seems to be, at least from what I’ve seen, not some of the stuff you’re talking about necessarily, but the stuff that gets out more in the popular literature seems to be all about caloric restriction and fasting and fasting mimicking diet and things that limit damage, but don’t necessarily stimulate growth.  So it’s interesting that they chose growth hormone as one of the strategies.

Dr. Stickler:                         One of the things they look at with hormones is you look at when the body functions optimally. What are the parameters that meet that?  And growth hormone, testosterone, these are two parameters that deteriorate with age.  Is this a natural process?  Sure.  Is it a healthy process? And most of us feel that it is not. We do note that function improves dramatically and markers of aging improve dramatically when hormones are put into healthy, youthful levels. I’m not talking about super physiologic doses in this, but in dosage levels that maintain the health. I mean, growth hormone in itself is a double edged sword. Too little is unhealthy and too much is also unhealthy. So you’ve got to keep in that Goldilocks zone of that.

                                            When it comes to calorie restriction, recent analysis has kind of pushed back a little bit on that too.  I mean, calorie restriction definitely has an impact, but calorie restriction to the point that’s required to match what they see in animal studies is pretty unpleasant state to be in.  I mean, there’s no question that total calorie restriction is beneficial, but to achieve really substantial outcomes, I mean, the hunger that you would experience wouldn’t make life worth living, I don’t think, which is a big impact and now they’re actually leaning towards the chronic calorie restriction is not the best way to do it, but that you do spurts of it.  So intermittent periods of it that allow the body to adjust.  I mean, stress is a good thing for the body. It makes the body adapt and severe calorie restriction is a stressful event on the body.

Dr. Weitz:                            So for those of us who haven’t seen this study, they used the combination of growth hormone, DHEA, metformin, which is a popular drug for diabetes, because it reduces insulin resistance, but they also used 50 milligrams of zinc and 3000 milligrams of vitamin D. One of the things they showed was that there was increased stimulation of the thymus gland, which tends to degenerate with time, and that’s what they mean by immunorestoration. As your immune system weakens, you become more vulnerable to bacteria and viruses, just like older folks are dying at a higher rate from COVID-19. So keeping your immune system robust is important.   We know zinc and vitamin D are crucial factors in immune function, but I haven’t heard too much talk about the potential benefits of zinc and vitamin D from this intervention study.

Dr. Stickler:                         Yeah and I mean, zinc and vitamin D are one of the first line interventions for COVID right now.

Dr. Weitz:                            Yes.

Dr. Stickler:                         From the consensus in the medical community.

Dr. Weitz:                            Yes.

Dr. Stickler:                         And since vitamin D is generally deficient in about 60 to 80% of a given population, it is important to supplement that and the zinc is also a double edged sword, because you can get some zinc toxicity with that.

Dr. Weitz:                            Sure.

Dr. Stickler:                         One of the things we look at is the genetics that relate to cautions with zinc and base our recommendations on that personalized approach with them. But there’s, I mean, when it comes to aging, there’s a lot of available stuff on the market right now. I mean, Rejuvant, which is calcium AKG, which was developed at Stanford’s Buck Institute on Aging, was developed by Brian Kennedy and it’s got really amazing aspects to it.

Dr. Weitz:                            Can you repeat that? That’s not something I’m familiar with.

Dr. Stickler:                         Rejuvant is the brand name of it.

Dr. Weitz:                            Okay.

Dr. Stickler:                         But calcium AKG, alpha-ketoglutarate.

Dr. Weitz:                            Right.

Dr. Stickler:                         We know deteriorates over time with aging and replacing that has, I mean, it impacts about five of the nine hallmarks of aging that need to be targeted. You have NMN, which is over the counter, and you have vitamin D, of course. You have senolytics now. I mean, supplemental senolytics. I mean, we have prescription senolytics, which take out those zombie cells that accumulate over time that the body can’t get rid of and they secrete toxins. They take up metabolic aspects of the body and when we can reduce them, we dramatically change the outcome. We use the senolytic formula that has quercetin and fisetin in it, which are two different over the counter senolytic compounds that have shown really impressive benefits. I mean, quercetin has been around forever and…

Dr. Weitz:                            It’s also a zinc ionophore and so we’re using that in our immune protocols these days.

Dr. Stickler:                         Absolutely and they found quercetin because they ran a study through a bioinformatics platform and they said, “These are the pathways we want to hit, what’s available that works on this?” And it kicked back to quercetin and dasatinib. I mean, dasatinib is a prescription, but these are two senolytic compounds that have a profound impact on aging. The key is really knowing how to take these in combinations that can create the outcome that you’re looking for.

Dr. Weitz:                            I looked at a PowerPoint presentation that Dr. Horvath had and one of his first slides shows a 71-year-old guy who’s an amateur body builder and he looks very good for his age, but it says on the slide that if you use clinical markers of aging such as body mass index, grip strength, blood pressure, he will probably be considered young for his age, though he is probably old according to molecular biomarkers such as the epigenetic clock. Dr. Horvath says that the message is that … This is what he says on the slide. That the message is that molecular markers will not be misled. What did he mean by that?

Dr. Stickler:                         Well, again, this is an area that what we’ve found, and you know, it’s funny because I found it in several of my clients, because I work with some professional athletes and their epigenetic age markers were, some of them 10 years older than their chronologic age and these were very fit, healthy people. There was a follow up study that was recently published looking at athletes and epigenetic age and they tend to be older. I know I was … I did a podcast not too long ago with Ben Greenfield and he got tested and he came out older than his chronologic…

Dr. Weitz:                            I saw it. I think his age is 38 and he was 43 or something.

Dr. Stickler:                         Yeah and so the study though that came out, some of the markers that they’re using to establish epigenetic age were methylated, which means the genes were turned down or turned off and it was interesting, because they picked out like three or four of these in particular that actually code for better health in the sense that it reduces cancer rates and heart disease. So even though the accumulation is over time, there’s benefits there. So are we truly measuring that? And that’s the issue right now, and this is what I love about True Diagnostics is they’re looking at 900,000 methylation points. How many of those do we know about? Well, maybe 5% of those that we actually have information on.   So what they’re doing is not only storing this or keeping this report together, but as data accumulates, it will update that report for you so that you can contribute to it too. You provide feedback on other aspects of like lab work and your social behaviors and suddenly we can start narrowing this down. I mean, this is the age of bioinformatics and the more data we have, the more accurate we can get with what we’re doing. This epigenetic age for these athletes and these really significant exercisers, I don’t think is a reflection of their true physiologic age. So it has to be taken with an understanding of what you’re actually measuring there.

Dr. Weitz:                            So how does the test determine if a gene is methylated, if it’s methylated too much to a point where that J shape curve now is going the opposite direction or not methylated enough, does it take into account all that? Can it?

Dr. Stickler:                         You’re asking me a technical question that’s more for the biochemist, but I don’t believe it goes into specifics of the degree of methylation. Just the specific markers they’re looking at, is there a methyl group added to that marker on the DNA is the primary focus.

Dr. Weitz:                            Right, so interesting, in the Functional Medicine world, one of the things that we’ve been looking at for a number of years is potential for methylation based on doing genetic testing and then seeing if somebody has certain genetic markers like the methenyltetrahydrofolate reductase gene and if they’re heterozygous or homozygous for two defects, they may not be able to methylate and then we may use specific methylated, activated B vitamins to try to stimulate that methylation.  But then we’re also cautious to try to make sure we don’t over-methylate, which certain genes that are over-methylated can lead to increased breast cancer risk, et cetera.  So I’m wondering if there’s a way that this methylation testing could be used for feedback, say, I have a patient, they are homozygous for MTHFR and we give them methylated B vitamins. Is there a way that we can then tell are we properly methylating their genes? Are we under or over methylating them? Can we titrate the dosage?  I’m wondering if there’s something like that, that is or might be available.

Dr. Stickler:                         Another great question, because again, we don’t have the answer to that. How does the body’s ability to methylate affect the aging methylation of the DNA? And there isn’t an answer. I mean, again, using genetics, and I run a genetics company and we test MTHFR 677 and 1298, and I have seen clients that had homozygous on both of them, which means that they have less than 25% function of the MTHFR, yet they have normal homocysteine levels and most of the time it’s because they’re consuming adequate methyl folate in the diet.  And looking at these polymorphisms, which is what we’re testing in, in genetic testing right now when we’re talking about 23 and Me, when we’re talking about the Apeiron test, Ancestry, they’re looking at polymorphisms and these are not mutations.  I think this has been taken to the point where it’s very misunderstood by the general public.   These are variations that have inherited through your ancestry that are designed to optimize your system for the environment that you’re in.  The problem is now we move around all over the world and we’re not in that ancestral environment that our genes are optimized for, so we have to make adjustments to our environment to match our genetics. This is nutrigenetics. It is basically eating for your genes as opposed to nutrigenomics, which is eating to change expressions of your genes.  I really want to see this whole idea of these polymorphisms as mutations to kind of go away, because it really is … It’s putting a lot of fear into people that essentially are unnecessary. So really understanding not only the genetics, but the markers that occur with that and the lifestyle of the person that has them. I mean, I have plenty of homozygous MTHFRs that I’m just like, “You don’t need any exogenous treatments on that. You’re doing well with what you’re eating, apparently, because you don’t have the expression that is showing.”

Dr. Weitz:                            Right. Yeah, good. Yeah, we gauge a lot of the recommendations based on things like homocysteine levels, et cetera.

Dr. Stickler:                         Yeah.

Dr. Weitz:                            So what is the difference between the True Diagnostics True Age test and the Horvath clock? It’s using the Horvath clock or it’s…

Dr. Stickler:                         There are aspects of it in there. Also, Dr. Hannum’s and the Duke clocks that are being used. So it’s a combination of them and it’s really designed to be the largest database of epigenetic marks on the market. I mean, honestly, we can’t give you a great deal of knowledge with these reports yet. We can give you an overview of the knowledge that we’ve accumulated, but over time, as more and more people do this, we’ll be able to dive deeper and give you insights into what’s happening. The great thing is we have all these markers now and so now that we know that we’re looking at these markers, we can run it through the AI that we have that will mine this stuff and say, “Here’s all the people that are smokers. What do you see in common with them that’s not in non-smokers?” And so we can start diving into the bioinformatics, which is going to be huge for people. I mean, this is truly the next three years, we’re going to see such advances in epigenetics and I think a lot of the genetics stuff is going to fall by the wayside from that point.  It’s not that we won’t need genetics, but we have to look at it as just another biomarker and the epigenetics is going to be really the top piece that we’re going to be focused on.

Dr. Weitz:                            So as I understand it, the Hannum clock used blood and measures methylation on white blood cell DNA, right?

Dr. Stickler:                         Right.

Dr. Weitz:                            But the Horvath clock or the newer version of the Horvath clock, uses DNA not just from white blood cells, but from other tissues.

Dr. Stickler:                         Mm-hmm (affirmative).

Dr. Weitz:                            Is that improvement? Your test basically is using the white blood cells, right?

Dr. Stickler:                         Right, and that’s always a question, because like I said at the beginning, every cell has different methylation. Every cell type in the body has a different methylation pattern to it, but what we’re looking at are these common denominator methylation patterns and generally you’re going to get correlation with the epigenetic markers that have been selected with like a buccal swab where we’re looking at epithelial cells from the skin or we’re looking at the blood or we’re looking at salivary accumulation. Whatever we’re looking at, the idea is that there is tissue specific methylation patterns, but then you’re also going to get universal methylation patterns that can be derived from any cell type that you get and that’s the focus of the epigenetic testing right now.

Dr. Weitz:                            So how can clinicians use this True Age test?

Dr. Stickler:                         Well, the way I use it in practice is that I will get the epigenetic age. We’ll do an intervention for a year or a series of interventions, and then we will retest. I have to say, right now, and this is being reported by several of the epigenetic companies, is that this year in particular, relative to people who got tested last year at this time, we’re seeing an acceleration of aging and what we are assuming this is relating to is the stress of this whole COVID-19 issue.

Dr. Weitz:                            Sure.

Dr. Stickler:                         It’s impacting people in ways that they don’t fully understand. I mean, the stress of anything that changes your habits in any way is a stressor on the body. We see these elevations in cortisol levels, despite the fact that we’re working with people to mitigate these, so I think that…

Dr. Weitz:                            People are eating worse. They’re exercising less.

Dr. Stickler:                         Yeah.

Dr. Weitz:                            I saw the CEO of Kellogg’s on TV bragging about the fact that more people are having breakfast cereal for dinner. They’re afraid to have time with other people, so they have less social connections. There’s a whole series of things along with the stress.

Dr. Stickler:                         Absolutely. Yep.

Dr. Weitz:                            So what are some of the things that negatively affect our aging? I noticed on the True Age test they mention exposure to heavy metals, pesticides and other toxins.

Dr. Stickler:                         Right, there’s eustressors and then there’s mal stressors. The ones that … A eustressor is good, because we have a certain kind of bandwidth that we function in and within that bandwidth, our gene expressions are set to really optimize the human body’s function within that realm. Little excursions outside that realm create stressors. Just like if you haven’t exercised in six months and you go back to exercise, suddenly you’re exceeding the body’s baseline of that comfort zone and creating a stress response. Is that a bad thing? No, that’s actually a good thing. It’s a hormetic response that the body responds and says, “Hey, this is an unfamiliar environment. I have to make adjustments to create a healthier, more resilient, anti-fragile human,” and so you get beneficial effects in that way, but there are some stressors that will take you too far out of that zone.  Those can be things like heavy metals. Those can be things like smoking. Those are parameters that don’t have really an established eustress type of benefit that the body will respond in a positive way and make you more anti-fragile. It actually drops you down outside of that familiar zone and makes the system weaker.

Dr. Weitz:                            I notice you also mentioned adrenal cortisol dysregulation as pointing a role in biological aging.  Is it in general, can you say, is it more of a lower, flattened cortisol curve or increases in cortisol that tends to correspond to worse aging?

Dr. Stickler:                         I mean, it’s not a … It’s that double edged sword again. Too little is not good and too much is not good. So you want to kind of keep within certain parameters with slight excursions outside of your familiar zone to create the positive response.

Dr. Weitz:                            Right.

Dr. Stickler:                         But most of the time … We do a lot of work with adrenals and we look at diurnal variations in the cortisol secretions and what we’ve found generally is we tend to blame the adrenal gland for it and the adrenal gland is nothing but the messenger. We find that when we work with stress response as far as what the perception of stress is and how the brain responds to it and how it stimulates the adrenal gland, that’s the win for the mitigation of this where we train through bio feedback mechanisms to do that.   Now, using adrenal adaptogens and that, they’re nice bridging pieces for it, but really you’ve got to get to the real central aspect of what’s creating the stimulation or lack of stimulation to the adrenal itself.

Dr. Weitz:                            Bringing up nutritional supplements, you mentioned a few already. We talked about zinc and vitamin D. You mentioned quercetin or quercetin, I’m not sure how it’s supposed to be pronounced, and that calcium supplement you mentioned. What other nutritional supplements … I think you mentioned nicotinamide riboside or…

Dr. Stickler:                         NMN.

Dr. Weitz:                            NMN, okay. You think that’s a preferred version over NR?

Dr. Stickler:                         Again, that’s something that we don’t have good data on.

Dr. Weitz:                            Okay. Okay.

Dr. Stickler:                         I mean, one of the biggest problems is people report doubling or tripling of NAD levels and when you see that, always question the study, because what we care about is absolute levels, not change from baseline, because somebody that’s got a 1% of where they should be and they triple that, they’re at 3%. What kind of boost is that? That’s not.

Dr. Weitz:                            Right. Yeah, yeah.

Dr. Stickler:                         So looking at the ideal way to do this, and really, I’m not a big fan of the NIDIVs. I mean, they give you a short burst, but the body gets rid of that in the next 24 hours. I think a lot of what people experience as a stress response that creates a euphoric feeling and they perceive that they’re getting benefit from it. So what most people are looking at is how do we chronically supply new NAD to the cells and so the debate is do we do intramuscular injections daily? Do we do IVs? Do we do supplementation? Should we do NR or NMN? There’s going to be some data coming out from James Clemons’ lab that I think is going to probably shift us more towards using NMN iontophoresis where we actually put a patch on, an electrical patch, that we put the NMN in to that will absorb based on electrical charges and we can do that even twice a day or a couple times a week and create the higher levels of NAD in the cells, which is really the ultimate goal in that.

Dr. Weitz:                            Interesting. What about resveratrol?

Dr. Stickler:                         Resveratrol is … I wouldn’t look at it from a standpoint of what they were initially looking at it. I mean, they were looking at it as a SIRT receptor stimulant and creating more NAD, but I think resveratrol actually has antiaging benefits.  Are they from what we think we are saying?  I’m not sure.  I think resveratrol for somebody who is interested in age rejuvenation, and we add that to our senolytic formulation.  I think that there is some benefit, we just don’t know what it is right now and I think it’s kind of minor, but we’re still looking at what’s the complete complement that can create the system?  One thing that people tend to neglect is a daily multivitamin.

Dr. Weitz:                            Right.

Dr. Stickler:                         We have so many micronutrients that are deficient when we look at our nutritional intake and our nutritional needs and so I have a core that I put everybody on. It’s a foundational multivitamin, and not an excessive one. If some people are taking like six or seven multivitamins a day. I’m just like if you’re taking more than two, you’re probably taking too much. Just eat healthy, take a small dose of it. The vitamin D, and we use a 5000 IU or D3 plus K2 fish oil, so we do use fish oil and this is because of epigenetics. I mean, there’s always debates about is fish oil good for you?  Is it bad for you?  Different outcomes in the same week from the research.  But what we do know from epigenetics and nutrigenomics is the chronic intake of fish oil really up-regulates metabolic gene activation and down-regulates pro inflammatory gene expression.  So we do use fish oil, usually just two gram a day, and we also recommend B12 supplementation and either through injections or through a sublingual.  Those are essentially our core, what we call foundational supplementation and then from that point on, we go into more bio-specific or more longevity focused or performance focused lines of vitamins, but we just have that foundation of we pretty much recommend for everybody as a core.

Dr. Weitz:                            Okay. What about specific diet? Has there been any work on … I noticed on the True Diagnostic website, Mediterranean diet was mentioned. What about Mediterranean diet versus vegan versus paleo or et cetera? Do we have a sort of…

Dr. Stickler:                         It again comes from [crosstalk 00:47:57].

Dr. Weitz:                            Depending on the person? You know?

Dr. Stickler:                         Yeah. I mean, it’s genetics again. When we look at gene expressions based on dietary patterns, there is no perfect human diet. I mean, if you take somebody that’s got an ancestry with [inaudible 00:48:17].

Dr. Weitz:                            We’re getting a weird echo.

Dr. Stickler:                         Yeah, there’s actually a lawnmower outside.

Dr. Weitz:                            Oh my gosh.

Dr. Stickler:                         Sorry. Yeah, didn’t expect that.

Dr. Weitz:                            Okay, not much you can do about that.

Dr. Stickler:                         Yeah. But if you have somebody with ancestry of Inuit Eskimo, their genetic polymorphisms that they’ve inherited are optimized for that environment, so a high fat diet is going to work very well for them. If you have somebody who is southeast Asian and more of a starchy diet works for them. Most of us in the United States have some kind of a core background of a Mediterranean heritage and around that, so European, Mediterranean, you’re going to find that the genes respond best to the components of the Mediterranean diet. A fish-based, high vegetable and significant intake of olive oils, we’re finding that the markers that we look at in aging, we are personally, from an anecdotal experience, finding that seems to correlate best with the outcomes.

Dr. Weitz:                            Yeah. So essentially as we’ve been talking about in functional medicine for a long time, you’ve got to match the right diet to the right person. What medications have been shown to slow down or reverse epigenetic aging?

Dr. Stickler:                         Well, the first one I talked about earlier was the dasatinib. That is a senolytic that’s really powerful and what we typically do is we’ll do…

Dr. Weitz:                            Is there another name for that? For those of us who are not familiar with it?

Dr. Stickler:                         Not that I’m aware of.

Dr. Weitz:                            Okay. Okay.

Dr. Stickler:                         [crosstalk 00:50:06] is, but I can’t think of it right now.

Dr. Weitz:                            Okay.

Dr. Stickler:                         That’s the generic name. D-a-s-a-t-i-n-i-b.

Dr. Weitz:                            Okay and what was that drug originally developed for?

Dr. Stickler:                         It was used as a … I can’t remember exactly, but it’s been around for many years. This was the one that they found in the bioinformatics platform that found that it limited that, but the way you use that is you typically take it for two days, like a Monday and a Tuesday for two to three weeks in a row and then you stop and then six months later you may take it again.  The thing with senolytics is they tend to target specific organ types. So the skin, the liver, the fat. You will target different areas that it will reduce the senescent cells, so you want to use combinations of those. We also have rapamycin. Rapamycin is wonderful. This was developed as an adjunct for people that have had kidney transplants to suppress the immune system.

Dr. Weitz:                            Right.

Dr. Stickler:                         But we use it in lower doses and dasatinib is a [M4 00:51:25] inhibitor, which is one of the aspects that we know creates more youthful expression in the body as inhibiting M4 over time. But the other thing they found is that, when we talk about senescent cells, and I think this is the most important thing that rapamycin does, is it mitigates what are called SASPs that are secreted by senescent cells and those are the toxic elements that are secreted by these cells. So the rapamycin seems to mitigate that and you don’t do a lot of this. I mean, it’s like a once a week dose of two to three milligrams that is effective in that and you have to watch for side effects with it.

                                                The other one is metformin. I mean, classic. Metformin is one of those ones that anybody focused on longevity, we typically work with on the metformin. It is a true M4 inhibitor. It’s one of the most potent ones that we have available to us and a lot of people will say, “Well, doesn’t inhibiting M4 limit the ability to grow muscle?” Which frailty is a hallmark of aging, but all the studies that have been done have been using metformin as an individual piece. Now, with our clients, we will use things, other things like testosterone or growth hormone, releasing hormone, and we monitor DEXA scans to see what their lean body mass is doing over time. We’re finding that the metformin is not indicative of muscle growth in that way, so we like the metformin in that regard.

                                                You’ve also got some peptides, which don’t have a great deal of research behind them, but they’re finding that they do have significant impacts on aspects of aging. I mean, we look at things like mitochondrial rejuvenation and mitochondrial biogenesis and we have things like GW501516, which is not a peptide, but a research chemical. We have things like SS31, which is a fairly new one. We have things like MOTSC, which are peptides that have the substantial impact on mitochondria. Those are also ones called [inaudible 00:53:53] which we don’t have a great deal of data on and there’s things like [Hepatilon 00:53:57] which from the Russian researchers, they have a six and a 12 year study using Hepatilon. We have things that can rejuvenate the thymus like Thymoline or Thymosin alpha, which boosts the immune system.

Dr. Weitz:                            What about BPC157?

Dr. Stickler:                         BPC157 I really like. I love the oral form for the gut. I mean, you talk about something that heals the gut almost 100% of the time, [inaudible 00:54:27] oral BPC. Talking about working on really neuro-protection or soft tissue recoveries, BPC is wonderful for that. It accelerates the recovery for that. I don’t find that it happens very well with the oral, but the oral is awesome for the gut, for sure.

Dr. Weitz:                            Cool. Good. So I think that pretty much concludes my questions. Any final thoughts you want to leave us with? And then give us information about how to find out about this test as well as anybody who would like to get ahold of you?

Dr. Stickler:                         Yeah. The one thing I always like to emphasize is that everything starts with lifestyle, first and foremost. I mean, and that’s what I tell people, 90% of what I do in my program is lifestyle orientation and you can’t focus on the standards of just nutrition and exercise. I mean, if you’re not addressing stress, if you’re not addressing brain health, if you’re not addressing even mindset. I mean, mindset is a huge piece. Love and relationships, a huge piece. So all of these lifestyle components play together and trying to isolate them into silos and thinking you’re going to have an impact is naïve. So really working with all aspects of the way you function is really important.

                                                Now, to get the epigenetic test and really to be part of something that’s pretty exciting, go to truediagnostics.com and you can find out how to order the test. You can order it direct, even. You don’t have to have a physician, but I recommend having a physician that can help you interpret it or a health coach that can help you interpret it. I mean, there’s probably more non-physicians that understand epigenetics better than the majority of physicians. I mean, I think physicians are moving into a world where it’s going to be sick care only and because 90% of our health is lifestyle, I think you’re going to see the functional practitioners, the coaches, all of this are going to be the go-to’s for really optimizing health and maintaining your baseline. So for anybody who wants to look into us, we have … Our website is apeironzoh.com, so it’s a-p-e-i-r-o-n-z-o-h.com. Apeiron Zoh is great for limitless life and that’s really our mission is to help create that limitless aspect of what’s possible.

Dr. Weitz:                            Great. Thank you, Dr. Stickler.

 

Weitz Sports Chiropractic and Nutrition
Weitz Sports Chiropractic and Nutrition
Supercharge Your Metabolism with Steph Lowe: Rational Wellness Podcast 183
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Steph Lowe discusses How to Supercharge Your Metabolism with Dr. Ben Weitz.

[If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on YouTube at https://www.youtube.com/user/weitzchiro/]

 

Podcast Highlights

4:30  The Low Carb Healthy Fat (LCHF) diet.  The high carb, whole grain diet promoted in western countries leads to blood sugar issues, inflammation, and weight gain. We should focus on eating foods that come out of the ground, off a tree or from an animal–foods that have the least amount of human interference and the highest nutrient density.

5:56  Healthy fats include olive oil, olives, oily fish, nuts, seeds and avocado.  We should avoid pro-inflammatory seed oils like canola, corn, and soybean oil.

9:04  Saturated fats have been demonized for five decades, but the idea that saturated fats cause heart disease has been disproven in the literature.  Steph supports the use of foods like coconut oil, grass fed butter, and ghee, as well as grass fed animal fats found in meats.  Our brain is 25% saturated fat and saturated fats are important components of our cell membranes and are the building block for hormones.   She also does not think that we should be eating a huge plate of steak with a slab of butter on top.  Her version of LCHF is actually largely plant based has a lot of fiber and she recommends eating six or more cups of vegetables per day. If we look at the Blue Zones, the areas in the world where people live the longest, people think they’re vegan, but while they don’t eat a lot of meat, they do eat eggs and seafood in small amounts and the common denominator is plants.

12:07  You get better blood sugar control and better long term energy when you rely more on fats than on carbs.  When you eat a lot of carbs, esp. high refined carbs, you are on a blood sugar roller coaster.  When you reduce the carbs and eat more healthy fats, you get fewer cravings for carbs.

20:11  After high intensity exercise Steph believes in ingesting some extra carbs, such as fruit in a smoothie. She finds that eating carbs prior to working out may cause digestive issues, since digestion is impeded by exercise.  The carbs after exercise do not need to be within 30 minutes but can be somewhat after that.

32:10  Some of the negatives of following a low carb diet are that people may have emotional attachments to foods like bread and therefore have trouble following it, so she recommends an 80:20 rule where they can follow it 80% of the time and deviate 20%.  There are also negative health consequences of following an imbalanced low car/high fat diet where you are eating a number of coffees with cream and eating a big steak with butter and cheese and very few vegetables. You will be missing out on essential vitamins, minerals, and important phytonutrients. Steph believes in eating some fruit like berries and some sweet potatoes and lots of vegetables. Having some sweet potato can make it easier to sleep.  It is also not healthy to get too extreme about following a ketogenic or low carb diet and being obsessed with your macros, your online diary, your finger pricking or your breath ketones.  It is better not to be too extreme.

 



 

Steph Lowe is a sports nutritionist and yogi from Melbourne, Victoria and she is the founder of The Natural Nutritionist and author of Low Carb Healthy Fat Nutrition.  Her website is TheNaturalNutritionist.com.auHer podcast is Health, Happiness, and Human Kind.  On Instagram Steph is @thenaturalnutritionist.

Dr. Ben Weitz is available for nutrition consultations, including remote consults via video or phone, specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111 or go to www.drweitz.com. Phone or video consulting with Dr. Weitz is available.

 



 

Podcast Transcript

Dr. Weitz:            Hey, this is Dr. Ben Weitz, host of The Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field, to bring you the latest in cutting edge health information. Subscribe to The Rational Wellness Podcast for weekly updates, and to learn more, check out my website, drweitz.com. Thanks for joining me, and let’s jump into the podcast.

                                Hello Rational Wellness podcasters, thank you so much for joining me again today. Today our interview is with Steph Lowe, who’s a sports nutritionist and Yogi, all the way from Melbourne Victoria in Australia, and she’s the founder of The Natural Nutritionist and the author of the Low Carb Healthy Fat Nutrition book. And, so we’re going to talk about the low carb high fat diet and especially as it relates to metabolism, so thank you so much for joining me today Steph.

Steph Lowe:       Awesome to be here, thank you.

Dr. Weitz:            Good, so maybe you could start by telling us your own personal journey, how you came to become a nutritionist, and how you found now the low carb high fat diet?

Steph Lowe:       Yeah, for sure. So, I mean, like a lot of people in the industry I do have my own personal journey with food, which started back as a teenager when I decided I wanted to lose weight to achieve this happiness that I thought that being thin would create.

Dr. Weitz:           Did you achieve happiness?

Steph Lowe:       I did not. I cut all fat from my diet, I became very disordered, and my poor mother was so worried that she took me to see a dietitian. And I still remember sitting in the dietician clinic thinking how amazing this woman’s job was, that she gets to sit here and talk about food, so I definitely know that the seed was planted then. Not surprising, when you cut all the fat from your diet you start to have mental health issues because your brain is predominantly fat.  So I then experienced what was never diagnosed but certainly felt like depression, and I met someone who convinced me to cut gluten from my diet. This is over 15 years ago, I wasn’t a nutritionist, really no one knew what gluten was and how to maintain a gluten free approach, but I was pretty desperate to feel better that I was willing to try anything.  And for me personally, the difference was night and day.  So, I started to have a lot more clarity of focus, a lot less issues with regulating my mood that I was really inspired to learn more.  So, it started as gluten free but it quickly became understanding more about the healing power of food, and when you learn that for the first time it’s pretty mind blowing that we haven’t been taught that from a young age.  So, I was inspired to go back to uni and study my post grad in nutrition, so I had what we call- 

Dr. Weitz:           We learned about the food pyramid, right?  12 servings of bread and pasta every day.

Steph Lowe:       Yeah, exactly. And in Australia, and it’s obviously the same way you are, that’s what we define as healthy, and we certainly over the last five or more years have really understood how wrong we had it. So, I set myself a mission to unpack a lot of the myths in the nutrition space, especially the food pyramid and how fats have been demonized for five decades, so I got my qualifications as a nutritionist and started The Natural Nutritionist in 2011. So, that was a while ago now if we think about how rapidly the real food space has evolved in that time, but I was a triathlete doing long course distances like 70.3s or half Ironman, and naturally that will is really high carb.  I remember going for long bike rides and being told to take multiple gels that just make you feel sick, and when you read the ingredients the logical mind would definitely tell you that it doesn’t make sense to be fueling with all this sugar.  So, I was determined to find another way.  So, I do work with a lot of long course athletes to this day, but my niche is different as my journey has evolved because, as you would know, real food movement and certainly the low carb movement is pretty big now which is amazing, because we need to be having this conversation and moving away from the food pyramid.

Dr. Weitz:            So, tell us about the low carb high fat diet and why should someone follow it?

Steph Lowe:       Yeah, so there’s a lot to discuss there because my version of LCHF, it stands for lower carbohydrate healthy fat, so lower as in context to the food pyramid. So, you said before 12 serves or sometimes we see six to eight serves of whole grains per day, but regardless, that’s 400 or more grams of carbohydrates per day. And what that creates is what we see in western countries, we see not only blood sugar issues and cravings, and the weight gain that occurs with excess carbohydrates, we’re now seeing chronic diseases that are all inflammatory in nature, that have origins in excess refined carbohydrates and sugar. So, it’s a disaster. Versus lower carbohydrate healthy fat, we’re actually talking about real food. So, food that comes out of the ground, off a tree, or from an animal, and the latter is an option of course, you don’t have to eat animal products, but we’re looking for food with the lowest degree of human interference, because we know it all have the highest degree of nutrient density, the opposite is true to right, so if we see food or we look at food that has a high degree of human interference it’s nearly always going to be really nutrient poor, and that’s not what our body needs.

Dr. Weitz:            So, what are healthy fats?

Steph Lowe:       Healthy fats should be predominantly Omega-3s. So, our anti inflammatory fats that come in whole food forms like olive oil, olives, oily fish, nuts, seeds, avocado, for example.

Dr. Weitz:            Olive oil and avocado aren’t necessarily high in Omega-3s.

Steph Lowe:       Well, they certainly contain Omega-3s and they are these beautiful whole food forms. Avocado, for example, naturally contain some omega six, but we don’t want to be eating too many omega sixes, but the real issue are the pro-inflammatory seed oils like that we used through the 80s and 90s.

Dr. Weitz:           Which are those?

Steph Lowe:       Well canola is a big one that still really popularized to this day, but it’s really any- 

Dr. Weitz:           Now, some people like canola because they say it’s higher in Omega-3s.

Steph Lowe:       Yeah, look and certainly the vegan movement really celebrates canola oil. I personally disagree with that, because we know that the optimal ratio for health is a one to one ratio between our Omega-3s and omega sixes. So, we’re not saying don’t eat any omega six, but using it as your predominant oil can’t makes sense because you would be creating a pro-inflammatory environment, and there’s incredible studies in the literature around the role of that one to one ratio.

Dr. Weitz:            Well, that one to one ratio is kind of extreme, I mean, that’s not I don’t think generally accepted.  I’ve certainly heard people say the one to one ratio is maybe what our paleolithic ancestors ate, but if you look at most of the normative values for, say, Omega-3 to six ratio, they typically say under four to one is considered normal, is considered optimal.

Steph Lowe:       Depends on your health goal, it’s like our blood test reference ranges. You can certainly set yourself a goal of “normal”, or we can look at what optimal is, and everyone has their own goals around what they want their health and their longevity to look like.

Dr. Weitz:           One to One is tough to achieve though.

Steph Lowe:       Do you think so?

Dr. Weitz:           Oh yeah, I need-

Steph Lowe:       On a whole food diet?

Dr. Weitz:           I think so. I think so, because most of the fats are still not going to be Omega-3s, olive oil is basically omega nine, and there aren’t that many foods that are really high in Omega-3 other than fish oil, flax seeds, so it’s hard to get one to one in Omega-3. I know I measure mine regularly and I try to keep it at two to one, but to do that I have to consume about eight grams of fish oil a day. So, it’s not easy to get to one to one, there aren’t that many foods that are super high in Omega-3, even if you have grass fed beef it’s still not predominantly Omega-3, it’s higher in Omega-3, but… Anyways, but so what are other healthy fats besides olive oil, avocado,…

Steph Lowe:       So, then we need to look at saturated fats, which naturally have been demonized for five decades. Now, it’s been disproven in the literature, but unfortunately it’s a myth that is hanging around quite strongly. And, again, I think it’s perpetuated by specific food trends, but if we, again, think about what food has the lowest degree of interference, I support the use of things like coconut oil, grass fed butter, and ghee. And then there are additional grass fed animal fats for those that are inclined. We only need to be having about 20% saturated fat from that component of healthy fats, but we do need to acknowledge that when we look at what saturated fat is, by weight 25% of it is in our brain, it’s a really important component of all cell membrane, and is a foundation building block for hormones.  So, we need to stop demonizing saturated fat but, at the same time, we don’t need to be eating just a huge plate of steak with a slab of butter on top. I think there’s lots of extremes in the health space, whereas my version of LCHF is actually largely plant based, where eating about six, if not more, cups of vegetables per day on a good day. And that’s what everyone can agree on, almost everyone, I’m not talking about the carnivore here, but almost everyone can agree on the role of a fiber rich diet with plants predominant. If we look at the Blue Zones, for example, people think they’re vegan, they’re not really, they don’t eat a lot of meat but they do eat eggs and seafood in small amounts, but what the common denominator is, is plants. And I think that’s an important conversation, because if you look at the food pyramid it doesn’t really celebrate vegetables; it celebrates bread and cereals, and almost everyone I meet is probably eating between one to two cups of vegetables per day. And so, it’s well under our goal of that six cups.

Dr. Weitz:            Yeah, it’s hard to get a lot of vegetables in, most people are not used to eating vegetables and they’re not super tasty or super rich, so you have to get used to eating a lot more vegetables to get yourself off that rich, super palatable, standard American, standard Australian diet.

Steph Lowe:       Well, yeah. The addictive food, you’re right, when you’ve got poor blood sugar control and you’re addicted to carbs, you’re not going to crave broccoli, it’s going to taste quite bitter and you’ll find it more of a chore to eat, versus one of the major immediate benefits of LCHF is blood sugar control. So, you can do way more than a 12 hour fast without being hungry, you can eat every four or five hours, you don’t have cravings, you don’t crash at 3:30, or 4:00 o’clock, and your taste buds change. So, food that once you thought was delicious will taste ridiculously sweet or unpalatable, and then vegetables will start to taste really nice, and pumpkin will taste sweet, and you’ll actually really enjoy that food, it just takes time to adjust, like anything.

Dr. Weitz:            And, so you get better long term energy because you’re relying on fats rather than getting carbs.

Steph Lowe:       That’s the thing, carbohydrates, especially refined carbohydrates, cause that blood sugar rollercoaster. So, it’s a disaster during the day for energy and productivity, but by the afternoon it becomes pretty impossible to deal with when we’re having cravings and really struggling to stay awake, for a lot of people were relying on more caffeine, perhaps, whereas LCHF you have just beautiful stable energy, stable blood sugar, great satiety, and my clients they will definitely notice that shift in their cravings, which is, that’s proof in the pudding. We don’t need these carbs and high sugar foods to prop us up anymore we’re burning fat that energy.

Dr. Weitz:            Are there certain specific patients or categories of patients who maybe don’t do as well with a higher fat diet? I’m thinking of perhaps people with unfavorable lipid profiles and a history of heart disease, or maybe people who have one or two copies of the apoE4 gene.

Steph Lowe:       Yeah, so there are definitely some more detail that we need, and that’s why I think testing is really important. So, if you’re going to embark on a low carb diet there’s lots of different tests that you would do, and certainly your blood lipid profile and some genetics could be fascinating. Now, the thing is about how we have interpreted a blood lipid profile over the last five decades is, we’ve done that very incorrectly, we’ve just basically look at total cholesterol, and if it was high we’ve assumed heart disease risk, which we know is hugely incorrect.  So, the first thing that we actually want to look at is what the inflammation is, or is not. So, we look at triglycerides less than one, which would pretty much almost always rule out any heart disease risk, but we do want to dig deeper than that.  So, we look at the total cholesterol to HDL ratio- 

Dr. Weitz:           Triglycerides less than one, maybe in the United States that would be under 100, I think.

Steph Lowe:       Yes.

Dr. Weitz:           Yeah, okay.

Steph Lowe:       The units are always going to catch us up, but the ratios are fine. So, when you look at a total cholesterol to HDL ratio we want at 3.5, and that tells us that even if we have LDLs, or high LDLs, that they were large and fluffy, so they protect the heart. Whereas the higher that total cholesterol to HDL ratio is, and certainly five and above, will tell us that there’s small dense particles that carry plaque and that’s problematic for cardiovascular health. So, we definitely need to be interpreting our blood lipid panel differently, and then it will-

Dr. Weitz:           And even better would be to get advanced lipid profile that includes lipid particle size.

Steph Lowe:       Yeah, you can do testing now, can’t you, so rather than just interpreting and using correlated information, you can do advanced profiles and look at your lipids.  Anyone that’s, say, older who might have more risk factors like family history or carrying extra weight around the middle, you can do Lp(a), a coronary calcium score, there’s many more diagnostics that are far more indicative of cardiovascular disease health, than just looking at total cholesterol.

Dr. Weitz:           Yes, for sure. So, how is your low carb high fat diet different than, say, paleo or ketogenic?

Steph Lowe:       Yeah, there are some obvious similarities in that with focusing on real food, so that’s very much the Paleo model. But, the thing is with keto is, by definition it’s- 

Dr. Weitz:            By the way, real as opposed to refined, or processed?

Steph Lowe:       Yeah, exactly. Food that comes in a packet or a box.  So, keto is quite low carb, so it’s somewhere between 25 and 50 grams of carbs a day usually, and more typically the lower end of that, especially if someone’s got Type two diabetes or metabolic syndrome, but that is quite low and should be prescribed when someone has a metabolic condition, and we would know that by diagnostics, again, so glycated hemoglobin or HbA1c, the higher it is, the more say on the other side of 5.3 it is, the more you’re insulin resistant.  And so then the obvious solution to that is to address the insulin resistance by lowering the carbohydrate, but if you have a HbA1c of 5.3 or lower, like a five, you don’t need to be only eating 25 to 50 grams of carbs per day.  If you’re a male athlete who does some intensity, you could be eating up to 150 grams of carbs a day, so that’s more than three times a keto diet, but for some people, not everyone, but they’re still experiencing all the benefits from a clarity of mind, a concentration, a performance, a recovery, and a longevity benefit, and it’s a lot more food and a lot more sustainable. So, I think it’s important that it’s really individualized.

Dr. Weitz:            Does it matter the time of day people eat their carbs?

Steph Lowe:       There’s a lot of different theories on that, as you would know, so what we want to understand is a lot more about the exercise program or schedule, because certainly high-intensity exercise is naturally going to be utilizing muscle glycogen as the fuel. And so, many people feel like they recovered better if they eat whole food carbs like fruit in a smoothie the hour after a high-intensity workout, the same doesn’t apply for anything aerobic in nature because that’s naturally a more fat burning session.

Dr. Weitz:            What about carbs before the exercise to fuel the exercise?

Steph Lowe:       There are some people that feel much better if they do pre-load with carbohydrates before high-intensity exercise, but the thing about high-intensity exercise is that it’s really- 

Dr. Weitz:            By the way, what do we mean by high-intensity exercise?

Steph Lowe:       Well, there’s lots of formulas, but as a general rule we use the MAF formula, so it’s Phil Maffetone formula, and so 180 minus your age would tell you where essentially that crossover point is. So, higher than that would be considered high-intensity, whereas lower than that would be aerobic or low intensity. So, it’s a formula that you use, 180 minus your age.

Dr. Weitz:            So, if I were doing a traditional heavy weight training session where I’m doing sets of, say, maybe eight to 10 reps with as much weight as I can, and maybe taking a minute or two rest in between. Is that a high-intensity or are we talking about doing maybe a circuit training where you’re going from one exercise, or one set to the other with very little or no rest, and maybe lighter weight. So, are those both high-intensity, what’s high-intensity?

Steph Lowe:       It all depends on the heart rate response, so everyone is going to be really different.

Dr. Weitz:           So, it all depends on the heart rate?

Steph Lowe:       Yeah, they both sound like they’re potentially high-intensity to me, because of the volume of weight in the first example, and then of course the circuit nature is nearly always high-intensity. But, then it becomes really individual, which is why we tend to use heart rate, so it’s not so subjective. Some people use RPE which is that rate of perceived exertion, but it’s very vague, we need to know how to interpret that.  And so it’s not a clear definition, whereas, if you get to the end of a session you know what your average heart rate is, you can call it, so you know what you really need to refuel with.

Dr. Weitz:            And you’re saying for high-intensity you don’t necessarily need carbs before, but you should have carbs afterwards to refuel your glycogen?

Steph Lowe:       Yeah, the thing is about that, if you have it prior, a lot of people find I start to get digestive issues, because when you start exercising naturally your blood flow goes outwards, so to heart, lungs, legs, extremities, et cetera. So, you don’t have the blood flow coming into the gut, so we tend to find our digestion it’s compromised, and we see many examples of that certainly in Ironman races where people experience a lot of unnecessary gastrointestinal distress, and it can happen in much more mild versions of that when people eat before exercise.  If it’s later in the day and we’ve been up for many hours and we’re training in the evening, and lunch has been hours ago, and dinner is not for another couple of hours, then usually we’re going to feel better if we’ve eaten, but the same wouldn’t apply to the morning, because if we wake up we haven’t depleted any muscle glycogen, we’ve only depleted a little bit of liver glycogen overnight, and that’s irrelevant for training. And so, we don’t have anything to replenish, and we feel more often much better without having anything prior.

Dr. Weitz:            And so, is it important to get a certain amount of carbohydrates within a certain period of time after the exercise, do you believe in that glycogen replenishment window concept?

Steph Lowe:       I do, but it doesn’t need to be 30 minutes or anything ridiculous, because that’s the other thing, the same applies to our digestion on the other side of high-intensity. Almost everyone will say to you, they don’t feel like eating straightaway, and that’s because their body is diverting the blood flow outwards again it’s not coming into the gut. So, we tend to want to wait until we’ve actually cooled down, maybe do your stretches have a shower and get yourself organized, and then think about eating, rather than running to the kitchen for fear of not recovering, which is a myth that’s been perpetuated by the protein powder industry.  So, I think it’s going to be quite individual, but I’d say roughly an hour.  And it’s only between 30 to 50 grams of carbs usually for a female up to–it’s not bowls of pasta or anything like, again, we might have been told.

Dr. Weitz:            What about endurance athletes who maybe are going to go on a two hour bike ride?

Steph Lowe:       Yeah, so it depends on how fat adapted you are or are not. If you’re just starting out and you’ve been following a high carb diet, then naturally you’re not going to be able to do two hours without fueling because your body is very sugar burning in nature, so that’s why we see people needing to have gels or Gatorade or different versions of that. But, when you’re fat adapted, and in fact, a good barometer of how fat adapted you are, is when you can do two hours fasted, when you have the ability to do that on water, lemon, and salt, our natural electrolytes.

Dr. Weitz:            Should fat burning athletes maybe have a packet of peanut butter or almond butter, in other words, should they have the fat version of the carb load in the middle of their training session?

Steph Lowe:       So, it depends on the goal of the session. So, certainly if the session continues to be aerobic in nature, so under that 180 minus your age, and you want calories, you can definitely be doing that from fat sources. It’s just going to depend on whether that’s practical for the type of exercise you’re doing, there’s nothing wrong with having some carbohydrates after that two hours, but what we don’t want to choose is gels or Gatorade which play with our blood sugar and spike and crash us. So, that’s why we tend to look for more natural carbs or products like Generation UCAN, or SFuels, because they’re designed to support that fat burning metabolism, but give us a small amount of carbohydrate to help us extend those long-

Dr. Weitz:            What are those products you just mentioned?

Steph Lowe:       So, Generation UCAN is made from a modified corn starch, so it’s been heat treated in such a way that it has a slower release, so it’s a slower release in terms of that carbohydrate, a bit like how you do low GI.  We want it to be slower release, and so we can fuel off those carbs rather than spiking and crashing and needing more. And SFuels has a similar concept, they use some MCT oil in there, as well, which we know increases fatty acid oxidation, and they’ve got their own proprietary blend but the concept is quite similar in terms of it being a fuel to help us for that longer session, without impacting our metabolic goals and our fat burning capacity.

Dr. Weitz:            Is this high fat training program catching on among athletes, if we were to say survey athletes in the Olympics, what percentage of them you think are using a high fat fueling program?

Steph Lowe:       I don’t know if the Olympics is the right example because that a lot of high-intensity exercise there, so-

Dr. Weitz:            Okay, so what’s a right example?

Steph Lowe:       I think that’s why we see it happening in sports like Ironman Triathlon, because it is a really perfect example of where you need to be fat adapted, because some people are out there for 17 hours. So, it’s not possible to consume that many grams of carbohydrates every hour upon hour when you’re out there for seven to 17 hours, and so it really does suit the more aerobic athletes, ultra runners, triathletes. Now, I’m not saying that people in the live Olympics can’t do it because they’re all going to do aerobic sessions as part of their training, but I just don’t think it is as popular as they are yet. It should be because it is the best approach for longevity and managing inflammation, which naturally helps recovery and longevity, but we just need to acknowledge that it would need to be applied, very specifically for someone who’s doing a lot of high-intensity exercise.

Dr. Weitz:            Yeah, how does low carb/high fat benefit metabolism?

Steph Lowe:       So, if you’re eating a food pyramid and you’re eating those 400 grams of carbohydrates per day, your body relies on sugar so you’re in that constant sugar burning state, when we burn sugar we also produce those reactive oxygen species and they are pro-inflammatory, so that’s why we see issues with recovery, issues with our inflammatory markers, and then unfortunately those chronic lifestyle diseases that happen after time. Whereas fats burn clean, there’s only byproducts of carbon dioxide and water, so there are no inflammatory species, reactive oxygen species, and we, again, create this fat burning metabolism which means that we have fat to burn as our fuel, so as our Diesel, versus sugar which acts more like petrol.

                                And then we have those benefits that I was talking to you about before, like the blood sugar control and the satiety, but it really is the inflammation that’s the most important piece because, again, we know that there’s so many lifestyle diseases that have that inflammatory nature, and most of them could be avoided, like type two diabetes doesn’t need to exist. It is a lifestyle disease that comes from a high carbohydrate diet in someone that’s genetically inclined to become insulin resistant, and I meet people who still think that type two diabetes is a life sentence. And to me that’s tragic that no one’s told them that there’s a dietary fix to put that disease into remission, they think it’s a life sentence of taking medication and running the risk of lots of side effects which come from the medication, and the increase in medication required when the weight continues to go up, and their diabetes continues to get worse. That’s a real tragedy of this century.

Dr. Weitz:            Oh, absolutely. Yeah, I’m a chiropractor and I also do the Functional Medicine, and so when patients come in for chiropractic, and we had a patient a couple of weeks ago, and I was helping him with his back and then I noticed that he had some blood sugar issues and was pre-diabetic, and I asked him what he was going to do about his pre-diabetes and he said, “Oh, my doctor said, just wait until the blood sugar gets higher and then we’ll put you on medication.”

Steph Lowe:       And so we have, unfortunately, a reactive health care system, whereas you and I are very proactive. So, a blood sugar issue can be addressed with a lower carb diet, so you don’t need to wait until you’ve been diagnosed with diabetes to fix it, and I think-

Dr. Weitz:            Oh, it’s absolutely insane but our system which is controlled by insurance companies actually doesn’t recognize that concept, so his doctor probably can’t even bill for pre-diabetes, so we can’t really under the insurance system do anything until the patient can get a diagnosis of diabetes.

Steph Lowe:       I know, and so that’s why you go to a doctor when you’re quite sick, and perhaps a chiropractor or a nutritionist when you’re looking to improve your health, right?

Dr. Weitz:            Exactly.

Steph Lowe:       Because we would obviously be able to be much more proactive than that.

Dr. Weitz:            And it’s insane to just get put on medication and not change your diet and lifestyle for a diseases caused by diet and lifestyle.

Steph Lowe:       And there are many examples of that. I think it’s the same with, unfortunately, what we’re seeing with the Alzheimer’s and Dementia epidemic. That has come partly from the low fat era, it’s a metabolic disease, and we’ve depleted our brain of its primary building block, we shouldn’t be surprised that we’re seeing this but it’s absolutely heartbreaking that people are going through this, when they’ve been on statin drugs totally stopping their cholesterol production for years, if not decades, and no one’s really talking about this until the year 2020, and that’s another tragedy that we could have avoided.

Dr. Weitz:            Oh, absolutely. Another factor there is the incredible amount of toxins that get into us from our environment, from the food, from the air, from all the chemicals being dumped into our environment. And so, those toxins-

Steph Lowe:       Again, lifestyle.

Dr. Weitz:           Yeah, absolutely.

Steph Lowe:       For sure.

Dr. Weitz:           Yeah.

Steph Lowe:       I agree, and I think there’s so many lessons. I’ve got a little one, she’s 18 months, and I think to myself, “I don’t know what the world is going to look like when she’s my age, but I hope that we won’t have as many regrets as we do now.” Like when we look at, say, my parents who are in their 60s and 70s, unfortunately I think that generation have been the unluckiest so far in terms of health, because they’ve live through the low fat era, they’ve lived through the polypharmacy era, they’re the ones that have been taking proton pump inhibitors, statin drugs, blood pressure medication, et cetera, et cetera, 16 pills when they get up in the morning. And no one has taught them about the power of food and what you can do to actually come off many of those medications, whereas with my knowledge my children won’t be taking medications, and hopefully that will continue. And it’s important because Big Pharma unfortunately are not interested in our health, they’re really just interested in profit, largely.

Dr. Weitz:            Oh absolutely. Unfortunately I’m in the same generation with your parents, but not following the same path.

Steph Lowe:       Yes, exactly, of course there are many exceptions to the role, but you probably see it in your friends. Do you have friends or people, friends of friends that are taking lots of medication, and I think that’s something that-

Dr. Weitz:            Yeah, it’s tragic.

Steph Lowe:       … could be… Yeah, again, avoided.

Dr. Weitz:            A polypharmacy route, and then the medications counter the side effects of the other medications.

Steph Lowe:       I know, and it continues, that’s how someone could possibly end up on 16 meds.

Dr. Weitz:            Oh, absolutely. So, what are some of the drawbacks, what are the negative aspects of following a low carb high fat diet?

Steph Lowe:       Yeah, so I said to you off air that I think because people like bread, and I’m joking but I’m not because people have these real attachments to certain foods. Now, the way I approach things is 80, 20. So, when I work with a client one on one, I’d never tell them I could never eat bread again, if that was their thing, of course we talk about quality and maybe looking at homemade examples, or how to do it better, what to eat with that bread, et cetera, for blood sugar control. But, ultimately I think if we take an approach to low carb that’s balanced, there aren’t going to be many drawbacks because in that 20% of your week you could technically eat whatever you want.   Now in my 20% I’m still not going to drink heaps of wine and eat rubbish food, but that’s each to their own right, I’ve just learned over the years that sort of food and those choices would make me feel horrible, and I’m just not willing to pay the price, but I don’t make that decision for anyone else. It needs to be sustainable and that’s the main goal.

Dr. Weitz:            Right, so I think one of the important things to emphasize is, there are versions of following a low carb high fat diet whereas, when we were talking off air, the person’s having a big steak with butter and cheese and very few vegetables, and so they have a very unbalanced high fat low carb diet. And that’s where I think you’re going to get into problems with missing out on important phytonutrients, and others essential vitamins and minerals that you would get from having a high plant rich low Carb high fat diet.

Steph Lowe:       Yeah, I agree with you, and that’s why I think keto has gone a bit wrong. I meet a lot of people doing keto, and the amount of dairy that they’re eating and the number of coffees with cream and drinking, it’s really misguided that we need to be even consuming dairy at all, there’s no nutrient that we’re going to miss out on if we don’t eat dairy. Now, if you like it any preference quality and you treat it as an occasional food, then go for your life, but I’m talking about people that have cheese with everything for their fat, and cream and every coffee, and so on and so forth. But, really, vegetables are an afterthought or, as I said earlier, we want this to be plant based, you can eat fruit, you should be eating berries, and you can eat sweet potato.  And you asked me before about what time we can eat carbs, there’s a lot of people that feel like if they do have some sweet potato at night they sleep a lot better because of that serotonin and melatonin relationship, and that’s something that is good to trial and error, as well, because you don’t want to do keto or low carb and then not be sleeping, because the impact of poor quality sleep is horrific, that’s going to take 10 years of your life.

Dr. Weitz:            Right, so there are potentially some negative hormonal consequences of having too few carbs.

Steph Lowe:       There’s negative hormonal consequences of being extreme, honestly, people, I think it’s the diet industry, we’re so used to being 1200 calories, eat less, move more, or starve yourself to be skinny, or only chicken and broccoli to put on muscle, and there’s all these things that we’ve seen over the last 20 or 30 years. And then when you jump into keto or low carb, you become so obsessed about your macros, your online diary, your finger pricking, or your breath ketones, or whatever it might be, that you lose that capacity to see the forest for the trees, because you want to take an approach that’s sustainable. And I just don’t think being extreme is the answer ever.

Dr. Weitz:            So, you’re advocating on your high fat program that people are essentially running on ketones, but you don’t advocate measuring ketones through urine or blood or breath.

Steph Lowe:       You can, so I’m not not advocating, I’m just not… I just think, for many people, it’s not going to suit them, and those that want to do it can do it, and that’s awesome, but we just need to realize that certainly initially we can get some good numbers and understand when we hit that 1.5 to three millimoles of that therapeutic ketosis. But after that, if we’re really efficient at using ketones we’re burning them, so they’re not in the bloodstream, so we might get low ketone readings, but we fast for 16 hours, we only eat, every five we can do two hours aerobic training fasted and there are all these incredible barometers, no inflammation in the blood markers, et cetera. So, there’s so many other barometers that I think give us much more powerful information beyond trying to get so obsessed about every day being in this goal, or in this range, when perhaps we’re actually burning those ketones for fuel.

Dr. Weitz:           So, if people want to measure ketones, should they measure them in blood or should they do the breath testing that’s now available?

Steph Lowe:       I think both can really be good, I many years ago I bought one of the breath ketone meters, and I found that quite easy to use and quite practical, it’s certainly more affordable than doing it via blood, like people that are finger pricking all day will start to really chew through those sticks obviously, so there’s a few variables that one would consider. I don’t mind either, do you have a preference?

Dr. Weitz:           No, not necessarily, I think the blood is probably more accurate, but less convenient.

Steph Lowe:       Yeah, I’d agree.

Dr. Weitz:           Yeah, so you also advocate intermittent fasting, a 16 hour fast as part of your program.

Steph Lowe:       It depends on the individual, so if it’s a female who’s got some hormonal issues going on we wouldn’t be jumping into 16, eight. We know that the sweet spot for women is 12, 12 or 14, 10. We have to acknowledge that most of the- 

Dr. Weitz:            So, you’re talking about 16 hours of fasting, eight hours window of eating, or 10 hours of fasting and 14 hours-

Steph Lowe:       So, If I said 14, 10, it would be a 14 hour fast with a 10 hour eating window, and we find that’s the sweet spot for women usually. Most of the research that’s done around intermittent fasting is in college aged male athletes, so we don’t want to take that data and apply it to women. Now, there are some women that have been doing low carb for many years that are either postmenopausal, so they can jump into 16:8, or those that are really well versed and have a good hormonal balance as referenced by what is a healthy menstrual cycle, and they might do 16:8 twice a week, but I don’t prescribe more than that for a female.

                                But, men tend to have more free rein here, due to that lack of hormonal fluctuation across the month, so they can do 16:8, but like anything you want to qualify it. So, you don’t go into the gym and start swinging 80 kilo kettlebells, so you want to start where you’re at and then build on from there. So, it’s the same with fasting, you want a minimum of 12 hours, so don’t eat from 8 until 8, and then you might add on from there and just make sure you’ve got good blood sugar control, craving control, and that the day doesn’t unravel because you fasted too long, you don’t have your head in the pantry by four or 5:00 PM.

Dr. Weitz:            And what are the advantages of adding this intermittent fasting?

Steph Lowe:       It’s just the perfect opportunity to accelerate that fat burning, because when you’re not eating your body moves into that fat burning state, so you’re really accelerating your ability to be fat adapted, and then 16 hours is incredible because we start to promote autophagy which is that cleaning out of dead and disease-like cells. So, it’s like PAC-MAN goes in, mops up all the potential issues that could be occurring, we know that’s great for managing inflammation, resting the gut, for anyone that’s got digestive issues it’s magic, and then there’s some really powerful longevity benefits that we see with fasting when it’s done appropriately.

Dr. Weitz:            Great, and of course exercise is a great way to promote [inaudible 00:40:47], often not mentioned.

Steph Lowe:       Yeah, very true. What’s the three eat introduced strategies that are about longevity? I think we’re still waiting for a magic pill, but so far there isn’t one. It’s real food, it’s sleep, it’s movement, it’s fasting, it’s nature- [crosstalk 00:41:07]

Dr. Weitz:            Actually, the latest anti-aging compound I’m hearing about is Spermidine.

Steph Lowe:       Oh, really?

Dr. Weitz:            Yeah, there’s always a new one, so…

Steph Lowe:       There is, there is. When we will probably continue to be magic pill orientated, but I think when we go back to the proven answers, they’re right in front of us so far, which is good to know.

Dr. Weitz:            Yeah, which is sleep, rest, healthy diet, exercise…

Steph Lowe:       Time in nature, time with loved ones.

Dr. Weitz:            Time in nature, yeah. Okay, thank you so much for joining us Steph, how can listeners and viewers get a hold of you?

Steph Lowe:       Yeah, my online home is thejnaturalnutritionist.com.au, and I hang out mostly on Instagram @thenaturalnutritionist.

Dr. Weitz:            Okay, that’s great. Thank you so much.

Steph Lowe:       Thanks, Ben.

 

Weitz Sports Chiropractic and Nutrition
Weitz Sports Chiropractic and Nutrition
GI Map Tutorial with Dr. Tom Fabian: Rational Wellness Podcast 182
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Tom Fabian, PhD discusses How to Interpret the GI Map Stool Test with Dr. Ben Weitz at the Functional Medicine Discussion Group meeting on October 22, 2020.

[If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on YouTube at https://www.youtube.com/user/weitzchiro/]

 

Podcast Highlights

2:01  Quantitative PCR vs Whole Genome Sequencing.  The GI Map stool test uses quantitative PCR, which is the best way to detect specific, clinically relevant bacteria or other microorganisms. It also tells you specific quantities, which is important to detect overgrowth and to allow you to see if levels are increasing or decreasing over time.  It can also allow you to detect microorganisms, like H. pylori, that are in pretty low concentrations.  Whole genome sequencing technology is better for getting an overall picture of the microbiome, but it is not good for clinical diagnosis and does not include any physiological markers, like calprotectin.  While quantitative PCR is highly accurate, the ability to detect something comes down to the choice and the design of the primers. Primers are designed for specific, individual strains or organisms.

12:50  The team at Diagnostic Solutions has designed the GI Map stool test with a focus on both research and clinical experience and it helps clinicians to understand the relationship between physiology and the gut.  You can see three common dysbiosis patterns: 1. Insufficiency dysbiosis, 2. Inflammatory dysbiosis, and 3. Digestive dysfunction.  Insufficiency dysbiosis is a lack of beneficial bacteria. And there can be a combination of these three.

15:56  There is some confusion that stool tests do not provide information about the upper gut but only about the lower gut/colon.  But this is not true.  There are a number of bacteria on the GI Map stool test that are more common in the upper gut, including H. pylori, which grows predominantly in the stomach, and the bacilli class of the Firmicutes phylum that includes species like streptococcus, lactobacillus, enterococcus and staphlococcus, which grow predominantly in the small intestine.  These species thrive in higher oxygen environments like the small intestine, whereas the colon is more anaerobic. Bile is present in the small intestine and the species mentioned above are also bile tolerant.  The Proteobacteria phylum, which we tend to think of as inflammatory microbes, are also much more prevalent in the small intestine than the large. Pseudomonas is linked to inflammation in the duodenum and it is also linked to issues with gluten and other food sensitivities.  Also, pseudomonas thrives on simple sugars and amino acids, which are prevalent in the small intestine.  They are also very bile tolerant and you can find these in the bile ducts and in the gall bladder.  Some of the data as to which species thrive in the small intestine comes from Dr. Mark Pimentel’s group, which mapped the microbiome of the small intestine, the Reemagine Study, which was published earlier this year.  [Mapping the Segmental Microbiomes in the Human Small Bowel in Comparison with Stool: A REIMAGINE Study]  

In the colon, the Clostridium class of the Firmicutes phylum tends to dominate and one of the key species is Faecalibacterium Prausnitzii, which is a major butyrate producer.  The Bacteroides group of the Firmicutes phylum is a major group in the colon. Akkermansia is a well known species in the Verrucomicrobia phylum, which is also one of the key groups in the colon. They thrive in an anaerobic environment and tend to thrive on complex fibers, as well as the mucus ecosystem, and the mucus layer in the colon is much thicker than in the small intestine.

22:17  Here are a list of organisms seen on the GI Map that are predominantly in the upper GI Tract: 1. Enterotoxigenic E. coli, 2. Vibrio Cholerae, 3. Yersinia enterocolitica, 4. Cryptosporidium, 5. Giardia, 6. Norovirus, 7. H. pylori, 8. Lactobacillus, 9. Bacillus, 10. Pseudomonas, 11. Staph, 12. Strep, 13. Citrobacter, 14. Klebsiella, 15. Fusobacterium, 16. Candida. 

Here are a list of microorganisms on the GI Map that are predominantly in the lower GI tract/large intestine:  1. C. difficile, 2. Enterohemorrhagic E. coli, 3. E. coli 0157, 4. Enteroinvasive E. coli/Shigella, 5. Entamoeba histolytica, 6. Bacteroides fragilis, 7. Clostridia, 8. Akkermansia mucinophila, 9. Faecalibacterium, 10. Methanobrevibacteriacea, 11. Microsporidium, 12. Blastocystis hominis, 13. Dientamoeba Fragilis.

25:47  H. pylori’s presence can be clinically relevant, esp. if it’s high, even without any virulence factors present.  Tom said that the presence of H. pylori is often associated with reduced stomach acid.  If the virulence factors are present, the two that stand out as most significant with the most research are cagA and vacA.  Virulence factors tend to work together, so the more that are positive, the more likely they will be significant.

33:26  Dr. Sam Rahbar, Integrative Gastroenterologist in Los Angeles, asked if bacteria like Klebsiella and Citrobacter fruendii are found in the stool, should these be seen as markers of dysbiosis or are they potential pathogens that should be targeted for treatment? Dr. Fabian explained that they are opportunistic pathogens that can exist in the gut without any effects or can potentially be part of a pathogenic process. For example, Klebsiella can be associated with certain autoimmune conditions, including inflammatory bowel disease, psoriatic arthritis, and ankylosing spondylitis.  [Here is one article discussing the connection between Klebsiella and Crohn’s and Ankylosing spondylitis:  The Link between Ankylosing Spondylitis, Crohn’s Disease, Klebsiella, and Starch Consumption.]  While a pathogen in the gut may be a trigger for autoimmune disease, it’s not yet clear whether eliminating this bug will improve the autoimmune condition. 

38:58  If a potential pathogen like H. pylori is present as either high in red or a number above the <DL that is black color on the report, whether it creates a problem for a patient depends upon the overall health of the gut and the microbiome.

43:00  If Pseudomonas is high on the stool test, that does not imply that it has colonized the large intestine. This bacteria mostly colonizes the small intestine and the stomach. 

43:57  If the secretory IgA level on the GI Map is low, that is an indicator that the bacteria in the microbiome that produce butyrate, like Faecalibacterium, are at low levels.  While it is a good idea to build up these beneficial butyrate producers in the microbiome with probiotics or prebiotics and more fiber in the diet, that can take some time. In the short term, some clinicians will recommend supplements like colostrum, Saccharomyces boulardii, L-glutamine, and even vitamin A to increase secretory IgA levels.

46:06  Calprotectin is a marker of inflammation in the colon.  If calprotectin is low and the patient appears to have a lot of gut inflammation, the inflammation is probably in the upper GI tract.  For example, Pseudomonas has been shown in research to cause inflammation in the upper GI tract. Candida is inflammatory and if often colonizes anywhere in the upper GI tract, even the oral cavity.  If you have H. pylori, which can cause inflammation in the stomach, you will not see an increase in calprotectin.

52:14  Inflammatory Dysbiosis.  There are particularly inflammatory bacteria in the Protebacteria phylum and some are in the subclass called Gamma Proteobacteria.  These include: E. coli, Salmonella, Shigella, Vibrio cholera, Yersinia enterocolitica, Enterobacter, Morganella, Pseudomonas, Citrobacter, Klebsiella, and Proteus. A lot of them have been shown to secrete the inflammatory type of Lipopolysccharides.  Dysbiosis in the mouth, like with periodontitis, leads to the increase of pathobionts like Klebsiella and Enterobacteria, which can then translocate to the gut.  If bacteria like Klebsiella are able to colonize the gut, this can activate the inflammasome.  If there is a lack of beneficial bacteria in the gut, then bacteria like Klebsiella will be more likely to colonize.  When you see Klebsiella, you should look at the patient’s oral health. You also want to look at indicators of low stomach acid, such as H. pylori or are they taking proton pump inhibitors.

55:48  Digestive Dysfunction Dysbiosis.  Elastase is a marker for pancreatic insufficiency.  If we see H. pylori, then often stomach acid is low. Also if we see overgrowth of Pseudomonas, Enterococcus, or Staph or Strep or if we see Faecalibacterium low, these indicate that stomach acid is low.  Research suggests that if Kebsiella is overgrown, this is a bacteria that often comes from the oral cavity or the respiratory tract, esp. if there is low stomach acid.

1:16:33  Are Blastocystis Hominis and Dientamoeba Fragilis pathogenic organisms (parasites) that should be treated or normal parts of the gut that should not be treated?  I recently interviewed Dr. Jason Hawrelak, well respected Australian Functional Medicine Doctor and expert on gastrointestinal disorders and the microbiome, and he said that these protozoans are extremely common and are generally irrelevant to that person’s symptoms. [Rational Wellness podcast episode 169 on Gut Parasites with Dr. Jason Hawrelak.] Dr. Fabian explained that Blasto and D. Fragilis are not commensal, since they are not present in the majority of patients tested. When we see them present, they are often part of a digestive dysfunction pattern. These protozoans are often seen in the context of things like H. pylori, candida, and general overgrowth. 

 



 

Tom Fabian, PhD is an educator and medical consultant with Diagnostic Solutions Laboratory to help clinicians learn to better interpret the GI Map Stool test. Clinicians can sign up for a professional account to order the GI Map stool test by going to DiagnosticSolutionsLab.com

Dr. Ben Weitz is available for nutrition consultations, including remote consults via video or phone, specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111 or go to www.drweitz.com. Phone or video consulting with Dr. Weitz is available.

 



 

Podcast Transcript

Dr. Weitz:            Hey, this is Dr. Ben Weitz, host of the Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to the Rational Wellness Podcast for weekly updates, and to learn more, check out my website, drweitz.com. Thanks for joining me. And let’s jump into the Podcast. Our topic for tonight is we’re taking a deep dive into the GI MAP stool test.  Tonight, we have Tom Fabian, PhD of Diagnostic Solutions and so I’m sorry for everybody who’s missing the [Biden vs Trump] debate.  And I’m sure there’s going to be a lot of poop discussed, but we’re going to have a much higher level discussion of poop tonight. So Tom, thank you for joining us tonight and I’m sure we all have a lot of questions about our favorite functional medicine stool test, and so we hope to develop some clinical skills to be able to better help our patients.

Tom Fabian:       Absolutely. Well, thanks so much Dr. Ben for inviting me to join your discussion group. And I look forward to interacting with everyone here, and hopefully giving everyone a better understanding of GI MAP and how to better apply it in clinical practice. All right.  So I’m going to go ahead and fire up the PowerPoint here.  So first I’ll just share my screen.  So tonight we’re going to be focusing on a deep dive into GI MAP. So this presentation is meant to be flexible since this is a very interactive group.  So Dr. Ben, if you have any questions in the meantime, definitely feel free to interrupt, or if anyone has anything that I’ve found over, they don’t really understand. I’m happy to stop and we can just cover whatever we can cover in the amount of time.

Dr. Weitz:            Maybe I’ll ask just one quick question since there’s a lot of different types of stool tests that are out there. Can you talk about the difference between the technology used for the GI MAP stool test, which is quantitative PCR, and how this is different than say whole genome sequencing, stool testing?

Tom Fabian:       Sure. Yeah, so they are different technologies for different purposes and you get different types of information. So starting with meta genome sequencing–that’s a DNA based method as is qPCR, at least the type that GI MAP is using. So we’re looking at detecting the DNA, for specific organisms or for genes, specific genes. So for example, in the instance of toxin genes, you can basically detect any aspect of DNA either way with either type of test but that’s kind of one of the areas where the similarity stops. So metogenomics is used, especially if you look at research for kind of a broad overview, a survey of the microbiome and the genes of the microbiome encodes to get a sense of the overall community. So there’s a lot of ongoing research in that area to figure out of the hundreds of species that you can potentially detect with that method. What does that actually mean? So that’s a lot of ongoing research and there’s really not a whole lot of conclusions we can make definitively about most of the species.  A lot of them just have not been well studied yet, of course we’re learning more every day.  So that’s one of the advantages of sequencing as you can potentially get kind of a more high level, bigger picture of the ecosystem.  But the challenge is if you want to measure specific clinically relevant organisms particularly quantitatively, so you can see what their levels are, whether they’re increasing or decreasing over time and with treatment, you really need a more quantitative method.  And especially when you look at sort of the composition overall of the microbiome, so you have very abundant species all the way down to species that are barely detectable. So there’s a really wide range of abundance levels for different species. Some of the species, in fact, quite a few of them on the low end of that range are clinically significant classic example would be H. pylori. H. pylori is mostly in the stomach by the time it’s in a stool sample, it’s usually pretty low concentration if it’s present.

                                So that’s difficult to pick up these low abundance species in typical kind of commercial based sequencing, because the ability to detect these low abundance organisms and to detect them in a way that’s at least reasonably quantitative depends a lot on the number of sequencing reads. So you may have heard the terms, sequencing depth, sequencing reads and that’s expensive to do that. So most of the commercial type testing doesn’t really go that deep. So you get a picture of the more abundant ones at the top, and that may include some of the ones in the middle, but oftentimes cannot identify the ones that are on the low abundance and of things very accurately. So that’s really where qPCR shines. In fact, it’s kind of like a technology that you want to use to find those needles in the haystack. And I’m actually going to go through a few examples here in this presentation. And I do have a couple of slides about qPCR as well, I can elaborate on that just a little bit, but that’s one of the main differences. Also a lot of the metagenome sequencing companies. In fact, I’m not aware of any right now that also include physiological markers. So to really get some insights clinically into what’s going on in the gut, you need to know both sides of the equation, microbiome, as well as what’s going on with digestion inflammation and things like that.  So you get a more complete picture, even though you have fewer markers because these types of tests focus on organisms that have been established to be clinically relevant and also these physiological markers. And then with that careful quantitation, then you can start to really see patterns and trends and things like that. And I kind of like it to say, you’re just looking at blood glucose levels on our standard lab test or a hemoglobin test. If all you got was plus or minus, higher or low, or sort of high, medium, low, that gives you a kind of a rough idea of what the levels are, but hemoglobin A1C of 5.6 is very different clinically from say 7.5. Although, in some measures, both of those might be considered kind of on the high end. So quantitation really is important in that’s part of a really a big part of what makes a marker more clinically relevant. So that’s kind of, sort of at a high level tip of the iceberg. What’s some of the key differences are.

Dr. Weitz:            Okay.

Tom Fabian:       Technologies.

Dr. Weitz:            Good.

Tom Fabian:       Okay.  You can tell from the title here. So we’re going to really focus on clinical insights, how to get some clinical insights out of GI MAP, particularly by connecting the dots.  So that’s really where the more advanced users get the most clinically relevant information out of GI MAP has learning how to connect those dots on the test with what’s going on clinically as well. And then of course, that’s all the point of all that is so you can get better clinical outcomes by really understanding what’s going on in the gut. So really in terms of connecting the dots, you have to know something about the dots, and which ones are most important and then how to connect them. And that really has to do with the microbial ecosystem as well as GI physiology and those two interact heavily. I’m going to go through a couple of examples in this presentation as well for basically illustrating how those dots are connected and can really yield some great clinical insights.

                                So in terms of qPCR which is also known as quantitative PCR or real-time PCR, so sometimes we’ll see ages RT-PCR on the purpose of that, the reason it was developed in research and is also used a lot clinically now is it’s really good for highly accurate identification and quantitation of microbes. I have heard some sort of… When you look at social media and you look at some of the comments that are out there, there’s a lot of misunderstanding of methods. So I’ve heard some sort of competing companies and other prominent folks that are out there in the community say that GI MAP uses 16 sequencing, which is pretty far from what we actually use. So we actually again use qPCR, quantitative PCR, but that it’s ability to identify something accurately comes down to the choice and the design of the primers. You can design primers that are highly specific for an individual strain, for example, you can detect right down to the strain level, for example, that’s how we detect pathogenic strains of H. pylori, C. diff, some of the other pathogens, is based on detecting them at the strain level.  So again, it’s especially good for low abundance microbes, there’s also the issue of absolute versus relative quantitation and it’s a little bit technical. I don’t want to get into that right now, unless anyone has questions, but absolute you’re looking at how much of that organism is present per say, gram of stool versus sequencing, which is all relative to what else is there. That could be a problem because if something goes up, that can make it look like something else is going down, when in fact it may be the same level, it’s just that it’s all relative. So it treats every sample as if it’s the same amount.  I do have one quick figure here to kind of illustrate that. And that’s actually in this figure from this particular article, which is quantitative microbiome profiling links gut community variation to microbial load. So it was published in a prominent journal, Nature, a couple of years ago where they compared relative versus quantitative approaches and they actually found that the absolute quantitation, especially when they looked at a Crohn’s disease patient was extremely important because without looking at absolute quantitation, you miss the whole picture of general decrease in microbes in the gut. And that’s a key feature of for example, Crohn’s disease. So I’ll look at… Show that data here in the next slide. So this is a pretty complicated diagram, but the main point here is on the left is a different samples that basically where the data is expressed in a relative sense. So every sample is treated as if it’s the same amount, starting amount, and all the different taxa indicated by different colors. So all the different types of microbes make up percentage of that pie, but you don’t really know if in person A, that the overall levels have gone down say F after antibiotics or after an infection unless you look at it from an absolute standpoint, and that’s what you see here. This is the breakdown, also expressed in terms of total amount per gram. You can see here on the side, it says per 10, they live in cells per gram.

                                So essentially you can see that they’re some individuals that have quite a bit less overall sort of total microbiome in their gut. And they found that to be very clinically significant. That’s one of the big difference between sequencing and qPCR. A qPCR is basically looking at things from an absolute standpoint. So the big question there is really why is that important? And again, I kind of alluded to some of those important clinical relevance type aspects, but it really allows you to differentiate low, normal and high levels at a much more detailed level.  So you can identify trends and patterns and that’s a big part of the connecting the dots with GI MAP. And that’s also critical for assessing the clinical relevance and your treatment approach, because you want to see if you do a retest, that organism may still be there, but it may be responding well, you may have gone down a couple of orders of magnitude in quantity showing that your approach is working. That’s really where quantitation is important.

The other thing that we bring to the table in terms of kind of a differentiator for GI MAP is, how we present our interpretive and educational information. So our staff has a really wide range of expertise, industry experience in Functional Medicine, clinical testing, several PhDs, et cetera.  And so we bring all that kind of cross disciplinary expertise to the table, particularly with clinical experience mixed with research and we really focus a lot on the latest research so that we can focus on these interactions, and GI MAP is really all about the second part of the equation helping clinicians understand the potential interactions between the microbiome and gut physiology.  So a key thing to understand here is there’s a lot of different aspects of physiology and the gut that really come into play once we understand them at a certain level that can help us understand how to interpret a stool test and what it may mean as far as these underlying issues. So we may, for example, see that, you’ll see here on the list pH is one of the major factors throughout the gut that affects the microbiome and vice versa, same with oxygen, the first nutrients from the diet as well, flow rate digestion, especially stomach acid and enzymes, immune factors, et cetera.

                                So a lot of factors can affect the interaction between the microbiome and our health. And that’s really reflected in GI MAP through three common dysbiosis patterns that we’ve identified over time, just in our overall experience with GI MAP, so those really boil down to 1. Insufficiency dysbiosis, which is a lack of beneficial bacteria, so that’s important to understand how to identify that on GI MAP, 2. Inflammatory dysbiosis, again, very important for a wide variety of diseases, autoimmune inflammatory diseases, and it’s also important to understand how to identify that. And then lastly, 3. Digestive dysfunction dysbiosis, which is kind of a generic term that we use because various aspects of digestion may be compromised or reduced and have an effect on the microbiome and the microbiome in some cases can actually have an effect on digestion. So once again, I’ll go through examples of this and in many patients, they can have a combination of these types of dysbiosis that reflect that interaction between physiological imbalances and the microbiome.

                                So just to note, we do have a resource on our website, a downloadable PDF that lists what markers constitute these different patterns. We will be updating that sometime shortly within the next couple of weeks or so, and then we will make that available on our website. But we do have that as a current resource that was created a couple of years ago, so it’s just a little bit out of date at this point. The other thing that we really kind of weave into this based on research, and how that applies clinically beyond sort of this holistic high-level integrative perspective of looking at the whole gut, a big part of that is recognizing upper versus lower GI MAP microbes. That’s something that you may have heard.

                                Some clinicians claim that with stool testing, you can’t get any insights at all, except into what’s going on in the colon that you basically don’t really understand from a stool sample what’s going on in the small intestine for example, it turns out there’s a lot that you can gain from that. You don’t get necessarily a completely accurate picture of the composition in compartments that are sort of higher up in the GI tract, but sort of the classic example is H. pylori.        We didn’t know that that is detectable in stool, and that certainly yields important clinical information with regards to what may be going on in the stomach, so think of this as kind of a domino effect that you want to get a bit of an understanding of what’s going on higher up in the GI tract, even as high up as the oral cavity.  And one of the examples I’ll go through that’s features one of the markers on GI MAP, for a lot of patients that may actually come from dysbiosis originally in the mouth. And then you want to understand how these physiological imbalances result in its presence in the gut and what it may be doing there.  So to really get into this a little bit more, it’s important to understand a little bit about the composition of the upper GI MAP microbiome.  It’s not as well studied as the lower GI, the colon microbiome, but we’re learning much more about it especially in the last few years.  Mostly what’s dominant in the upper GI from the mouth down to small intestine are a large class in the Firmicutes phylum called the Bacilli.  So that species and groups like streptococcus, lactobacillus, enterococcus and staph. We do have these groups on GI MAP when you see them overgrown, it’s likely that they may reflect imbalances in the upper GI tract. And there’s some just basic information about the physiological conditions that they thrive in, they like higher oxygen environments.  So they don’t like the anaerobic environment in the colon, unless the colon environment’s been disrupted.  They like simple nutrients that are highly available in the small intestine.  Bile is in the small intestine, so they’re bile tolerant, et cetera,.  Also, organisms from the Proteobacteria phylum, which we tend to think of more of the inflammatory microbes, the dysbiotic microbes, they’re much more prevalent as a percentage in a small intestine. So typically they constitute say 20% of the microbiome in the small intestine and only 2 to 5% in the large intestine. So proportionally they’re much smaller in the large intestine.

                                A lot of the research has come out on Pseudomonas, which you do have on our tests, actually going to go back to that, linking Pseudomonas to inflammation in the duodenum, for example, and linking that to issues with gluten and kind of the broader picture of food sensitivities. They also thrive in a higher oxygen environment, also thrive on simple nutrients like sugars and amino acids, highly bile tolerant, you can actually find many of these in the bile ducts and in the gallbladder.  So they’re very bio tolerant, so really important group in the upper small intestine.  Composition of lower GI microbiome at a high level, the most abundant groups in some ways fairly simple, the Clostridium class really dominates and that’s the..in the colon, the largest class or largest group in the Firmicutes phylum, and one of the key species is Faecalibacterium Prausnitzii which we do have on GI MAP as well. That’s a major butyrate producer, again, it’s in the Clostridium class, which is the dominant group in the Firmicutes phylum. And then there’s a Bacteroides group, which is the major group, typically in most people in the bacteria Firmicutes phylum, Akkermansia is a well known species in the Verrucomicrobia phylum, which is also one of the key groups in the colon. They thrive in an anaerobic environment, generally that whole ecosystem, at least in a healthy individual thrives on complex fibers, as well as the mucus ecosystem.  So the mucus layer in the colon is much thicker than in the small intestine. So that’s one of the reasons why there’s a more significant you can see ecosystem in the colon. So this is data from Dr. Mark Pimentel’s lab that was published just earlier this year. This is just basically showing… You can see at the bottom here on the X axis duodenum, jejunum, FD, which is their term for the furthest distance the scope could go in the ileum. So it essentially means ileum for the most part compared to a stool sample. So the take home point here is the different colors represent the different major groups in the different compartments here, but it’s fairly consistent across the small intestine and then suddenly you have this huge change in the large intestine, which is reflected by the fecal sample. So that’s really reflecting that big change in physiological parameters from the small intestine, which again has a higher oxygen content, et cetera, usually lower acid levels, higher pH, then the colon very different environments particularly because of the fact that it’s anaerobic.  So that’s why anaerobic species thrive there that ferment carbohydrates. So a big difference and that’s really key to understanding this sort of localization aspects to interpreting stool tests. And this is the Tyler study mapping, the segmental microbiomes in the human small bowel in comparison with stool, the Reimagine study. And again, this is a study that was just published earlier this year by Mark Pimentel’s lab. [Mapping the Segmental Microbiomes in the Human Small Bowel in Comparison with Stool: A REIMAGINE Study]

Dr. Weitz:           Yeah. We were lucky enough for Dr. Pimentel to join us several months ago.

Tom Fabian:       Oh, you did? Okay, great. I have to go back and make sure I check that out.

Dr. Weitz:           Yeah.

Tom Fabian:       So this is a summary of markers on GI MAP based on research that indicates where they’re predominant in the GI tract. We just sort of broke it down between upper GI and lower GI, with the upper GI being on the left and then the lower GI being on the right. So not all species or groups are known in terms of research that’s available in terms of where their predominance is, and then in other cases, they may be prevalent in both but both of these groups here research supports the predominant primarily either in the upper or the lower GI tract. So once again, there’s quite a few markers on GI MAP that are likely reflecting what’s going on in the upper GI. Again, the classic one being H. pylori, GRD is another, well-known microbe that basically thrives in the upper small intestine. The two that I’m going to focus on here just briefly in this presentation are Klebsiella and C. diff. So one example of an organism that’s present more commonly in the upper GI and also the oral cavity and then less prevalent in the lower GI except in cases of potential inflammation.

                                So as far as stool composition, just to kind of summarize it primarily reflects the colon composition. So that’s sort of intuitive, but also that’s what research shows as well. And of course within the column, there’s a mix of luminol and mucus associated microbes, with the composition primarily dominated and fecal samples with luminol microbes. But definitely you get a sense of the mucus associated microbes such as Akkermansia. It’s also dominated by anaerobic Fermenter bacteria in particular, the Clostridium class in the Firmicutes phylum and then the Bacteroidetes genus in the Bacteroidetes phylum. Those are far and away, the two most dominant groups in the microbiome in most individuals, at least in Western countries. Microbes from the upper GI tract can be present in stool, but usually in really low numbers.

                                So that’s of course where qPCR comes in, because we can still get some good insights based on the presence of some of those low abundance type organisms. So once again, this is just sort of back to the figure from the Pimentel study showing the breakdown of these major groups across the small intestine and stool. Of course, the question is why we’ll get into some of that a bit more as well. So that guy somehow made a mark there. So really, I think it’s important to consider since we can detect potentially some of these upper GI microbes. Some of them are better established as being pretty exclusive to the upper GI tract. Again like H. pylori and Giardia. Pseudomonas, mostly research does indicate that it’s likely thriving in the stomach and the upper small intestine and so far, most studies indicate that it’s not present and are not active, usually not active in the large intestine.

Dr. Weitz:            Are you going to have time to go into H. pylori? And if not, can I ask a couple of questions now about H. pylori?

Tom Fabian:       I’m sure. Yeah. I’m happy to answer questions right now, but it’s H.pylori.

Dr. Weitz:            Okay. So if we see H. pylori present, but there aren’t any virulence factors essentially it’s my understanding that that’s not super important. Correct?

Tom Fabian:       So as far as H. pylori its presence without virulence factors, it is important apparently, we certainly see a potential clinical impact quite often when it’s present and especially if it’s high.

Dr. Weitz:            O.K., so when we look at the numbers, like the normal says 1.0 e3, now what’s considered high?

Tom Fabian:       High is generally that’s what that cutoff level is indicating. So above that number is considered high, below that number is considered detected.

Dr. Weitz:            Like if it’s 5.0 e3, is that a little high or a lot high? Is it a lot high if its e4, e5 that makes it a lot high, right?

Tom Fabian:       Right. Yeah. I mean, because those are orders of magnitude, but definitely clinically in the E three range is high and it’s of course you have to take everything into the context of the patient and how that patient’s presenting symptoms that may be related to that, but also we can see a pattern on GI MAP. And so there’s a lot of research showing, for example, the H. pylori, regardless of virulence factors likely reduces stomach acid in majority of people that have a chronic infection, and so we have an overall digestive dysfunction pattern that I mentioned briefly earlier that is often associated with H. pylori, and it’s one of the ways that we can gauge based on just the test markers and connecting the dots, doesn’t look like this is having an impact in the ecosystem and then of course the clinician has to decide, is that relevant to the patient’s symptoms and how the patient is presenting?

Dr. Weitz:           So you’re saying if we have a patient with elevated H. pylori and it seems like it might correspond with the symptoms, it might be worth treating, even if there’s no virulence factors?

Tom Fabian:       It would be worth considering, a lot of clinicians do, but I think the… When it comes to functional integrative type clinicians, a lot of clinicians will often focus more on antimicrobial approaches versus going straight to antibiotics. So it’s not a scenario that would be kind of in conventional medicine it’s the more looking at the potential virulence in relation to things like potential for stomach cancer ulcers also things like that. Some of the more serious outcomes that are tied, the risk for those types of outcomes are tied to the virulence factors. But the more mild sort of to moderate effects based on just depression of stomach acid still can be clinically relevant for patients, but it may not warrant sort of complete eradication for example.

Dr. Weitz:           And in some of the virulence factors more important than others?

Tom Fabian:       Based on research so far, the answer is yes. The two that stand out the most, partly because they’ve been well-researched, but seem to be especially required for the more significant inflammatory outcomes and that would cagA and vacA.  That’s important to point out though that virulence factors tend to work together and so generally the more you see on the test, so the more that are positive, the more likely than that could be a more significant scenario.

Dr. Weitz:           One more quick question, just in general, in terms of any bacteria or pathogen or potential overgrowth when we see the number there, but it’s less than the normal that could still be significant?

Tom Fabian:       Right. Now, again that’s really where clinical judgment comes into place, so-

Dr. Weitz:           Because it’s really well, it’s has <dL> right? Like super low.

Tom Fabian:       Exactly. Yeah. That either means it’s just not there at all or it’s presence at a low level.

Dr. Weitz:           Okay.

Tom Fabian:       We often do see that based on interacting with clinicians that their judgment is, and also based on what we see on the pattern on the test that [inaudible00:30:31] can be clinically significant for some patients, again, mostly in that context of potential for contributing to dysbiosis and reduce digestion.

Dr. Weitz:           Okay, great. Go ahead.

Tom Fabian:       So that’s really kind of… It was actually a great time to talk about H. pylori because that is kind of the classic example when you hear certain folks out there saying you can’t really get any information about the upper GI from a stool test, that’s simply not true because H. pylori is sort of the case in point. We can certainly get some great insights into what may be going on in the stomach in that case.

Dr. Weitz:            And of course, zonulin gives us some information about the upper bowel as well. Right?

Tom Fabian:       Right, exactly. So qPCR, again, just kind of that analogy that it’s great at finding these needles in the haystack. H. pylori is a good example. There are a lot of the metogenomic type tests, metagenome sequencing that generally aren’t as good at detecting H. pylori let alone quantitating it. So when you really want to know about a clinically relevant organism, qPCR is a very effective way to assess that. So let’s talk a little bit about the insufficiency type of dysbiosis. So this is something that probably a lot of clinicians who worked a lot with GI MAP have seen, you may see a really broad insufficiency like we see here for this patient where there are a lot of markers in the normal bacteria section that are deficient, at the phylum level that’s certainly one of the most important levels to look at because those two groups together make up the bulk of the microbiome, particularly in the colon.  So when they’re both deficient, that’s telling you the microbiome overall is probably deficient and then all those beneficial functions that they serve are probably also deficient. It’s also a great to focus, particularly on Akkermansia and the E. coli bacteria, and those are two Keystone species. So once again, when one or both of those are low that can be pretty significant in terms of indicating that the colon ecosystem is not so healthy. The other thing I want to note about kind of connecting the dots on GI MAP is we do lots of research.

Dr. Weitz:            Let me just see if I could throw a question in Dr. Rahbar who’s joining us tonight is a integrative gastroenterologist. Let Dr. Rahbar ask a question. Let see, I’m going to unmute you Sam, why don’t you go ahead and ask your question. Did I unmute you?

Dr. Rahbar:          Can you hear me?

Dr. Weitz:            Oh yeah. Now we can hear you.

Dr. Rahbar:          Okay.

Tom Fabian:        Yes, I can hear you.

Dr. Rahbar:         Yeah. I have several questions since we use this lab quite frequently, and I kind of use my common sense approach to it.  For example, I see sometimes practitioners wanting to treat Klebsiella and Citrobacter fruendii in the stool. And I always question, are these specific pathogens, or are these markers of dysbiosis?  It means that, do you need to look at it as dysbiotic flora or like if I got Shigella or something in the stool I would say, okay, you’re going to have some specific bug that I have to treat it.  Or campylobacter.  At least from the literature that I see, I don’t recognize these as specific pathogens of the gut, indications of disease.  So I usually respond that maybe you treat SIBO some other dysbiotic scenarios, but I wouldn’t target a specific one, but Dr. Fabian, I wanted to get your opinion on this one without just saying something. 

Tom Fabian:       Absolutely. Yeah. I mean-

Dr. Weitz:           And these are two markers that are listed in the section potential autoimmune triggers.

Tom Fabian:       Right. And that actually is one of the examples I’ll be covering here in this a little bit, so that’s really why it’s considered an opportunistic pathogen. So opportunistic pathogens can exist in the gut without any effects at all or they can potentially be part of a pathogenic process. So they’re not generally recognized at least in the gut as being outright pathogens. That picture is probably going to change a little bit with some of the organisms like Klebsiella, where we do see that it’s more frequently now associated with things like inflammatory bowel disease, et cetera.  So it’s beginning to square where it’s not thought of as sort of an outright infection, a specific infection like salmonella, but it is part of the pathogenic process in some cases. So it’s kind of in that gray area, and that’s a perfect example of where clinical judgment really to come into play in combination with really understanding how to connect the dots with a test like GI MAP.  So you can really get a sense for, does look like this is a problem, or does it look like it’s for this patient probably not much of a problem.  And that’s, well-documented research some people can have relatively high levels of Klebsiella and no evidence of inflammation.  Other people can have high levels and have inflammation, but the big difference often is the ecosystem.  If they don’t have as many of the beneficial bacteria, they may be more likely to have inflammation.

Dr. Rahbar:        Right and if I may say something, obviously we need to evolve into this to understand if we correct that, whether it reverses the immunological abnormality or not.  We can say that this is part of the autoimmune trigger but if you fix it, does it fix your autoimmune problem?  And that answer obviously is not clear.  And so far, I don’t think if you just change that bug, you’re going to see it, but we have to see how that answer is going to evolve.  I wanted to ask you a question regarding the H. pylori.

Dr. Weitz:            So actually, let me just ask that same question again. Tom, is there any data showing that if we have a stool test that shows potential autoimmune triggers and we reduce that particular bacteria, that we may have a positive effect on their autoimmune disease?

Tom Fabian:       That’s a good question. So I’d have to go back and kind of dig through some of the research that I have to see what specific studies there are, mostly to date what I’m aware of is, those are associations and a few cases, there may be some kind of mechanistic insights suggesting there might be a causal link. But mostly to date, a lot of those are based on associations. I’d have to go back and again, dig through the research to see if I do have some studies that specifically talk about whether or not if they’re addressed, does the disease reverse or do some of the symptoms improve?  Not entirely sure.

Dr. Weitz:            Yeah. I just had a patient today who has Ankylosing Spondylitis and he has high levels of Prevotella [I meant Klebsiella] and there’s data showing that that can be directly related to how the Ankylosing Spondylitis is created in the body.

Tom Fabian:       Right. Yeah, definitely for some of them, at least it’s suspected, and some evidence that there might be some kind of molecular mimicry, for example where the immune system reacts to protein on the pathogen or the opportunist that then looks very similar to a protein in the body and then the body develops an immune reaction to those proteins as well. So that’s kind of an ongoing thing. I think it’s mostly well established for one of the oral microbes, which is Porphyromonas gingivalis, but there’s probably a growing list of examples there.

Dr. Rahbar:         Dr. Fabian, may I ask a question regarding H. pylori, we occasionally find this in duodenal aspirate as interesting that even in the stool test sometimes the marker comes up as red and sometimes it’s black. I agree that the best value is below <DL, below the detectable levels. So if any amount is showing would it be abnormal whether it’s in the black or red zone?

Tom Fabian:       That’s a good question. So certainly below detection limit, if you’re aiming for eradication or greatly reducing its levels from a therapeutic goal, then certainly that’s what you’d be looking at. Now there’s with any sort of microbe, I mean, except for outright pathogens and H. pylori is kind of more on the opportunistic pathogen category versus something like enterohemorrhagic E coli, which is not really pathogen. Those you generally don’t want to see those in the gut at all of course.  When there’s H.pylori there’s some debate as to whether or not complete elimination is always desirable. It really depends on kind of looking at all the risk factors, but some data indicates that there may be some increased risk for other conditions by completely eliminating H. pylori. So what we know mostly from research is that most of these types of opportunists in the gut like Klebsiella, H. pylori, as long as they’re kept in check by healthy gut and healthy microbiome, they may not be a problem.   So that’s kind of where that gray area, low levels for some people may be fine, because maybe they have an overall healthy stomach, they have a lot of Lactobacillus, for example, in the stomach, which is definitely one of the known healthy groups in the stomach and a healthy ecosystem. Then they may be fine and there may be no reason to target H. pylori, but if people are having symptoms that could be ascribed to it, plus we see a signature on the test and there may be other considerations as well.  Some clinicians may decide that they want to at least try to reduce that and see if that helps symptoms for that patient.

Dr. Weitz:           Does it make sense to also do a H. pylori breath test or antibody test to confirm it?

Tom Fabian:       Some clinicians feel that because it really depends again, on the scenario and the risks, say if you have lots of virulence factors and there’s a history, family history of stomach cancer or anything like that, there may be scenarios where you really do want to make absolutely sure that it’s eradicated, if you’re trying to eradicate it or even just verifying the levels over time. So there are some clinicians that prefer to do multiple tests. Just to really get a better handle on it. PCR is very sensitive. So it is often a scenario where we’ll see a low level detected where a breath test or a stool antigen tests may be negative.

Dr. Weitz:           By the way, is PCR ever too sensitive?  Is it ever the case that it’s picking up things that maybe are no longer there?

Tom Fabian:       That’s a highly unlikely scenario as far as past infection. So it’s a very different scenario than say antibodies, which can linger for a long time. DNA from organisms, especially in the gut is highly unlikely to linger, partly just from the simple fact that materials moving through within a certain period of time.  So if the microbe isn’t attached and to be attached to it has to be alive, because it has to actively produce those proteins that allow it to attach.  So it’s not likely, that it would be detectable past a certain relatively short period of time on the order of days.

Dr. Weitz:            Okay. And Dr. Greenberg asked if the Pseudomonas is high, does that imply that it’s overgrown in the small intestine or that it has also colonized the large intestine?

Tom Fabian:       So far there is no research supporting that it can colonize or at least colonizes on any sort of frequent basis in the colon. All the research to date supports that it’s mostly in the upper GI and stomach.

Dr. Weitz:            Okay.

Tom Fabian:       Really it’s niche where it thrives. I haven’t yet come across a single study. It can be detected, of course that’s how we pick it up. It really doesn’t seem to thrive in the colon. In fact, specific studies have looked at that based on transcription gene expression, and Pseudomonas is one of those that when you look at gene expression methods is not detected in the gut, meaning it’s not active.

Dr. Weitz:            Okay. Yeah, go ahead.

Tom Fabian:       Okay. So coming back to this section where were talking a little bit about the beneficial bacteria and what to look for when there’s a lack of beneficial bacteria. In addition, of course, to the normal bacteria section you really want to make sure you pay attention to secretory IgA. So we do know that, the main stimulus for normal physiological ranges of secretory IgA is the normal commensal microbiome, through secretion of Butyrate and other products that stimulates the production of secretory IgA. So we see a really strong correlation there.  Typically when there’s a lack of at least, one of the key groups of beneficial bacteria, we often see low secretory IgA.  Clinically it appears that the lower, the number like we see here, the more likely that is to reflect lack of Butyrate producers.  So you’ll often see, for example, really low secretory IgA below 100 when Faecalibacterium, for example, is also very low.  So it’s kind of a great overall marker for lack of beneficial bacteria.

Dr. Weitz:            So, if we see this on a test with a patient who maybe has some other infection or parasite at the same time, would we best be trying to improve their microbiome with probiotics or prebiotics, or would be better to directly try to stimulate their immune system with colostrum or some products like that have an immunostimulatory effect?

Tom Fabian:       A lot of clinicians will focus on both building up, the microbiome can take time depending on what’s going on. So if you need a more immediate effects then those types of supplements, Saccharomyces Boulardii, L-glutamine even Vitamin A, has been shown to be necessary for normal secretory IgA levels. So supplement approaches certainly can help bridge that gap until the beneficial bacteria are recovering. So again, that’s a really important marker to pay attention to that has a very strong correlation with lack of beneficial bacteria.

Dr. Weitz:            I just want to ask about the fecal calprotectin, which is a marker of inflammation. I’ve had a number of tasks where that was normal, and not particularly high, but the patient has a lot of gut symptoms and it just seems like their gut is really inflamed. So, why would that number be low if their gut’s really appears to be inflamed?

Tom Fabian:       That’s a good question. So it’s a good marker for inflammation particularly in the lower GI. So if you look at studies on Calprotectin, for example in relation to H. pylori, so Calprotectin in stool, there’s not much of a correlation, so we know the H. pylori can cause inflammation in the stomach but that doesn’t reflect so much, in ability to detect it in stool. So one possibility is that you may have upper GI inflammation, if they’re inflamed and that’s likely in a lot of cases. So for example, Pseudomonas, lots of new research shows, that when that’s overgrown that’s likely causing inflammation, doesn’t always mean it is. So again, you want to take into account the big picture but if it’s significantly overgrown that’s a significant possibility that could be causing inflammation the upper GI. Candida is known to be inflammatory often colonizes pretty much anywhere in the upper GI tract, even the oral cavity. So that’s one of the major reasons if they seem to be inflamed and Calprotectin looks fine, maybe more on the upper GI.

Dr. Weitz:            One of the patients [I meant practitioners] asked that, she had a patient with Ulcerative colitis. Calprotectin was 660 on the GI MAP a week later, the calprotectin was 150 on a standard lab.

Tom Fabian:       So, it’s difficult to kind of compare among labs due to, we know what our lab does. Our lab certainly does everything that’s required of a CLIA lab and then some, so we know that our markets are internally validates very well, but we can’t speak to other labs in terms of how they perform the test and also do their validation, but also be aware that Calprotectin is a marker that can change over time.

Dr. Weitz:           So if you change, can it change quickly in a week?

Tom Fabian:       But actually, yeah.

Dr. Weitz:           Okay.

Tom Fabian:       Yeah. Because, it’s really responding to what’s going on in the gut. Now, if you have chronic inflammation, that’s not necessarily changing, you shouldn’t expect to see that changed. Generally though, if you’re doing a retest say after treatment and you want to see what’s happening with the levels, it’s always recommended to use the same lab that you started with. So you have that consistency and baseline because otherwise, you’re factoring in possible methodological differences.

Dr. Weitz:           Yeah. I have to say sometimes this sort of question comes up when I’m managing a patient as a Functional Medicine practitioner/Chiropractor, and then the patient goes to see a standard GI doctor and they send them to LabCorp or Quest and get a different result and then they scoff at this test.

Tom Fabian:       Right. Yeah. I mean, that’s always going to be an issue when you’re comparing tests. We see that, like I mentioned with H. pylori where a patient may be negative with a stool antigen test, they do a PCR test and because of the sensitivity level, we pick it up and the other lab with the other method, didn’t pick it up. So, it’s ideally you’re doing the same if you’re kind of comparing time points with the same test.

Dr. Weitz:           Okay, good. Go ahead.

Tom Fabian:       Okay. So on the next slide, it’s just kind of a visual reminder of what we’re looking at. So, we’re so used to looking at tests, the numbers and kind of thinking about things a bit more in the abstract when it comes to the gut, because we can’t see the ecosystem.  It’s important to really kind of come back to sort of the visual understanding that we’re talking about the bugs, and this is the lumen side towards the top, and you can see the bugs here. And if these are largely representing beneficial bacteria, there’s secreting, creating factors, particularly short chain fatty acids that are absorbed into the mucosa. That then basically elicit effects, particularly from the immune cells and the Epithelial cells, certain Epithelial cells, the Goblet cells, respond by producing mucus and then certain immune cells, the Plasma cells respond by producing secretory IgA, and the secretory IgA is secreted in the mucus layer. So just kind of another quick little clinical Pearl is you’ll often see low secretory IgA along with low Akkermansia. And that’s indicating that likely this mucus layer that includes mucus and secretory IgA could be deficient. You can see here, it’s representing that this mucus layer is keeping the microbes away from the mucosa, which is important to keep the reactivity of the immune interactivity down. So that’s part of the whole immune tolerance type, a phenomenon is preventing overreaction of the immune system to harmless microbes.

And so just a little bit more about the Firmicutive bacteria to these phylum, just to reiterate they’re anaerobic and they’re dominant in the colon and the main source of short chain, fatty acids, and those short chain, fatty acids have many important effects. One of which public have a little bit of time to go through here and a little bit when I go through one of the studies, but there are definitely overall key for colon health particularly in terms of protection from pathogens and opportunists. So it’s not common to see some of these opportunists, particularly under Autoimmune triggers, for example. And when we do see them, that suggests possibly the overall beneficial bacteria may be deficient.

So the other information you’ve already talked about, so we’ll move on.  I just want to touch briefly on inflammatory Dysbiosis. So this is a subset of the inflammatory kind of the main inflammatory types of organisms on GI MAP.  So there are particularly inflammatory bacteria in the Proteobacteria phylum. Most of them tend to be in a subclass or subgroup called Gamma Proteobacteria. So they’re all fairly related. A lot of them have been shown to have the more inflammatory type of LPS, for example. But quickly I want to focus on Klebsiella.  So that’s something we’ve talked about a little bit so far here, as an example, there’s this really interesting study that just came out a little while ago.  Actually just this past summer.  So the title is Intermucosal connection between the mouth and the gut and commensal pathobiont-driven colitis.   So this is basically showing that the connection between Dysbiosis in the mouth and Dysbiosis in the gut, and then what can happen in between. So they say here real quick, Periodontitis leads to expansion of oral pathobionts, including Klebsiella and Enterobacteria species, which were both on our tests and the oral cavity amassed oral pathobionts are ingested, then translocate to the gut.

                                So basically swallow pass through the stomach and then end up in the lower GI tract, particularly if there’s not enough stomach acid, where they activate the inflammasome in Colonic mononuclear, Phagocytes triggering inflammation. And I want to go on to a little bit more information here. So they say in the article, this evidence suggests that at least two conditions must be met for oral pathobionts to topically colonize the gut.  First, the colonization resistance of the gut resident microbiota must be disrupted often, meaning that you have a lack of beneficial bacteria enabling the oral microbes to invade the gut.  Hence intestinal inflammation favors the growth of Enterobacteriaceae, that’s kind of a subgroup that includes E-coli, Salmonella, Klebsiella, et cetera in cleaning bacteria transmitted from the oral mark, because one more thing I want to highlight from this article is alternatively neutralization of gastric acid or inhibition of acid secretion could promote ectopic colonization of oral bacteria in the gut.  For example, it has been reported that the use of Proton pump inhibitors, which reduce production of gastric acid leads to increased colonization of mouth resident bacteria in the gut, consistent with his observations been reported that gastric acid inhibitors worsen clinical outcomes in IBD. So definitely this is an important article that kind of follows up on earlier research showing this integrative approach. You’ve got to take the whole GI tract into account.

                                When you see Klebsiella come up on a test, the questions you want to ask are, is there evidence it’s causing inflammation? You may even want to check with the patient, ask the patient about their oral health. You may want to look at indicators of stomach acid because it may be telling you this patient might have insufficient stomach acid. So lots of, kind of connecting the dots there when you see these various organisms. So that’s talked a little bit about the insufficiency Dysbiosis, inflammatory Dysbiosis. Those two are really linked. As you can imagine, when you have a lack of beneficial bacteria, that’s one of the key factors that allows these inflammatory microbes to grow in the lower gut. I just want to touch on the Digestive Dysfunction Dysbiosis. When we think of digestive dysfunctions, most clinicians go straight to this digestion section and look at the markers.  Steatocrit is looking at fat malabsorption in this case, it’s high.  Elastase is a marker for pancreatic enzyme deficiency or our production in this case it’s low. But if you see those normal, does that mean digestion is fine?  And often times the answer is no. Fortunately we can get some additional insights by looking at the patterns of the microbes and what we know about certain microbes, such as H. pylori.

                                So it’s just kind of coming back to what I talked about that this review article basically came to the conclusion that most patients chronically infected with H. pylori have Gastritis and also Hypochlorhydria, not necessarily all.  It’s important to know that not everybody that has H. pylori has low stomach acid but a pretty large proportion of them do seem to have low stomach acid and that low stomach acid for various reasons on this case, they’re looking at Proton pump inhibitors leads to certain types of Dysbiosis that’s really reproducible. So they mentioned here in the highlighted area that Streptococcaceae and Enteroccaceae species are among the most common that you see elevated. Also PPIs are risk proceeded infection. So I’ll get to that. Hopefully we have a little bit time later on here too. Sometimes decrease with E coli bacterium as well. So these are the patterns that we can see, for example, in relation to low stomach acid, there’s a lot of research backing this up, particularly with the Fermicutes phylum. Many studies have replicated that, finding that you see elevated levels of those in stool when patients have been shown to have low stomach acid. And so this is just an example of a patient that had high H. pylori, so suspected low stomach acid, again, not diagnostic for low stomach acid, but something to think about. You’re looking for an overgrowth pattern. We’d see the overgrowth pattern typically in the normal bacteria section.

                                This would be pretty significant. We don’t always see it, this prevalent with so many markers elevated. But we often do see this overgrowth pattern, particularly with the Firmicutes phylum. And then in this case, we also saw Faecalibacterium was low, which really follows that particular study that was found to be low as well. With low stomach acid, your opportunistic bacteria is really where you’re going to see the most common evidence of overgrowth. That’s where the Enterococcus species are and Streptococcus. So if those are high, then suspect that stomach low stomach acid may be an issue. And then some of these others too, like Pseudomonas can also be overgrown and stomach acid is too low, or there’s other.

Dr. Weitz:            Can I ask about Methanobrevibacter?  So we know that methane SIBO is now IMO according to Dr. Pimentel. And so therefore it’s an overgrowth of methanogens, like methanobrevibacter, Methanobrevibacter smithii, and so if the patient has a positive SIBO breath test for methane SIBO, would we necessarily see elevated levels of Methanobrevibacter and, what if they don’t correlate?

Tom Fabian:       That’s a good question. So they generally do seem to correlate as far as we can tell but not always. So that is an important factor to consider that sometimes you can have an increase in bacteria or in this case, microbials because Methano bacteria is they actually are archea, not bacteria kind of closely related, but and so you can have an increase in function, of microbes in some cases without necessarily a significant increase in their numbers. Now that said, on our test and based on looking at literally thousands of tests over the last couple of years then the methanobacteria family on our test tracks very closely with overall evidence of overgrowth on our test. And you’ll see here in a moment, if I get a chance to get to the one of the slides here that talks about that more, it’s, it’s really a direct reflection of the level of fermentation, particularly in the colon.  So when you see methanobacteriaceae in our experience it seems to be clinically relevant anytime it’s in the E nine range, not even above the cutoffs.  It’s highly correlated with this. So generally, yes. I would say when, when patients have also had a breath test, they will have some level of methane detected. But it’s not necessarily a hundred percent correlation for example.

Dr. Weitz:            And somebody asked a question about H. pylori, which is can it also increase stomach acid production, depending upon where the H. pylori is?

Tom Fabian:       Yeah, that’s true. So there is some evidence that in some cases that can be the case during more than acute sort of early infection. And it really does depend, apparently there’s some conflicting research on it. So it’s not really all that well studied, but it does depend on where in the stomach it’s infecting and the extent of the infection. Now, there is some evidence based on a couple of studies I came across that typically the infection can migrate in the stomach over time. And I forget which direction if it’s antrum to corpus or corpus to antrum, but the overall conclusion was that it tends to long-term be more consistent with hypo or Hyper. But some patients may have an increase in acid depending on where the infection is.

Dr. Weitz:           Okay.

Tom Fabian:       So this is just kind of showing you in this example that Klebsiella was elevated which again is something we often see when there’s other evidence suggesting low stomach acid. And that goes along with that research that suggests Klebsiella may often come from the oral cavity or possibly the respiratory tract, which is also another common location for Klebsiella. And then it may get into the GI tract to those routes when stomach acid is insufficient. I’m going to go ahead and skip this here other than, of course, whenever you see an overgrowth of inflammatory species and we had that list higher up on one of the other slides oftentimes, but not always, you’ll see Calprotectin elevated. So there is a correlation there. We see it most commonly in, for example, patients that have already been diagnosed with inflammatory bowel disease we often will see that connection between higher Calprotectin and higher levels of inflammatory species.

Dr. Weitz:           By the way, if pancreatic elastase is low, is the best recommendation is to recommend that they supplement with pancreatic enzymes or are there other recommendations?

Tom Fabian:       That’s a good question. So a lot of clinicians do take that route to help compensate. But of course you want to also ask the question what may be contributing to that.

Dr. Weitz:           Right.

Tom Fabian:       So there may be issues with the pancreas itself. Of course, Pancreatitis, things like that may play a role for some patients, but even low stomach acid can lead to lower release of digestive enzymes. That might be another factor for a lot of patients that can be gut-brain axis issues.

Dr. Weitz:           Interesting. Low acid leads to low pancreatic enzymes?

Tom Fabian:       It’s a contributor. Yeah.

Dr. Weitz:           Okay.

Tom Fabian:       It wouldn’t be considered, if you say you have really low elastase are rate sufficiency. That’s, well below that 200 cutoff it would probably be unlikely that that’s the sole contributor unless for example stomach acid is exceptionally low. You may be wanting to look into some other contributing factors at that point.

Dr. Weitz:           And if steatocrit is high, that’s fat in the stool, is the best recommendation to give them a lipase, fat breaking, fat digestive enzymes, or is bile going to be more beneficial or both?

Tom Fabian:       Good question. So just based on the presence of the excess fat in the stoool you can’t tell directly just from that which upstream process is affected.  Now, if you do see that our last days is really low, particularly if there’s outright insufficiency, meaning well below 200, then it’s more likely that, the highest steatocrit would be caused by lack of lipases from the pancreas as well. But you can also have a scenario where there’s insufficient bile but it’s probably less appreciated is issues in the small intestine, which is where fats are primarily absorbed, where they’re supposed to be absorbed in a healthy gut. So if you have an inflamed, small intestine, and you’re not able to really absorb fats as efficiently.

Dr. Weitz:           Such as if you have SIBO.

Tom Fabian:       Exactly.

Dr. Weitz:           Okay.

Tom Fabian:       Right. Just have a few more things to go through and then based on time, do you want me to stop here or take more questions or do you want me to continue on for a couple more slides?

Dr. Weitz:           Go a couple more quiet slides.

Tom Fabian:       Okay. so again, these are the three main Dysbiosis patterns that learning to recognize them can give you a lot of insights into what’s going on in the overall gut, in terms of physiology and the microbiome, and even some insights into say lower versus upper GI issues, I’ll skip this, but we all know that of course pH is one of the key factors along the GI tract. We mostly think of stomach being the key kind of checkpoint. So when you may unfortunately ingest pathogens, for example, food poisoning if you have good stomach acid, then they’re less likely to survive the transit, but what’s less appreciated is that slightly acidic levels in a healthy colon, especially the ascending colon, are almost as important and helping to keep pathogens and other opportunists from colonizing your colon. So I’m just going to go through a quick example of that here. This is a really interesting paper that was published recently, so the title is Inhibiting antibiotic-resistant Enterobacteriaceae by microbiota-mediated intracellular acidification. So that’s in the Proteobacteria phylum, that’s a particularly inflammatory group.  So inhibiting that group by microbiota mediated, intracellular acidification. So just to kind of cut to the chase, they mentioned Klebsiella and E coli as kind of the examples they’re looking at here. And then the highlighted in orange part towards the bottom says Klebsiella pneumonia, Escherichia coli, Proteus mirabilis by acidifying the proximal colon and triggering short chain, fatty acid mediating intracellular acidification. So essentially what they showed in this study is that normal levels of beneficial microbes that are producing adequate levels of short chain, fatty acids literally inhibit the growth of these pathogens by basically producing the short chain fatty acids that then are taken up by those cells and that satisfies the cells and basically prevents them from growing.  So that’s one of the ways in which these beneficial bacteria, like Clostridia, Bacteroidites can help to keep those pathogens in check. So once again, when you see those at high level particularly Klebsiella or Proteus that’s one of the things we’ll be looking at is evidence for low beneficial bacteria. And they actually showed in this study that just restoring the beneficial bacteria and the short chain fatty acids can be enough to address those pathogens. So that’s kind of an example where you don’t always have to resort to antimicrobials.  Restoring gut balance may be sufficient.

Dr. Weitz:           Can I just ask a question about anti-microbials?  I interviewed Dr. Jason Hawrelak a few months ago, and he mentioned that he thinks that taking anti-microbials like Berberine can significantly damage the microbiome.  Do you think that that is something that is liable to happen?  Do we see evidence of that?  In other words, can natural anti-microbials produce damage in the microbiome?…   The way antibiotics can say, for example.

Tom Fabian:       Generally, no, we have not seen that. Not even close.

Dr. Weitz:           Okay, good.

Tom Fabian:       Mostly when we see a really broad deficiency pattern, it’s related to antibiotics or other pathology like IBD or something like that.

Dr. Weitz:           Good.

Tom Fabian:       Real quick though, I think he was referring to at least the research I’m aware of on Berberine in one study a few years ago, showed that it can long-term or high doses can reduce diversity. But it was in an animal model in mice. So that suggests maybe not taking super high doses for a long time would be-

Dr. Weitz:           By the way what’s a high dosage? Because for example I’m using Berberine not only for gut patients, but we use it to help manage metabolic factors and I also use it as a sort of a substitute for Metformin in anti-aging programs.

Tom Fabian:       Right. Good question.

Dr. Weitz:           It works synergistically with Metformin to manage blood sugars, so.

Tom Fabian:       Right. So that was really just one study and I have not come across any additional studies on that and again it was a mouse study. It was a very high dose though. Something maybe equivalent to a least more than five grams per day for humans. Again, you have to take those kinds of things into account that if it was just an animal study and it was super high dose, maybe it doesn’t apply to real world settings. Right?

Dr. Weitz:           Okay.

Tom Fabian:       But that’s not been our experience. The patient is on strong antimicrobial botanicals. Don’t seem to develop a deficiency pattern based on what we see on GI MAP so far.

Dr. Weitz:           Right. Good then that’s been my experience as well.

Tom Fabian:       Okay. So this actually, it’s kind of interesting that we talked about that, because I won’t go through this full case. It’s not really a full clinical case, but just a quick example of an older female history of bladder cancer was on long-term Amoxicillin antibiotic for five or more years. Main complaint was just Chronic diarrhea. So of course there was a suspicion of antibiotic associated diarrhea in this case.  You can see here very broad deficiency, which would be pretty much expected from such a long-term exposure to an antibiotic.  But just based on what we’ve talked about before with the insufficiency, you would expect that this would potentially lead to overgrowth of opportunists or pathogens.  And sure enough, you see Pseudomonas and Klebsiella overgrown and it turns out that those two are the ones that are known to be resistant typically to Amoxicillin.  So, we’re seeing exactly the pattern you would expect based on that patient being on that antibiotic.  This kind of scenario to me is very important. You’re thinking about, which gut tests you want to go with and how good is a gut test? And you can kind of debate validation approaches and all these things and sequencing versus PCR. But in the end of the day, it really comes down to “Does this clinically validate?” And as you know a patient for example, is on an antibiotic long-term, you would expect to see patterns of this. If you don’t see patterns like this, there may be some individual variation, but when you… So that’s just something to keep in mind as you’re going through some people may try different gut tests. You want to make sure that the test you’re using clinically validates and that it makes sense based on the patterns that you’re seeing.

Dr. Weitz:            Can I just comment your test looks at, if there’s a pathogen what antibiotics might be effective for those pathogens, some of the stool tests, in which in the past, I know used to use natural anti-microbials, how come you don’t include that?

Tom Fabian:       That’s a good question. So I’m not sure of all the reasons why I know part of it is we wanted to kind of keep our test to molecular that’s what our lab does, that other sort of approach to look at potential sensitivity involves culturing. So that’s part of the picture, but also how realistic is it from a couple of different standpoints that what you’re measuring on a Petri plate with one organism really translates to how effective that’s going to be in an actual, vast, complicated ecosystem. You don’t really know that plus most clinicians tend to use common formulations.  Some do use single ingredient approaches.  A lot of clinicians use formulations that they found to be generally effective.  So it’s not necessarily going to affect what they use clinically either.  So it’s not always clinically useful information.

Dr. Weitz:           Okay.

Tom Fabian:       I think I’ll skip all of this here just real quick. And one more thing about Klebsiella and also Morganella they have been linked to excess Histamine production.  So again, be thinking of these things, when you see Klebsiella overgrown you want to kind of look at the context are beneficial bacteria lacking. Does the patient also potentially have Histamine intolerance symptoms, et cetera. So the more you know about these microbes, the more you can potentially clinically connect those dots. This is the only thing I was going to show and I’ll stop at this one. This is a little bit of a complicated diagram, but it’s representing the colon on the left side is the proximal colon and moving on across horizontally to the right towards the distal colon. There’s a lot of research showing basically the dynamics in the colon so that you understand better, why a patient may have say a high Firmicutes, low Bacteroidetes why they might have Sulfur-reducing bacteria and methanogens.

                                So the main point I wanted to make here is generally in the first part of the colon is where most of the Fiber fermentation, Carbohydrate fermentation is going to happen, that can release hydrogen and then basically that part has to kind of start happening first before that hydrogen is available for the methanogens.  And then basically further down the line would be the Sulfur-reducing bacteria, which tend to be more in that latter part of the colon.  Where also bacteroidetes tend to dominate and that’s going to be affected by transit time and other factors too.  But there’s a lot of, sort of modeling that’s being done to understand the ecosystem.  And I think this is a great visual and understand why do we see high methanogens on our test when there’s high Firmicutes that are showing you that there’s a general overgrowth pattern, probably because they’re fermenting, generating H2 and then promoting methanogen growth.  All right.  So that’s in a few additional slides, a lot of material that we could always cover.  Maybe we’ll have an opportunity a part two at some point.

Dr. Weitz:            Okay.

Tom Fabian:       Yeah, so I bring that in, so really it’s all about connecting the dots and just learning. We have a lot of educational information because we offer the consultation. So I encourage everyone to take advantage of those resources because the more you can connect the dots, the more you can get out of the stool tests in terms of good clinical insights that can really help you be more effective in helping your patients and clients.

Dr. Weitz:            I have one more question I’d like to ask and then, I’ll see if anybody else has some additional questions. I’ve interviewed several clinicians. One of whom is very prominent and feels that some protozoa like Blastocystis hominis and D. fragilis are commensal and not something that we should be concerned with. And he’s been talking about that quite a bit.  And I think it’s common for a number of Functional Medicine practitioners to see that on a GI MAP stool tests and say here is likely the cause of your problem and are used to treating it and getting results.  And then I also talked to, in another recent Podcasts another practitioner Ilana Gurevitch and she felt that in patients where correlated with their symptoms, very important to treat blasto and D fragilis. What do you think are these pathogens, commensals or does it depend?

Tom Fabian:       Good question. So they’re not likely to be commensals based on our experience because we don’t see them in the majority of patients. It’s commensals tend to be present in the majority of individuals. I think the real answer is probably somewhere in between. So if you look at the research, most of the research suggests that Blastocystis in particular and possibly Dientamoeba their conclusion and in most of the research is that for the majority of people that have them, they’re not a problem because most of those people are asymptomatic, but I think they’re thinking of them asymptomatic in a conventional sense, not a functional sense. So they may be ignoring SIBO and these other things, mild GI symptoms, et cetera, and not taking those into account. With GI MAP, we only see, I would say probably more than 95% of the time when we see blastocystis and, or Dientamoeba Fragilis, it’s a long with that digestive dysfunction pattern. I don’t think I’ve ever seen blastocyst is just sort of by itself with no other patterns where it’s kind of like the obvious cause of things.   It’s almost always in the context of things like H. pylori, maybe candida, general overgrowth. So the question is what’s causing the symptoms?  Now trying to pin it on an individual organism, some may be more important than others.  H. pylori often is because of its effects on stomach acid.  Candida often is because we know it has, it can cause inflammation like you got Pseudomonas. Blastocystis I think is somewhere in between probably for some patients, if they have a certain subtype and it’s a really high level that may be more significant than if it’s there at a low level.

Dr. Weitz:            Okay. So one question that came in is what causes Insufficiency Dysbiosis? Is it low stomach acid?

Tom Fabian:       That’s a good question. So recent research indicates the antibiotics are often a major cause even long-term because what can happen is antibiotics can actually effect the mitochondria in the cells that line the colon, in a way that makes the gut environment less favorable to those beneficial bacteria. So, that’s at least one example of pharmaceuticals that may have that effect. Certainly lack of fiber in the diet. That’s been correlated with lower levels of these beneficial species, any source of inflammation.  So inflammation is highly detrimental to many of those beneficial bacteria. So whatever gets inflammation going that can really turn the tide.  One of the other contributing factors and it’s related to low digestion is too much protein in the colon.  That could be from just high protein diet or not digesting well.  But this process of sort of breaking down amino acids, which is called protein fermentation, and then breaking down carbs which is carb permutation. So primarily fibers they’re antagonistic.  So the less fiber you have, and the more protein you have in the colon, that can really also be detrimental to those beneficial bacteria.

Dr. Weitz:            So another question is how does the Ketogenic diet, and I would even throw in there, how about the carnivore diet impact the microbiome?

Tom Fabian:       I’ve actually only seen two cases so far and they were all almost identical and they were probably one of the… There were both among the worst cases I’ve seen as far as Dysbiosis. That’s a perfect example of this sort of… The sayings of tests don’t guess, or the opposite of that is treat the patient, not the test, right? Two different philosophies or ends of the spectrum. When you see that, so in both cases, the patient improved in symptoms, they had typical GI symptoms, gas bloating, apparently issues with carbohydrates. So they went full carnival symptoms improved. And yet you look at the gut microbiome and it looks terrible, lots of inflammation in both cases just massive Dysbiosis. So the question is, well, is short-term improvement in symptoms, are you setting the stage for long-term problems? And is there another way to address those symptoms without kind of ruining the microbiome? So good question. I mean, I guess time will tell, from everything we know about the microbiome, those results look terrible. They really would be considered by almost everybody is really bad [inaudible00:40:45]

Dr. Weitz:           Okay. And one more question, is it necessary to stop digestive enzymes before collecting the stool sample? In fact, are there any other recommendations that should be taken before collecting the stool sample?

Tom Fabian:       Not really a lot of us can depend on the clinician goals in terms of what you want to see. Do you want to see how your patient is doing on the treatments or do you want to see them of course, before treatment, et cetera?

Dr. Weitz:           Well, I guess if they’re taking enzymes, would that affect the pancreatic elastase levels?

Tom Fabian:       There’s not much evidence that does now.

Dr. Weitz:           Okay.

Tom Fabian:       Certainly, with acid, that’s typically not in the enzyme formulation, so, you wouldn’t literally affect it from just coming from the antibiotics or the main one, if you do take antibiotics we recommend waiting at least 30 days post antibiotic treatments, maybe 60 days to allow the microbiome to recover somewhat.

Dr. Weitz:           Okay. Excellent. Thank you so much, Thomas.

Tom Fabian:       It was my pleasure. Thank you.

Dr. Weitz:           Great. And thanks everybody. And we’ll see you next month.

 

Weitz Sports Chiropractic and Nutrition
Weitz Sports Chiropractic and Nutrition
Atrial Fibrillation with Dr. Aseem Desai: Rational Wellness Podcast 181
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Dr. Aseem Desai speaks about Atrial Fibrillation with Dr. Ben Weitz.

[If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on YouTube at https://www.youtube.com/user/weitzchiro/]

 

Podcast Highlights

9:58   Arrhythmia is an abnormality of the heart’s electrical system that can result in bradycardia, where the heart rate goes too low and often presents with fainting or extreme fatigue. It can result in tachycardia, which is when the heart rate becomes fast and in some cases can go above 200 beats per minute.  And then there are irregular heartbeats, which are broken down into two categories: 1. Benign, which include premature beats that can occur from the top chamber of the heart, the atria, or the bottom chambers of the heart, the ventricles. 2. Conditions like Atrial Fibrillation (AFIB), which are quite dangerous and can cause stroke, congestive heart failure, as well as reduced quality of life.

11:09  How dangerous AFib is depends upon your stroke risk factor, which is determined by the CHA2DS2-VASc scoring system. C is for congestive heart failure. H is for hypertension. A is for age. D is for diabetes. 2 is for prior strokes or blood clots. A higher score is correlated with a higher risk of stroke.  Even though age increases the risk of AFib, there are significant numbers of young people with AFib, esp. athletes. For example, NFL players have 6 times higher risk of AFib. This may be because athletes tend to have a lower heart rate and people who have a very low resting heart rate have an increased risk of having premature beats and these can be a trigger for atrial fibrillation.

14:07  Dr. Desai does not think it makes sense for those with a low heart rate, like athletes, to attempt to raise their heart rate with increased sodium consumption or by taking licorice.  Arrhythmia does not occur simply because you have a low heart rate. A resting heart rate of 40 or 50 is only one factor along with drinking a lot  of alcohol, sleep apnea, or goes on to gain weight after retirement goes on to develop high blood pressure or diabetes.  It is the over activation of the parasympathetic nervous system that can trigger arrhythmias like AFib. This is not to say that being stressed out, in flight or fight mode too much of the time and having overstimulation of your sympathetic nervous system is not also a problem and a risk factor for AFib.

18:01  Some of the most common risk factors for AFib include: 1. age over 65, diabetes, 2. high blood pressure, 3. thyroid disease, 4. heavy alcohol use, 5. sleep apnea, and 6. obesity. Even one glass of alcohol is associated with an 8% increased risk of an AFib episode.  Chronic high blood pressure increases the stretch in the left atrium, the the top left chamber of the heart, which is the trigger for AFib. There is an inflammatory component with AFib, which is why diet and supplements can be beneficial.  Environmental toxins can be triggers for AFib. And there is a close connection between the gut and the heart and gut issues can trigger heart problems.  Acid reflux can be a trigger for AFib, since the esophagus sits right behind the heart.  Even just eating really large, fatty meal can activate the vagus nerve and trigger an AFib episode.

27:37   Diet can play a role in preventing and controlling AFib, though this should be individualized to each person.  The Mediterranean diet is probably best for most patients, though some do better on vegetarian or a lower carb diet like Paleo.  Some patients are able to take care of their AFib purely with diet and lifestyle modification, though some need medication and some need a catheter ablation procedure. AFib is a progressive disease and AFib begets AFib.  It is an electrical cancer.  Early detection is important and in order to detect AFib, there are some great biometric tools out there, including the Apple watch and KardiaMobile, which you can buy on Amazon for $90.

 

 



 

Dr. Aseem Desai is a cardiac electrophysiologist (EP), a physician specializing in heart rhythm disorders.  He has been caring for people with atrial fibrillation (AFib) for over seventeen years and currently practices in Orange County, California.  He has published a number of scientific papers and he just published his first book, Restart Your Heart: The playbook for thriving with AFIB. His website is DrAseemDesai.com

Dr. Ben Weitz is available for nutrition consultations, including remote consults via video or phone, specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111 or go to www.drweitz.com. Phone or video consulting with Dr. Weitz is available.

 



 

Podcast Transcript

Dr. Weitz:            Hey this is Dr. Ben Weitz, host of the Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to the Rational Wellness Podcast for weekly updates, and to learn more, check out my website drweitz.com. Thanks for joining me, and let’s jump into the podcast.

                                Hello Rational Wellness Podcasters. Thank you for joining me again today. Our topic is atrial fibrillation with Dr. Aseem Desai. This is actually the most common form of arrhythmia diagnosed in clinical practice. It’s estimated that between 2.7 and 6.1 million Americans are living with AFib. I got that from Dr. Desai’s book. Interestingly there’s such a broad range I guess it’s not clear necessarily whether people know they have this or not, but that’ll definitely be something we want to understand.  But as our population ages AFib incidence is increasing. So I just mentioned arrhythmia, so what is arrhythmia? Well this is basically a problem with the rhythm of the heart which occurs when your heart beats too fast, too slow, or irregularly. Some forms of arrhythmia are harmless while others can cause serious damage and even death. Your heart has four chambers. There are two upper chambers known as the atria and two lower chambers known as ventricles. Your heart also has a built in electrical system that controls the coordinated contraction of the muscles of these chambers resulting in your heart beating between 60 and 100 beats per minute while at rest.  If the heart beats too fast this is a type of arrhythmia known as tachycardia. Well with slow heart rate is known as bradycardia. Atrial fibrillation is a type of tachycardia that originates in the atria and it can be a serious condition that can lead to stroke if it’s not controlled or managed properly.

Now we’ve had a number of discussions about the cardiovascular system on this podcast, but we essentially have focused on conditions like how to prevent and reverse atherosclerosis and hypertension.  So essentially we focused on, to use a analogy from construction, we’ve focused on the plumbing, and then the engine that helps drive the blood through the body which is the heart. But now we’re going to talk about the electrical system of the heart. Our interview today is with Dr. Aseem Desai who’s a cardiac electrophysiologist which means that he’s a physician specializing in heart rhythm disorders. And he’s been caring for people with atrial fibrillation for over 17 years and currently practices in Orange County, California. He’s published a number of scientific papers and he just published his first book Restart Your Heart: The Playbook for Thriving With AFib. Dr. Desai thank your for joining me today.

Dr. Desai:             Thank you very much Dr. Weitz. Thank you for having me.

Dr. Weitz:            So before we get into the specific questions about the cardiovascular system, I noticed that you and I have something in common which is that we both have an undergraduate degree in philosophy. How did you come to study philosophy with an interest in cardiology?

Dr. Desai:             I love it. I love that I’m meeting a fellow philosopher. We could talk about Aristotle the whole episode here. Yeah no so I was part of the seven year medical program at Northwestern so as a high school senior you gain admission to college and med school at the same time, and the idea was to foster an interest in liberal arts. And so we did have a double course load. Pre med as well as liberal arts major, but it really kind of opened my mind. I think I tend to look for challenges and I don’t know about you Ben but this was probably one of the biggest challenges was reading philosophy and writing the papers. And what’s interesting is to this day I still use a lot of the logical reasoning, the deductive reasoning even when I’m doing, when I’m taking care of heart patients and making diagnoses.

Dr. Weitz:            Right. I know for myself one of the things that I got out of philosophy is when you study philosophy you learn that there’s not a lot of concrete answers, but you want to get closer to those answers. And the way you do that is by being critical and asking good questions.  And so I think that’s also important in medicine to be critical when people make statements and challenge them and try to get closer to the best answer we’ll have at that point in time.  So I think that’s helpful–how philosophy has helped me.

Dr. Desai:             Absolutely Ben and to your point I also think it keeps you with an open mind, a beginners mind. 

Dr. Weitz:            Yes.

Dr. Desai:             I think that as physicians we do have a tendency to not have that and especially…

Dr. Weitz:            We think we know everything yeah.

Dr. Desai:             Yeah. Right. Exactly. And so I think that, I mean I look forward to learning as much from you as you will from me perhaps during the podcast and as well as your viewers. I always welcome feedback, your listeners. So I do think that these two philosophers on this podcast today will have a lot to say to each other.

Dr. Weitz:             So how did you come to specialize in heart rhythm disorders?

Dr. Desai:             Well it’s very personal. So when I was about three, my dad had a heart attack. He was 37 at the time and although I don’t have much memory of that, I think many things for kids, they get ingrained in your brain even if you may not be able to process what’s going on. And he was an oncologist so I actually saw him not only as a physician but I saw him becoming a patient and I saw how this heart disease really robbed him of enjoying his life and he was fearful that he was going to have another heart attack.  And so as I went through college, high school and then college, I had an interest in science and unfortunately in the middle of medical school, me second year of medical school he actually suffered a cardiac arrest.  And he was in India at the time and in most cases the cardiac arrest is actually due to abnormal rhythms from the ventricle, from the bottom chamber.  It’s called ventricular tachycardia and ventricular fibrillation.  And in many cases as you mentioned with regards to the plumbing of the heart, a heart attack or a blocked artery, the clot that forms in a plaque can actually induce the ventricular tachycardia and ventricular fibrillation and cause sudden death.  So I think that really got me focused on the electrical system of the heart. And as I went through training and residency and then in fellowship I just found the electrical system quite a challenge. To be honest I was terrified of cardiac arrhythmias when I was a medical resident.  I mean they were really hard to understand and interpret electrocardiograms which are the recordings that we do for the heart’s electrical system and I don’t know about you Ben but mentors kind of come across your paths in different ways.  When I was a medical intern at Stanford and I was sitting reading EKG’s as part of the cardiology rotation. And it happened to be right near the electrophysiology office and electrophysiology is the branch of cardiology where we do study and treat these rhythms.  And one of the attending physicians saw me reading EKG’S and came up to me and said, “Hey you want to write a paper with me on IV Amiodarone?”, which is a drug that we use for cardiac arrhythmias.  And the next thing I knew I was writing a paper. Had no idea what I was doing, but I did publish it and I think the story goes on from there.

Dr. Weitz:            Yeah I had sort of a recent experience with arrhythmia.  I had a EKG done and after the EKG was done my doctor left the room, came back, and repeated it. And then decided to leave the room and repeat it again, and he brought another doctor in. So in between I got up and looked at the sheet of paper that read out, and the paper read that this patient is having an acute MI and I was feeling completely fine. And he came back in the room and I said, “Hey doc. Whatever’s going on, I could have something wrong with my heart, but I am not having an acute MI.”  And so it turns out I have a early repolarization variant.

Dr. Desai:             Mm-hmm (affirmative).

Dr. Weitz:            And which is something that happens in people who are athletic and so then I also had to have hernia surgery recently and I had to make sure everybody was on board with this. That they suddenly weren’t going to freak out when I was under anesthesia and somewhere or anywhere along the line that somebody saw my EKG.

Dr. Desai:             Well I think you make a great point Ben that you actually should carry a photocopy of an EKG.  If you have an abnormal EKG and it’s truly normal just a variant of normal which is what early repolarization is it’s always a good idea to actually carry a copy of it.

Dr. Weitz:            I do I have it in my phone.

Dr. Desai:             Yeah. Yeah. Yeah because like a radiologist with chest x-rays, as cardiologists we often will look at an old EKG to really get a sense of is there a new change and it really illustrates the room that we have to move on our artificial intelligence algorithms and these EKG machines.

Dr. Weitz:            Certainly the readout from that machine was not correct. Maybe you could explain a little more about exactly what is arrhythmia?

Dr. Desai:             So arrhythmia is a generic term used to describe any abnormality of the heart’s electrical system and that can result in something called bradycardia where the heart rate goes too low and often presents with fainting or extreme fatigue. It can result in tachycardia which is where the heart rate goes too fast. A common symptom there would be a sense of a racing heartbeat, and sometimes if the heart rate goes fast enough, and in many cases it can go over 180, 200 beats a minute, people can faint with that as well.  And then you have irregular heartbeats and so irregular heartbeats are really broken down into two categories benign which include what we call premature beats that can occur from either the top chambers of the atria or the bottom chambers of the heart, the ventricles. Or conditions such as atrial fibrillation which are quite dangerous and can cause stroke, congestive heart failure, as well as reduced quality of life. So it really is a generic term, arrhythmia. And it encompasses bradycardia, tachycardia, and irregular heartbeats, AFib being the most common. But it’s important to mention that not every irregular heartbeat is AFib.

Dr. Weitz:            How dangerous is AFib?

Dr. Desai:             It’s actually very dangerous. It depends on your stroke risk factor score first off. So we use a scoring system called CHADSVASC. It’s an acronym and you calculate the number of points that include some such as congestive heart failure, high blood pressure, age, diabetes. And as you add up these points there’s a lot of large databases that have shown that once you hit a score of 2 or higher your stroke risk is actually quite high with AFib and it continues to go up as the points get added up and so we, just like many areas of medicine and I’m sure in your case as well, you look at a person’s health and you do a risk stratification, priority stratification and it’s no different with AFib. So you can have young patients actually that get AFib, especially athletes.  We’re seeing a larger population. Those patients tend not to be as high risk for stroke but certainly impacts their quality of life though.  NFL players have a six times higher risk of AFib compared to their counterparts. Most people don’t realize this.

Dr. Weitz:            Really? Why do you think that is?

Dr. Desai:             That’s a good question. So we’ve now learned that the nervous system is a big component of heart rhythm problems. So the nervous system, just like inflammation is a big part of many different illnesses including coronary disease and GI issues. The nervous system, the autonomic nervous system which includes the Fight or Flight which is the sympathetic and the Rest and Relax–the parasympathetic, actually is heavily involved in the genesis of cardiac arrhythmias. So for example, athletes have often a low resting heart rate and that has to do with the vagus nerve. The vagus nerve, being that part of the nervous system that helps to preserve your energy really. There’s no point in your heart rate being 90 beats a minute when you’re sleeping. So a good conditioned athlete often has a low resting heart rate.  But just like anything in life, extremes may not be a good thing and people who have a very low resting heart rate have an easier ability to have what are called these premature beats that I referenced earlier.  Why I said that premature beats are benign, that’s not exactly true.  If you have enough premature beats, especially from the atria and under the right perfect storm so to speak it can be a trigger for atrial fibrillation so one thought with the football players and other athletes including triathletes for example is that this low resting heart rate predisposes to these premature beats.  Because there’s a longer time interval between beats with a low resting heart rate so it’s easier for these extra beats to be a trigger and if you think of AFib as a fire, you have the matches and you have the wood.  And the matches would include something such as these premature beats, would include things such as alcohol, variety of other factors.  And then the wood are the risk factors for AFib which would include things such as age over 65, diabetes, sleep apnea, a whole host of things that we can get into.

Dr. Weitz:            So would it make sense for an athlete who has a lower resting heart rate, for example myself, actually when I was on when I was in the pre op, they, my heart rate was right around 50 and down to 48 and up to 55 and they kept going, “Oh. You’re an athlete. You’re an athlete.” And they were freaking out a little bit. Does it make sense for somebody with a low resting heart rate to try to raise their resting heart rate?

Dr. Desai:             Well it’s a good question and the problem with this is you can’t really do that from the standpoint of, I mean other than taking in stimulants such as amphetamines.

Dr. Weitz:            Well could you for example take in more sodium? Could you eat licorice? We just heard about somebody who ate so much licorice that they died actually.

Dr. Desai:             Right. Yeah the problem with licorice consumption is that it more predisposes to dangerous heart rhythms rather than purely increasing your heart rate.  And it’s not that low heart rate in and of itself.  It’s, with arrhythmias like AFib it’s the perfect storm.  So we’re now learning there’s quite a bit of complex genetics with AFib. So not every athlete with a heart rate of 40 or 50 is going to get AFib by all means, but if that athlete consumes a lot of alcohol, if that athlete has unrecognized sleep apnea, if that athlete puts on weight after they retire and goes on to develop high blood pressure or diabetes, that’s really, it’s that adding up of risk factors.  It’s just that when you have a low resting heart rate that kind of puts you at a little bit of a higher risk.  But we’re still working it out. We’re still trying to determine what’s going on. But you ask a good question which is, is it the heart rate itself? And I would say no it’s more, it’s that over activation of the parasympathetic nervous system.  And it’s not just the heart rate.  The actual vagus nerve, when you stimulate it either in laboratory models or even when we’re doing a procedure called catheter ablation, and you stimulate the vagus nerve which you can do, it’ll actually trigger AFib and it has nothing to do with low heart rate. It’s literally stimulating that nerve and the release of the acetylcholine and other components that can be a trigger for arrhythmias.

Dr. Weitz:            Now is it the overstimulation of the parasympathetic or the sympathetic?

Dr. Desai:             That’s a great question. So now we believe in most cases it’s actually the parasympathetic that’s the problem.

Dr. Weitz:            Well that’s interesting because and when we have patients who have anxiety or they have adrenal problems or they have fatigue, we’re always working with them to increase parasympathetic stimulation because the thought is everybody’s stressed, everybody’s in sympathetic mode all day long and that’s why they’re drinking caffeine because they want to be in this sympathetic mode because they’re not sleeping enough and they’re trying to get more work done, etc.

Dr. Desai:             Well you’re absolutely right. For emotional and mental stress and even physical stress, I mean the parasympathetic nervous system’s a very important part.  You I’m sure are aware of heart rate variability and using heart rate variability in certain breathing techniques activates your parasympathetic nervous system. 

Dr. Weitz:            Exactly.

Dr. Desai:             So it’s not so much as you mentioned about calming down your fight or flight.  It’s about enhancing your rest and relax.  It’s about enhancing your parasympathetic nervous system.  The only reason why I’m commenting on this from the standpoint of arrhythmias is that the parasympathetic has been implicated honestly both parts of the nervous system have been.  So we clearly see sympathetic triggers if someone’s under a lot of stress and their heart rate goes up, they can end up having more premature beats.  So it’s not, I would just say anything out of balance in the body, right, is not a good thing. And so when you come to AFib we love using this term the perfect storm.  You have a few risk factors, you have a few of these matches, you have a little bit of that wood, and then it creates the fire and that’s why on a given day there’s something or a combination of things that could lead to a patients first AFib episode.

Dr. Weitz:            Well it’s interesting when we’re talking about these risk factors because it seems like this comes up all the time. At this point we’re still going through this COVID-19 pandemic, and what comes up all the time is that people are likely to have a worse prognosis if they have any of these chronic diseases like being overweight, having hypertension, having diabetes, having sleep apnea, having lung disease. These are the same chronic conditions that are so prevalent in our society that they make it more likely that you’re going to have AFib.

Dr. Desai:             That’s absolutely right and if you look at obesity for example that it one of the number one risk factors for AFib and there’s a lot of different mechanisms that are thought of with regards to that. But obesity itself leads to many of the other conditions you mentioned. The diabetes, the high blood pressure. Chronic high blood pressure increases the stretch in the left atrium which is the top left chamber of the heart. That’s the trigger for AFib. There are so many different types of mechanisms, but as you mentioned with COVID this inflammatory component is critical right?  I mean that’s why people get this multi organ system failure. That’s why people get this myocarditis that you’re seeing in cardiac cases.  And so many cases, or many people believe I should say, that AFib is along the same lines. It’s an inflammatory disease. It’s, so you do see elevated biomarkers in the setting of AFib.  We just don’t know what to do with those biomarkers, but we do know that there is an inflammatory component like many things. I think that’s also why probably treating your body with food as medicine, that certain foods definitely and supplements definitely do help cardiac arrhythmias, but the other, I think what distinguishes it a little bit, AFib from some of these other things we’re talking about is this interplay with the nervous system so I think the gut, as you know the enteric nervous system and the gut there’s that secondary nervous system. The heart has it’s own nervous system, and so it’s interesting to see this sort of two way street between the brain and the heart and the brain and the gut, and I think when those things are out of balance and it’s usually nature and nurture, there are some genetics probably and then there’s environmental triggers.  So many things we’re not aware of right? We don’t even, there may be multiple toxins in the environment that are big components of causing AFib that’s to why one person gets it and one person doesn’t. So there are well defined risk factors: age over 65, diabetes, high blood pressure, thyroid disease, heavy alcohol use, sleep apnea, obesity is the big one. And then there’s one that we really haven’t determined yet. But I would say that you see this I call it the electrical epidemic, AFib. It’s an epidemic because as we get older we’re living longer, and so it’s arthritis of the electrical system. So when you get AFib when you get older, you could be a totally healthy person. Lived a totally healthy life, and still get AFib. And it has to do with scar tissue that builds up in your electrical system just like it would in your knee. So that is, that’s the age related factor of AFib. And then you have that obesity component that our society as you mentioned Ben, I mean we’re getting unhealthier and unhealthier and the obesity epidemic is probably a big reason why we’re seeing AFib.  We’re seeing a lot of AFib in our practice right now so our patients who have AFib are getting more AFib right now during COVID. Two reasons we think.  One is increased alcohol consumption.  One glass of alcohol is associated with an 8% risk of an AFib episode. It’s not a small thing. And then the lack of physical activity and weight gain.

Dr. Weitz:            Yeah and the stress as well.

Dr. Desai:             The stress is huge absolutely. We see, it’s interesting you mentioned the stress. Just in observation there’s a lot of people who, they’ll be in AFib, they’ll go into this AFib episode at home. Their heart’s racing, it’s going irregular, they’re feeling terrible because the heart’s an engine so when you go into AFib you lose about 30% of the pump efficiency of your heart. It’s almost like losing a few pistons in your engine. That’s what the atria do for you and when you go into AFib the part of the heart muscle beats very poorly, very chaotically. So people are feeling terrible and they go into the hospital and they’ve been sitting in AFib even sometimes for a few days and they go into the hospital and the doctor is getting ready to shock the heart back into rhythm called the cardioversion which is often something that’s done for AFib. And literally you’re getting ready to press the button and the person converts to a normal rhythm. And the hypothesis here is that people feel safe when they get into a hospital in this context. Not always. But in this context they feel safe.  And so we see it over and over again where people, that’s why I’m a big believer in mindfulness. I do a daily mindfulness practice. I have a lot of interest in that, and we definitely see through activation of the parasympathetic and calming down that fight or flight response. I mean I mentioned all of these things about parasympathetic and arrhythmias, but don’t get me wrong. It’s not that the parasympathetic is bad and it causes arrhythmias.  It’s just that we’re learning specifically in athletes, but what’s also interesting is GI triggers for AFib. So people who have acid reflux, the esophagus sits right behind the heart, or people who eat a really large, fatty meal activates the vagus nerve. So again it’s these, it’s over activation.

Dr. Weitz:            Yeah I mean, be honest with you in my practice we see a lot of patients with GI disorders, especially irritable bowel syndrome and reflux. These functional disorders, and they’re extremely common.  When you combine those with obesity, and 70% of the patients in this country are overweight, you add in the rates of diabetes and hypertension and some of these other conditions, it’s surprising that we don’t have more people with AFib.

Dr. Desai:             Oh absolutely and I’ve been on different kinds of shows and I’ve talked about these things and one of the things I started realizing and gotten humbled about is patients are saying to me, they’re like, “This is great. You’re telling me all these bad things. How do I change my life?” And I don’t know if you’ve heard of Thrive Global. It’s a organization funded by Arianna Huffington and it’s an amazing…

Dr. Weitz:            Oh I know who she is, but I haven’t heard of the organization.

Dr. Desai:             So yeah. So Arianna and I had a chance to connect as I wrote this book, partly because of my interest in mindfulness and I reached out to her to get her thoughts on the book, and she invited me to be a contributor for this website.  So for your listeners out there I would definitely encourage you to check out this website thriveglobal.com because they’re addressing so many issues of COVID right now.  Parents who are working from home, schooling people at home. I mean everything really under the sun. But what I like, their theme is microsteps.  So to make a behavior change, it’s a micro step.  It’s not what we used to think which is, 21 day challenge.  Give up this.  It’s really making those small changes every day and then, and building on that and having that accountability.  So I just wanted to mention that because you and I are having this great discussion about all these risk factors, but I don’t want people to be demoralized into thinking that there, it’s, there are ways to change, and I know that you do that you do that on a regular basis with your patients.

Dr. Weitz:            Absolutely and the greatest thing that could come out of this COVID crisis is if there’s more awareness about doing something about these chronic diseases that result from poor diet and lifestyle like we’ve just been talking about like obesity and hypertension and diabetes and etc. etc. We, America needs to wake up and get healthy and exercise and eat healthy and get control of their stress and all of these chronic, all of these conditions like AFib are, we’re going to see less of.

Dr. Desai:             Yeah I totally agree. I mean it’s interesting, a virus that is decimating part of humanity is also connecting part of humanity and waking up part of humanity that all of these thing’s we’re talking about, these are huge risk factors for massive COVID infection and poor outcomes.

Dr. Weitz:            Yeah.

Dr. Desai:             So I think you’re right. People are sort of saying well this is this end goal that we all have of not wanting to get infected and certainly not wanting to have a bad infection.

 



 

Dr. Weitz:                            I’ve really been enjoying this discussion, but now, I’d like to pause to tell you about the sponsor for this episode of the Rational Wellness Podcast. This episode is sponsored by Pure Encapsulations, which is one of the few lines of professional nutritional supplements that I use in my office. Pure Encapsulations manufactures a complete line of hypoallergenic research-based dietary supplements. Pure products are meticulously formulated using pure scientifically-tested and validated ingredients. They are free from magnesium stearate, gluten, GMOs, hydrogenated fats, artificial colors, sweeteners and preservatives.

Among other things, one of the great things about Pure Encapsulations is not just the quality products but the fact that they often provide a range of different dosages and sizes, which makes it easy to find the right product for the right patient, especially since we do a lot of testing and we figure out exactly what the patients need. For example, with DHEA, they offer five, 10 and 25-milligram dosages in both 60 and 180 capsules per bottle size, which is extremely convenient.

                                                Now, back to our discussion.

 



                           

Dr. Weitz:            Are there certain diets that are associated with less risk of AFib or that can be beneficial for patients that have AFib?

Dr. Desai:             Yeah I think that the… 

Dr. Weitz:            And keep in mind the background is that there’s a lot of confusion today as far as what the best diet is and it’s almost like partisan politics.  We’ve got the vegans on one side and the people who only eat meat, the carnivores on the other side.

Dr. Desai:             Right.

Dr. Weitz:            And then we’ve got the Paleo and the Mediterranean [crosstalk 00:28:12] and everybody’s claiming that their diet is the best.

Dr. Desai:             Yeah and I think it raises the point. This is for AFib, this is for diet. You have to individualize to your case. You may have a certain blood type if you believe that, where a certain diet is better or you may have a lot of chronic inflammatory disorders whether it’s fibromyalgia or lupus or even cancer and a vegan diet with all the data we know about reducing inflammation on that. So as cardiologists we typically recommend the Mediterranean diet. There’s a fair amount of data with regards to that. Lean proteins, good fats, but I think that it really comes down to balance. But you also have to look at your individual situation because whatever food plan you adopt, you want to adopt something that you can stay with the long term.  Yeah you can have your cheat day once a week or what have you, but you want something that’s really going to sustain you long term which is why I’m not a big fan of things like Atkins and really high fat diets. I agree sugar is not good, but I think you really have to individualize and AFib is the exact same way. No two patients with AFib are treated the same or are the same. So some people, they may be able to take care of their AFib purely with diet and lifestyle modification. Losing weight, not drinking alcohol, etc. etc. Treating sleep apnea which is very unrecognized as trigger for AFib.

Some people, they need a medication in some cases. Some people need a catheter ablation procedure and there’s other kinds of things that we can do, but AFib is a progressive disease.  AFib begets AFib. This is an electrical cancer. People need to know about this disease. They need to know how to screen themselves for it. They need to know how to help their loved ones with it because you don’t want to wait until someone has stroke to figure out that they have AFib.  And nowadays with all these great biometric tools, Apple has their EKG function on several of their watches. KardiaMobile has a device you can buy $90 on Amazon. These are devices that actually allow you to record an EKG and tell you with a reasonable amount of accuracy, not perfect that you may be having AFib.  So we are big proponents now of early detection, early intervention.  So if someone gets diagnosed with AFib for example you don’t want to just say, “Lifestyle and diet and let’s regroup in four weeks.” Every episode of AFib even if it’s five minutes and this is really important changes the cellular and electrical architecture of the heart to want to have more AFib. It’s a muscle memory thing.   So we’ve had cases of patients where they think they’re only having one or two episodes a year, where in fact they were having a lot more silent episodes, but that’s common actually while people are sleeping. Silent episodes of AFib they don’t feel anything and their AFib is progressed by the time they go to treatment. So early detection, learn how to take your pulse after you brush your teeth. It should be like a metronome. It shouldn’t be fast and irregular.  Many patients have very subtle symptoms. This is really common. 

Dr. Weitz:            Yeah what are the symptoms of AFib?

Dr. Desai:             Yeah I’m glad you asked. So the, it depends on your age, so younger people and we’ve seen people as young as 18 by the way, tend to get that rapid, irregular heart rate. The palpitations that we described. But it’s more than just skipping beats. It’s a tremendous amount of fatigue or shortness of breath because again the engine analogy, you lose pistons when you go into AFib. That’s different. If you’re having these skipping beats, these premature beats, you don’t lose pistons in your engine. You, they may be bothersome but you don’t feel terrible and with AFib that’s the big thing is this general sense of lack of energy, fatigue, shortness of breath. But what’s interesting is that as people get older, and especially people who aren’t that healthy who aren’t that active, they may not be aware at all they’re in AFib.

                                They’ll show up for gallbladder surgery as pre op and they’re in AFib. We that so commonly. And then you ask them, “Well over the last six months or year, have you noticed a change in your endurance or activity level?” “Yeah I have I just thought it was I was getting older.” We hear that so commonly. Well it’s not until you restore someone’s rhythm back to normal which is what we often do in those cases at least once. At least as a trial. When someone says they don’t have symptoms with their AFib, we believe as electrophysiologists that unless there’s a strong reason not to, everyone, or most people I should say not everyone, most people should have some kind of attempt at restoring the rhythm. Because you don’t know how much you’re actually having symptoms of something until you restore the rhythm. It’s like having a bad knee and doing less.   You don’t really, and decide to have a knee replacement and realize that you could do more. So that, it’s the same thing with AFib. It’s the great masquerader. It’s electrical cancer. There’s so many different presentations and that’s why the early detection and these devices that I mentioned are so important.

Dr. Weitz:            So the most common symptoms, list four or five of the most common symptoms.

Dr. Desai:             Yeah so most common symptoms, fast irregular heartbeat called palpitations, shortness of breath, sometimes chest discomfort, tremendous fatigue, and that would probably be, and then unfortunately stroke is an often common presentation of AFib where there’s no symptoms. But I would probably say the fatigue part and what’s, the key thing with any of these arrhythmias in the beginning, they’re episodic so what’s different with the heart, the coronary arteries, the three coronaries, they’re, it’s plumbing as you mentioned. So if you have a blockage, it’s going to show up on a stress test. It’s going to show up on a variety of testing. AFib, it can come and go. It’s like the electrical system in your car or your house. It’ll act up sometimes, and then it won’t be there. So you show up to a doctor’s office for an EKG and then you come back in six months and you’re in normal rhythm, you could be having AFib that night and you don’t know it and it’s not until you go from this in and out AFib which is called paroxysmal to continuous AFib which is called persistent that people really then get diagnosed.

                                And the problem is by the time you get to persistent, the treatments are much less effective. We have lots of ways of treating people with persistent AFib, that’s an important point. One of the reasons I wrote this book is people are, there’s so much misinformation out there. People are told they have to live in AFib. It’s too far gone, there’s nothing that can be done, and in the introduction of the book I talk about a man who was told that for five years continuous AFib and we got him to rhythm because of current technology. It’s also lifestyle changes. So those will probably be the most common symptoms. I wanted to circle back to your question which I really didn’t answer about diet. Magnesium is really important with regards to, and I think the important thing about magnesium is you can’t go based on a blood level. 90 something percent of magnesium is stored in your tissues, not in your blood [inaudible 00:34:59][crosstalk 00:34:59]

Dr. Weitz:            Right.

Dr. Desai:             And that’s the same with potassium as you know. So we have a low threshold to recommend a magnesium supplement to someone with heart rhythm issues unless they have advanced kidney failure that’s really the only time where you want to be careful about the magnesium. As far as a specific diet I wouldn’t say, I’d be curious to see if you’ve come across anything in your research. I haven’t come across anything that says this diet is really good for AFib, but I would definitely argue that anything that results in reduced inflammation in your body is likely going to be a good thing for AFib. If nothing else it’s going to help your risk factor’s right? It’s going to reduce your obesity and all these other things which then help your AFib so it’s really about trying to prevent the AFib. Now its [crosstalk 00:35:39]

Dr. Weitz:            There are now a number of forms of magnesium [crosstalk 00:35:44] we use frequently in our office and so there’s magnesium citrate, magnesium glycinate is known to be better absorbed and have less issues with bowel laxity. We’ll [crosstalk 00:35:59] use magnesium citrate if someone is constipated. We use magnesium threonate which has been known to affect the brain and central nervous system a little better. Is there a form of magnesium that you think is more effective for AFib?

Dr. Desai:             I’m so glad you asked that because a lot of people just go to Costco or what have you and pick up whatever magnesium is on the shelf and this is nothing against Costco by the way, it’s more [crosstalk 00:36:26]

Dr. Weitz:            I’m with you.

Dr. Desai:             Yeah magnesium oxide is one of the [crosstalk 00:36:29]

Dr. Weitz:            I got this big giant bottle of fish oil for five dollars.

Dr. Desai:             Exactly. Well there’s a reason why it’s five dollars. So, but magnesium oxide is probably one of the worst absorbed forms of magnesium. And it’s one of the most common sold ones in stores. So yeah the ones you mentioned are great. Magnesium citrate, it actually comes, I love Natural Calm. Natural Calm is a product that you find online, you find in stores. [crosstalk 00:36:54]

Dr. Weitz:            It’s a powdered form of magnesium. [crosstalk 00:36:57]

Dr. Desai:             Yeah it actually comes as a gummy. Now the gummy has some sugar in it, so you’ve got [crosstalk 00:37:01] to be careful about that one.

Dr. Weitz:            Forget the gummies.

Dr. Desai:             Forget the gummies. So but magnesium citrate is a good one, magnesium glycinate as you mentioned, Doctors Best is a really good brand for magnesium glycinate for example. Magnesium malate. Malate is a really good one. And taurate, magnesium taurate. So taurate has kind of more of a specific cardiovascular effect. Sort of derivative or related to taurine amino acid and there is data with regards to taurine and heart health and even rhythm. So there’s a company Cardiovascular Research Lab makes magnesium taurate that we will often prescribe to people. So it’s really about just getting people to take it. And I always tell people go based on the serving size of the bottle. People always ask what dose you should take. It’s really, it’s very manufacturer specific, company specific, but I would say those would be the main ones to consider.

Dr. Weitz:            Yeah I would like to say when it comes to magnesium, manufacturers are often very careful and often will recommend one tablet or something line that. But they have no idea your particular circumstances.

Dr. Desai:             Right.

Dr. Weitz:            And for the most part the only side effect of taking more magnesium is that you’ll get diarrhea and you’ll [crosstalk 00:38:12] know that pretty quickly. So- [crosstalk 00:38:15]

Dr. Desai:             Right.

Dr. Weitz:            You very well may need 400, 600, even 1000 milligrams would not be at all excessive for our magnesium need so a lot of time just what says on the bottle may not be [crosstalk 00:38:29] what you need.

Dr. Desai:             I’m glad you raised that point, Ben. A few things. One is we’ve seen cases where if we give someone magnesium glycinate. Hey go based on the serving size on the bottle, continue to have rhythm issues whatever the rhythm issue is and then we add in another magnesium. So the combination of magnesiums. Know that I’ve had one patient who said, “Well the glycinate didn’t work but when I added in the taurate and lowered the glycinate.” You know so you really have to titrate based on if you’re taking it for palpitations for example, or AFib you want to titrate it based on your episodes. Is your heart calming down? That’s the point of the magnesium is there’s what’s called phase two of the action potential in the heart and the electrical system is part of your heartbeat, and magnesium and calcium have this exchange pump in the heart cell and that’s the theory behind why magnesium helps so much as a stabilizer of the electrical system. And the point you made about the GI distress, so we do have a fair number of patients that just can’t tolerate any form of magnesium orally.

                                So you have magnesium foil. You have bath flakes. There are other ways of taking magnesium that you can absorb some. [crosstalk 00:39:34]

Dr. Weitz:            And the glycinate has less effect on the bowel. But [crosstalk 00:39:39] taurine is another supplement just used [crosstalk 00:39:41] individually. Have you had experience with using that?

Dr. Desai:             Yeah I have one gentleman actually who, and of course I’m telling you stories about different people. We don’t have [crosstalk 00:39:50] these large randomized crowds, but I have this one gentleman who, he struggled with premature atrial beat. So these are benign things but it just debilitated him because if you’ve ever had one it feels like your hearts going through this rollercoaster. And so he tried initially the Natural Calm. That didn’t really work for him, he switched to the glcinate that didn’t really work for him. So then we had him on magnesium malate, and then we added a little bit of taurine in. And that, not the full dose of taurine that’s often recommended. And that really calmed him down so I do think that there’s a role certainly for taurine. My go to if someone’s having rhythm issues or heart issues is to say start with magnesium. Start with glycinate as you mentioned is well absorbed. If it doesn’t work maybe consider magnesium taurate or Natural Calm. And then if you continue to have issues that’s where you start to think about these other things.

                                And it’s also important to mention just for your listeners, there are a lot of drugs that deplete your body of magnesium and you have to be aware of that. Proton pump inhibitors for example that block acid secretion for ulcer disease notice deplete the body of magnesium. The diuretics [inaudible 00:40:59] deplete your body of magnesium and potassium so to your point Ben, those are people who probably need to have a super dose of magnesium because they’re losing so much of it. And the last point about magnesium I’ll make is intravenous magnesium has a powerful anti arrhythmic effect and what that means is we have people who have come into the hospital with AFib or with what’s called ventricular tachycardia dangerous heart rhythm and you just give the magnesium even with a normal level and it has this amazing immediate calming effect and I mentioned with the magnesium that the serum level is not very helpful. You can ask your doctor to order what’s called a RBC magnesium level within the blood [inaudible 00:41:36] and that tends to be a little bit more accurate.

Dr. Weitz:            Yeah we use that regularly. A few other supplements. Have you had any experience with coenzyme Q10 which is frequently recommended for heart health?

Dr. Desai:             Yeah I obviously recommend it to my patients generally for heart disease [crosstalk 00:41:55] treatment or prevention. [crosstalk 00:41:55]

Dr. Weitz:            By the way CoQ10 since we’re talking about nutrients that are often depleted, cholesterol lowering drugs like statins deplete [crosstalk 00:42:01] the body of CoQ10.

Dr. Desai:             Yeah it’s so interesting how we have people and so many treatments that fight each other. I mean it’s just they’re in the ring together and they’re fighting each other and it’s sort of like you’re not really sure what that outcome you’re having.

Dr. Weitz:            Oh yeah. We, statins increase your risk of diabetes and some of the most common diabetes drugs increase your risk of heart disease so.

Dr. Desai:             Right. Exactly. So I’ll be honest with you. I don’t really have a lot experience or knowledge of specifically Coenzyme Q10 and it’s impact on the heart’s electrical system or AFib. Have you come across anything in that regard? [crosstalk 00:42:34] With Coenzyme Q10 [inaudible 00:42:34]?

Dr. Weitz:            I’ve, yeah I’d seen some studies on it and CoQ10 seems to have a lot of benefits for congestive heart failure for a series of issues with the heart, so it’s probably one worth experimenting with and another one is hawthorn berry which is often [crosstalk 00:42:52] included in supplements for hypertension and heart health.

Dr. Desai:             Yeah my feeling on supplements is as you know there’s a lot of criticism from western medicine on these I think having functional medicine is such an amazing step forward. That you have physicians and practitioners from all different disciplines really focused on maintaining function not so much on giving a pill or doing a procedure. But I think that people just need to be careful that the supplement alone isn’t going to necessarily fix the problem. And you really, there is definitely a role and we do a lot of catheter ablation so I’m a very integrative electrophysiologist, but I’ll be honest catheter ablation if you look at all the different treatment options for AFib, I’m talking about people now who have the disease that is not being managed by just diet and lifestyle. It is a highly effective form of treatment and there’s a lot of misinformation including from healthcare providers about the efficacy of catheter ablation that nowadays with early AFib, the early onset of AFib peroxisomal we have some trust rates of almost 85 to 90% with a [crosstalk 00:44:03] risk of around 1%.

Dr. Weitz:            What do you hear healthcare providers saying that’s incorrect about ablation? What’s [crosstalk 00:44:12] the common misconceptions?

Dr. Desai:             It’s too risky and it doesn’t work. And then number two is it’s not going to work for you, patient, because your AFib is too far gone. And so, and then the third is well it doesn’t make sense to treat your AFib or try to get you into rhythm because you’re not having any symptoms. So those are the three. And this book that I wrote is not just for patients or family members. This book is for healthcare providers. Not just for education, but It’s hard to, nowadays in a 20 minute patient visit how are you going to talk about such a complex disease and we just have these kind of five page pamphlets that really don’t tell you much. So the idea is really to provide people with a little bit more detailed information. But catheter ablation for the listeners who haven’t heard the term, it’s simply a way of destroying abnormal tissue and preserving normal tissue. So destroying cells that aren’t supposed to be there. So if you think of the sources of AFib which are called the pulmonary veins as capsules of AFib sending out sparks, then we, well with kind of the fire analogy that we used.

                                We’re essentially creating some insulation around the fire. We’re creating insulation around a broken wire. Drug therapy, there’s a role for it, but anti arrhythmic drugs, which is what we use, they have such a high side effect in toxicity rate and at best the most effective one which is amiodarone has only about a 40 to 50% long term success rate. So again our first step always with heart disease or any kind of disease including AFib is diet and lifestyle. Lose weight. That can make a huge, I’ve had patients that have had ablations and they were overweight and then, and their AFib kept coming back. And then when they lost the weight, their AFib didn’t come back. And that’s something that shame on us as electrophysiologist in our field that we’re now learning you have to optimize those risk factors before and after any intervention to have the best outcome. And there is this mentality unfortunately in our society about sort of quick fix. Do an ablation, there’s a lot of sort of altered expectations. People come in and think that the ablation is going to reduce their risk of stroke or fix their AFib.

                                And it’s a big [inaudible 00:46:26] this is what you do. It’s a big picture functional medicine holistic standpoint. You’ve got to manage everything. Everything’s got to get in balance.

Dr. Weitz:            Yeah. I guess when I think about AFib the idea of doing a procedure that could potentially cure it instead of having to take some of these drugs for the rest of your life that have all these side effects. To me that sounds much more appealing. On the other hand, when I watched one of your videos describing how you do the ablation, boy it is a really complicated procedure that involves threading this little wire into the vein, going through one side of the heart into the other side of the heart and it makes me realize you really want an expert who’s going to do that because it is, at first watch you think oh well just go into this part of the heart and just burn this little thing and everything’s fine. It’s like I just fix this electrical socket and it’s a really complicated procedure.

Dr. Desai:             I’m so glad you mentioned that. That’s important feedback for me. Because actually that’s how, electrophysiologists consider AFib ablation to be one of the easiest procedures we do. Because the femoral vein is a vessel in your groin, we put an IV in there, we thread the catheter through the IV so there is no cutting, and there’s a, it’s a straight shot into the heart. That’s our mindset because we deal with it everyday right? But we don’t think about the other side of it, and I should really think about redoing that video because if that video sent a message to you that this is a really complicated procedure, it’s actually changed a lot over the decades and so it’s actually become quite a simple procedure. There’s, for example we use something called the cryoballoon.  It’s a balloon. We go to these four different structures in the heart. We freeze each for basically 210 seconds and we’re done. The actual ablationt takes only 20 minutes. A lot of it’s set up, a lot of it’s technology and things like that, so.

Dr. Weitz:            Okay.

Dr. Desai:             I’m glad you mentioned that because I have to really rethink what I’m putting out there now because it can look a lot more complicated that it is, you know?

Dr. Weitz:            Yeah. Yeah. You were talking about some and the risk is you go through one [crosstalk 00:48:37] side of the heart to the other and you know.

Dr. Desai:             And I’m not discounting that. I mean [crosstalk 00:48:43] to your point, you don’t just want to go to, you know whenever you’re having a procedure done or any treatment you want to go to someone who has high volume, done a lot with a low complication rate. And that’s the case with anything that you do on your body.

Dr. Weitz:            Absolutely. Absolutely. Including getting chiropractic adjustments or- [crosstalk 00:48:59]

Dr. Desai:             Including getting chiropractic adjustment absolutely. Yeah I mean for sure.

Dr. Weitz:            So what are some of the most common medications that are used?

Dr. Desai:             So oftentimes beta blockers include drugs such as metoprolol, atenolol, these are drugs to what we were talking about earlier about the fight or flight sympathetic nervous system. Those are drugs that block the effect of that on the electrical system of the heart so naturally they lower the heart rate, they lower the blood pressure. And so they can be effective if someone especially has a rapid heart rate. There’s a drug called propranolol which often has an anti anxiety effect as well which can be helpful for premature beats. But the problem is that those drugs aren’t easily titratable and so especially for young people often don’t like being on them because it really blunts your heart rate response to exercise, so people feel tremendous fatigue. It can exacerbate depression. It can exacerbate insomnia. For men it can exacerbate ED. So there’s definitely trade outs.

                                But what’s nice about beta blockers is they typically don’t harm you compared to other drugs that we use. Calcium channel blockers such as one called diltiazem and one called verapamil, these lower adrenaline in a different way and what’s nice about them compared to the beta blocker is not as much fatigue but they do, they can cause constipation and some ankle swelling. Those two classes of drugs have about a 40% efficacy rate for AFib long term. So not the highest. And then you have the next tier of drugs called anti arrhythmic drugs and there’s about five or six that we choose from. And these drugs, if you think about the heart’s electrical system as a bunch of doors opening and closing those are what we call ion channels and this is what these different electrolytes like we’re talking about, magnesium and sodium and potassium and calcium, these move in and out of the heart cells and the electrical system and it generates current. Just like you think of any electrical thing it generates a current. And so the drugs actually block these different doors, these doorways called ion channels and so as a result the drug can manipulate the current.

                                Well sometimes that works well in treating AFib and other issues, but sometimes it manipulates the current too well and it slows the heart rate down too much or it creates a dangerous rhythm called ventricular tachycardia and so the problem with drug development with AFib is that there’s been no improvement in decades. And one of the reasons why is that we still don’t have a good handle on the genetics, and we still don’t have a good handle on how do you create a drug that’s just specific for the top chambers of the heart, but do not affect the bottom chambers of the heart? Cancer for example, oncology, wonderful drugs now targeting the immune system. Same thing for many other conditions like rheumatoid arthritis, psoriasis. We don’t have that quite yet for the electrical system, so those are the two, and so the anti arrhythmic drugs would include drugs such as amiodarone, sotalol, propafenone, flecainide, multaq, tikoson, in case your listeners if they’ve ever heard of those drugs they have an efficacy of about 50% long term with very high side effect profile.

                                And again I, my job here is not to push ablation. Obviously I am biased. I do a lot of ablation. Of course I am biased and I believe in it, but I have been humbled in many cases where we ablate, AFib keeps coming back, and one day a spouse comes to the office and mentions the husband snores and we have this aha moment, “Oh I should’ve done a sleep study.” And then I do a sleep study and the AFib disappears and it’s that much of a connection between sleep apnea and AFib.

Dr. Weitz:            Yeah. There’s a huge connection between sleep apnea and a whole series of [crosstalk 00:52:34] chronic conditions and it’s definitely underdiagnosed and I think part of it just because people don’t want to be put on a CPAP machine and they don’t [crosstalk 00:52:44] want to get diagnosed.

Dr. Desai:             Yeah I’m glad you mentioned that. Not that I’m a sleep specialist, but what I, I refer a lot of patients for either home apnea link studies which is where you can screen it at home, or a sleep study and the top number one reason why people don’t show up to the appointment or don’t want to have it done is they don’t want to get a CPAP machine. And my experience has been in many cases it’s because they didn’t have the right mask, they didn’t have the right pressure setting, they didn’t have the right education. They were just given a machine, it was ordered, they dropped it off one day and they suffered with it and then there was no follow up. So I think it’s important for people to know and then there’s a lot of other treatments. There’s dental appliances as you know. There’s stimulators now. Medtronic makes one for example for treatment of sleep apnea for different, for like the tongue for example the glossopharyngeal nerve. So, but it important to treat. And the number one way to treat is to lose weight and [crosstalk 00:53:37] that’s such a big trigger.

Dr. Weitz:            Yeah there’s also a correlation between low vitamin D levels and sleep [crosstalk 00:53:43] apnea.

Dr. Desai:             Yeah. I didn’t know that actually is that true? I didn’t know [crosstalk 00:53:47] that.

Dr. Weitz:            Yeah there’s a few studies on it. I interviewed a dentist who was described how he saw a number of his patients turn around with getting the right amount of vitamin D.

Dr. Desai:             I’m going to have to keep that in mind because so many of our patients have sleep apnea. [crosstalk 00:54:02]

Dr. Weitz:            Now in his case he felt it was important to get the vitamin D to the optimal level not the [crosstalk 00:54:07] normal level. So not [crosstalk 00:54:10] just over 30 but say in that 50 to 70 range.

Dr. Desai:             Okay. All right.

Dr. Weitz:            Nanograms per milliliter.

Dr. Desai:             Okay.

Dr. Weitz:            And then I guess blood thinners are recommended sometimes too to prevent stroke which is one of the side effects.

Dr. Desai:             Yeah I think it’s important you touch on that. So stroke is the most catastrophic and so the mechanism of a stroke is a blood clot forms in the heart through a substance called thrombin and the anti platelet drug such as asprin for example don’t work that well on thrombin. They work well on clots that form in the coronary arteries or in the brain but in the heart with AFib the atrium doesn’t beat properly, you have this sort of lifeless bag of contractions so the blood clot can form stagnant blood. And so we traditionally have had blood thinners such as Coumadine or Warfarin which has a lot of challenges. Efficacious but a lot of challenges. And then there are a whole host of neuro drugs that aren’t so new anymore. Eliquis, Xarelto for example, Pradaxa. And It’s nice these drugs actually have been studied in very large trials now showing relatively low bleeding risks. We use, it’s all about the risk assessment. So you have the CHADSVASC acronym I mentioned earlier, you add up the points to determine who’s at high risk for stroke and AFib.

                                And then you have what’s called HASBLED, H-A-S-B-L-E-D, and that is another acronym and that actually tells us who’s at risk for bleeding on a blood thinner. And we can compare the two to then say, well this 80 year old person who has a high risk for stroke also has a high risk for falls because they fell three times in the last year. So that is someone we may refer for there’s a set of procedures called left atrial appendage occlusion procedures. A device called Watchman for example that you see a lot on commercials now. [crosstalk 00:55:58] [inaudible 00:55:58] scientific. But these are devices that help isolate the part of the heart that is the source to the clot from traveling elsewhere. So the Watchman is like a little basket that get implanted in the heart, and it’s typically done, I mean these are invasive procedures, but they’re not cutting open the chest, you’re doing it still through the femoral vein for example. So there’s definitely options for people, but one thing I would definitely say to people is if you can’t take a blood thinner because you’ve had a side effect or for whatever reason, get evaluated by a cardiologist or I think especially and electrophysiologist because you may be a candidate for one of these other procedures and you don’t want to have a stroke. [crosstalk 00:56:36]

Dr. Weitz:            Right.

Dr. Desai:             That’s the most catastrophic thing.

Dr. Weitz:            Yeah. One more question. This is just kind of a personal case from one of my patients. I have a longstanding patient and he kept getting AFib from, he felt like it was coming from drinking something cold. Does that make any [crosstalk 00:56:54] sense?

Dr. Desai:             Yeah it’s that vagus nerve again. [crosstalk 00:56:57] [inaudible 00:56:57]

Dr. Weitz:            Oh okay.

Dr. Desai:             [inaudible 00:56:58] nervous system. Yeah [inaudible 00:56:59] a triathlete. Every time he drank Gatorade at the end of the race he went into AFib. How much of a reward is that? You just finished a race and you go into AFib because of the Gatorade. So yeah you get esophagal stimulation. Really hot, really cold beverages can stimulate the vagus nerve. And then the esophagus is right next to the vagus nerve so there’s actually a direct sort of mechanical type stimulation. So yeah there is actually reason for that [crosstalk 00:57:24]

Dr. Weitz:            Well interesting you know we talk about the vagus nerve all the time when [crosstalk 00:57:27] we talk about gastrointestinal conditions so.

Dr. Desai:             Yeah. Yeah. I  kind of feel like the vagus nerve is getting a bad rap now. It really is important. It [crosstalk 00:57:35]

Dr. Weitz:            Well absolutely it’s a pathway for communication through the body [crosstalk 00:57:41] between the brain and the gut, and the gut and the brain, and the gut and the heart, and the heart and [crosstalk 00:57:45] the gut.

Dr. Desai:             And it’s so important. When we mentioned earlier, and maybe this is a good parting note is stress is pervasive and there are so many great ways for creating toolboxes to deal with stress. The classic stuff like exercise and being in nature and things like that. But mindfulness and breathing techniques and even simple things a few minutes a day, it activates that parasympathetic nervous system that helps to counterbalance that fight or flight response. We were built to run away from dinosaurs the problem with this is that we think that a conflict at work is a dinosaur. And sometimes it actually may be [crosstalk 00:58:18] a person may look like a dinosaur. But sometimes not and so but our brain, our limbic system and our fight or flight response and everything interprets the threats that way so its important for us to always be mindful of how we are interacting with people. We can just, that way we can kind of show up as the best version of ourselves and not be so reactive that we have choices on how to act.

Dr. Weitz:            Yeah. Big scary arm chair dinosaurs. Doc.

Dr. Desai:             Yeah. That was a great way of saying it without saying it. I love that. I love that.

Dr. Weitz:            What’s the best way for listeners and viewers to get ahold of you and contact you and?

Dr. Desai:             Yeah. Yeah. So the book is called Restart Your Heart: The Playbook for Thriving with AFib. It’s on anywhere books are sold including Amazon, Barnes & Noble. If you go to my website which is draseemdesai.com D-R-A-S-E-E-M-D-E-S-A-I .com I have a ton of information about the book and where to purchase, but also I have a blog, lots of complimentary advice there. We have a variety of different videos and things like that. And then I am very active on social media so especially on Instagram and Facebook we even have AFib groups and things like that, so it’s @draseemdesai. That goes for Twitter, LinkedIn, Facebook, Instagram, and then I have a YouTube channel as well @D-R-A-S-E-E-M-D-E-S-A-I and you can direct message me or reach out to me or follow me.

                                I definitely, I thrive on feedback. So that’s the only way that any of us, I mean your feedback about my video, I’m going to go look at that video now because your feedback about my video is important because I may be scaring a lot of other people and I need to change the way that video looks, so yeah. That’s important feedback.

Dr. Weitz:            Okay good, doc. I enjoyed the conversation and then when I put it up in about five, six weeks I’ll send you links and hopefully you can share it with your followers.

Dr. Desai:             Yeah I’d love to and love to give you a roo. Thanks to Dr. Weitz for this conversation today. I appreciate you having me.

Dr. Weitz:            Great. Thank you. Thank you.