Jeff Gerber transscript

Written by Christopher Kelly

Nov. 17, 2017


Christopher:    Hello and welcome to the Nourish, Balance, Thrive podcast. My name is Christopher Kelly. And today, I’m delighted to be joined my Dr. Jeffrey Gerber. Hi Jeff!

Jeff:    Hi Christopher! Thanks for having me.

Christopher:    It’s my pleasure. The people who don’t know Jeff, Jeff is a board-certified family physician and owner of South Suburban Family Medicine in Littleton Colorado where he’s known as Denver’s diet doctor. He’s been providing personized health care to the local community since 1993 and continues that tradition with an emphasis on longevity, wellness and prevention. Congratulations on that Jeff. You don’t see that very often in primary care doctors.

Jeff:    Oh, thanks Christopher. It’s so great to hear it coming from a British-speaking person. It sounds so much more official.

Christopher:    Well, I’m glad to be of service. I should make it clear to listeners that Jeff is not a lipidologist. He’s not a research scientist. He is a primary care doctor and he spends his time in the trenches, working with real people which I think is incredibly important and honorable work. And I wanted to keep the emphasis of this interview on that clinical care. How does that sound, Jeff?

Jeff:    Yeah so I have no formal training in Lipidology other than just being a primary care doctor but I hope people would appreciate that it’s coming up on almost 30 years in the trenches as you say. My experience is clinical and having done lots of home work and research on my own, trying to better understand what’s going on in terms of cardiovascular disease and overall health.

Christopher:    And the reason I think this is important is because you’re the guy that has to look that patient in the eye and explain to them why it’s still not working after they’ve been doing it perfectly for 6 weeks or even 6 years. Have you ever had that experience?

Jeff:    Yeah so it’s not always as simple as it sounds and we have all these mechanisms and we have different theories and we have a traditional approach, we have a modern approach, we have ancestral approach. And sometimes, it just doesn’t work the way it’s supposed to work as it’s written in the book. And so, we have to come up with practical, simple and real solutions for our patients.

Christopher:    And am I right in thinking that you’d be meeting a low-carbohydrate maybe even ketogenic diet for t-decades now?

Jeff:    Yes.

Christopher:    Could you just tell me about how you became interested in that diet and thought it was a good choice for yourself.

Jeff:    Yeah so, in medical school we were just taught the traditional approach and just to accept what was out there, the low-fat, low-calorie. And it never made a whole lot of sense to me but about 20 years ago, patients started to approach me with these non-standard diets that were lower in carbohydrates and higher in fat. And I would follow them although they were going to drop dead from heart disease. But low and behold, they lost weight and felt great, metabolic markers improve. And at this point, I started to do my own homework reading about metabolic disease, metabolic syndrome in particular. It really helped me to understand the root cause of many chronic diseases that we see today in modern society. And I’ve just been continuing to learn ever since.

Christopher:    Tell me about your experience interviewing and reading the work of Dr. Joseph Kraft. I was listening to a presentation by either this morning where he says that Joseph Kraft thought that those with cardiovascular disease, not identified with diabetes are simply undiagnosed. Can you tell me about that and your experience with Joseph Kraft?

Jeff:    Yeah so that quote comes out of his book, the Diabetes Epidemic in You. And Irene and I went to meet him and interview in 2015 at the tender age of 95. And he just passed away last year at 96 so he outlived the odds to be honest. A funny story, a couple of years prior, a patient had actually given me his book. And it’s a very small book and it’s an interesting read. It’s not an easy read.

    Dr. Kraft was a scientist. He wasn’t really a writer. But if you sift through the book, it really is revealing but I actually put the book aside. I didn’t realize I had it sitting on the shelf. And then I had learned about Dr. Kraft actually through Grant Scofield and Catherine Cross from Auckland, New Zealand. And Ivern and I decided that we had to go out and interview Dr. Kraft.

    You know, what he was saying in that quote is that metabolic disease and how he measured it was through the 5-hour insulin. I know that’s something that you’ve been quite interested in. It was his tool to measure metabolic health and he said that healthcare professionals weren’t properly screening and measuring for hyper insulin anemia and diabetes. And so, through his discovery as a pathologist, he had done hundreds of autopsies and he noted that there’s this connection between hyper insulin anemia and heart disease. He suspected that the majority of cardiac patients probably had some degree of metabolic diseases measure through the insulin assay.


Christopher:    Obviously, you have a great deal of clinical experience. So, would you then agree with the statement?

Jeff:    Absolutely. And in my clinical experience, I’ve actually been doing glucose-tolerance test for over 18 years. I’ve actually been doing testing insulins during most of that time period. It was only after I met Dr. Kraft that I started doing the post-prandial 2-hour insulin which is a short version of the 5-hour insulin assay. And if you’re a good clinician and you understand metabolic disease, you can in a sense triangulate looking at other metabolic markers and have a pretty good hunch whether a patient is going to have hyper insulin anemia and insulin or glucose defect without doing a glucose-tolerance test.

    So, that was really our operative and when we started doing the 2-hour insulin, it confirmed out hunches. It confirms the hunch basically. But to our surprise, we find people that come into the office. I can even give you an example right now Christopher, who you wouldn’t think they were necessarily having a metabolic issue. And then you check their 2-hour insulin and then to your surprise, the insulin’s through the roof.

Christopher:    Did he describe the 2-hour insulin test? Some of our listeners might not be familiar with it.

Jeff:    Yeah so, the 2-hour insulin assay is similar to our glucose challenge which is a standard protocol in doctors’ offices where generally, you give 75grams of glucose or dextrose when the patient comes in fasting. And then traditionally, well you’re fasting glucose before you administer the oral solution. And then, you would measure a 2-hour glucose. And if it’s in the shoot standard, if it’s less than 140, it’s normal and anything higher is of concern.

    And over the years, we’ve actually increased the sensitivity by including the 1-hour glucose measurement which hasn’t been standardized and we found a group from Italy, a great paper that suggested that you can measure that 2-hour glucose if it’s over 155, that’s abnormal. Although Catherine Crofts from Auckland is a little critical, she says that the sensitivity and the specificity of a 1-hour glucose isn’t that great. I would agree but we’ve been doing it that way as well as measuring a fasting insulin. And there’s some debate as to what a normal fasting insulin is and so we generally think of a normal fasting under 5. And then anything higher is perhaps suspicious.

    And then, you can measure the 2-hour insulin. Fortune for us, in terms of the mechanics of it, we have a lab downstairs where we can send a patient down during the 2-hour test to get the 2-hour insulin drawn. Unfortunately, it’s a test you need a lab because it uses radio and assay. So the day that they invent an at-home insulin test measurement, that would be wonderful.

    We do the glucose measurement here in the office. We send them down to the 2-hour insulin. And what Catherine Cross in her PhD thesis, she also had met with Dr. Kraft but most importantly, she got access to his entire database which started out on a floppy disk and it was Dos Excel. But what happened is she went to Dr. Kraft’s house to meet with him. She flew from New Zealand. And during their discussions, she said “Well, do you have the database”. And he says “Yeah, let me go in the closet and have a look” and he pulls out floppy disks.

    Well, Catherine though it would just be handwritten stuff. So, I think Catherine new what a floppy disk was but she didn’t know if there was any data that she could extract. So she took it to her IT people at Auckland and they said yeah, it’s DOS Excel and she extracted the entire database which was wonderful. So she analyzed it and she wanted to come up with a simple clinical method for somebody just like me. And so, granted the 5-hour insulin assay. Really think about it, you have to measure insulin and glucose at 30 minutes, 1 hour, 2 hours, 3 hours, 4 hours and 5 hours. So that’s a challenge.

Christopher:    The challenge is to find a lab that’s open for enough consecutive hours, right?

Jeff:    Yeah! And I know you’ve done tests at home.

Christopher:    And they also have limitations. Sometimes the bloodspot doesn’t work as well as you would hope.

Jeff:    It’s hard. And so, the practical test is what Catherine came up with and you just simply measure a 2-hour insulin. If it’s less than 30, it’s normal. And if it’s over 40, you have a problem. And that’s what we do and so again, it often even surprises me when you see these insulins sky high.


Christopher:    Let’s take a step back and let me ask you the question; what causes cardiovascular disease? Because up until this point, we’ve made it sound like it’s all about insulin and traditionally, we’ve all thought or being told that it was more about cholesterol. And obviously, you’re disagreeing with this by your clinical practice that you’ve just describe. Can you tell me about some of the things that you think cause cardiovascular disease?

Jeff:    Yeah so, that’s a tough question, Christopher.

Christopher:    It’s the toughest question!

Jeff:    Yeah. Why did you have to ask it?

Christopher:    I’m sorry.

Jeff:    If I had the answer to that question, I would be Nobel laureate candidate but we can try to break it down simply. And so, what kind of heart disease are we talking about? The big one is what we refer to as atherosclerosis and plaque. And we’ve been looking at this for over a century. And the pathologists have first observed these fatty streaks growing in the blood vessel wall that were filled with cholesterol.

    And look, now we know that it’s not the simple idea that the plaque is clogging the arteries. And we’re getting a narrowing in the stenosis. It’s more that 90% of these plaques actually rupture and it spews these inflammatory materials out and then it causes a clog. That’s the main pathogenesis of a heart attack or a stroke in that matter. And it’s more about looking at the burden of plaque. And we’re not really looking at stenosis per se but the great pathologists from the 19th century, we have Carl Von Rokitansky. He was actually a German pathologist and he had done thousands of autopsies over his career.

    And then, you might be more familiar with Rudolf Virchow and he was an Austrian pathologist. We refer to him as the father of pathology and I remember learning all about him in medical school. They concluded that atherosclerosis was actually a process of damage control. It was trying to repair damage. And I have to thank Malcolm Kendrick because you know, he’s a GP; a family doctor like myself from Scotland. He’s written a couple of books on cardiovascular disease and he’s now written literally 40 blog posts on the question you just asked.

Christopher:    Right! Right!

Jeff:    And he thinks he’s getting close. He’s probably going to write a book. He’s brilliant. I’ve gained a lot of information from him but what he points out is that Virchow and Rokitansky were actually arguing about what was anthogenesis and what plaque was. They both agreed it was inflammation and Rokitansky said that plaque was simply a blood clot in the blood vessel itself trying to heal. And Virchow was saying “How can we have a blood clot in the blood vessel itself?” And it’s just that the epithelia grows over the top of it.

    But they both agreed that it was this damage control and it was a response to something. But interesting, they didn’t answer the question “Where did the damage start?” All they were seeing was the effect that the plaque was the result of. Now, the thing is maybe the plaque isn’t simply damage control. Maybe it is part of the problem. But they were looking at things that the problem starts in the endothelia lining. But there’s other theories now where maybe it’s deeper inside its vascularization.

    But then, we move into the 20th century and then we have another pathologist, Russell Ross. I’ve been following his work and he passed away in the 1990’s. He really followed the pathologists from the 19th century and he did his research in Seattle at UDUB. And in the 70’s, he referred to this as a response to injury hypothesis, really along the lines to what that other great pathologists were saying.

    But he was looking at it at a molecular and cellular level. And he was trying to determine what the cause of the initial injury and the insult was. And he still struggled with that, Chris. I have to tell you. But he did further define the inflammatory response. You know, looking into the plaque itself. He saw foam cells, macrophages, inflammatory cytokines and it was totally an inflammatory disease.

    And it somewhat brings us today that we recognize this as an inflammatory disease but we don’t really know the causes. And the other frustrating thing as you said is that we’ve lost sight of this as being a response to injury; an inflammatory disease we’ve just focused on cholesterol and reducing saturated fat. And it hasn’t work and I remember this in medical school. I remember Virchow tried it, which was talking about thrombosis in the blood vessel and it seemed to not have much clinical practicality. At least it had very little to do with what causes heart disease.


    And that was frustrating to me until I started doing my homework. There’s a lot of reasons for what causes heart disease. We just don’t know how to put it all together. So, what’s causing this damage? Does it have to do with a deficiency of vitamins or minerals? And please interject Christopher, by the way, because this is not a complete list. Does it have something to do with an excess of a macronutrient? A micronutrient? Is it a toxin suck as smoking, pesticides and I apologize because I wrote some of these things down? Air pollution? BPA’s as hydrocarbons. Maybe it’s cosmic radiation, who knows? Infection with something that Russell Ross was very interested in. Was it a genetic defect? Well, maybe. How about more than that, maybe it was a genetic mismatch or what we call the ‘evolutionary medicine’ where our ancestral genes don’t get along with the modern day environment. And then of course, I always like to put it on the bottom of the list, cholesterol.

    Right, we have to think about that. But my focus is to really deemphasize cholesterol. It is a player but as you can see, there are so many more factors to it. And how do you prove it out of anything? So when you look at studies, there’s associations. And so, we’re still looking. Oh, another one is we have a deficiency of nitric-oxide. That’s one that Malcolm seems to really focus on. And Nitric-Oxide plays a role in the elasticity of the blood vessel wall and also in inflammatory process.

    So, what I’m supposed to do from the clinical perspective in the trenches is come up with solutions. And when we don’t have all the answers. So what am I to do?

Christopher:    Yeah. I totally appreciate your situation. And clearly, it’s complex and my guess is that there’s many moving parts that are all interacting with each other and that’s what makes the initial spark so difficult to understand. But tell me, how does insulin fit into all of this? Clearly, we are or at least you and there are others decided that insulin is a major player in the pathogenesis of this disease. Can you talk about how insulin fits in all this?

Jeff:    Yeah so, first of all, you could say it’s a causal or it’s just a measurement or another bio-marker. And I think there’s arguments on both sides. It’s really jury-driven in the 1980’s along with the work of Dr. Kraft. Together, they defined metabolic syndrome that we like to call the insulin resistance syndrome and I believe we finally believed to calling it that in our book that’s coming out next year. It really defined inflammatory disease relating back to hormonal dysfunction. And of course, metabolic syndrome, there’s this criteria just to mention, abdominal obesity, blood pressure, hyper insulin anemia, cholesterol ratios interestingly that had nothing to do with measuring LDL.

    And they both define this hormonal dysregulation that leads to atherosclerosis and many other chronic diseases that we see in modern society. Now, there are some studies that suggest that certainly, glucose is directly toxic to endothelia lining in the blood vessel wall. Also, some suggestions that insulin itself is directly toxic. But again, we don’t have all the pieces of it but we have the association to know that if you have the metabolic syndrome, then you’re at a significantly higher risk of developing cardiovascular disease. And when you start looking at the research comparing insulin to dead cholesterol, the patters that we see is that there is a greater association between measurements of metabolic health and insulin versus the measurement of cholesterol.

    And in fact, I have a study here that shows exactly that that had come out a couple of years ago. That the correlation between events in this particular paper. And it was a large population. About 135 thousand people. That lead author, Gloria Lena-Vega, she showed that it correlated much closer to your ratio of triglyceride to HDL which is really just a surrogate to insulin versus cholesterol or LDL cholesterol. And it didn’t matter whether your LDL was I think 142 or under 142. What was important is; what was the triglyceride to HDL ratio in these particular patient? So that’s an example and so, this is why my focus for 20 years has been metabolic health looking at insulin. And we still consider cholesterol and on top of that, some cardiovascular imaging.


Christopher:    Is the standard lipid panel completely useless now? Is LDL a useless bio-marker?

Jeff:    I wouldn’t say that. It’s interesting in the old Framingham, they even come out and say that LDL cholesterol is somewhat useless unless it’s over 300. It’s like a ridiculous number. What Framingham also said but got buried is that HLD seems to correlate highly with cardiovascular risks; so that higher your HDL, the lower your cardiovascular risk is.

    But the problem is the whole lipid hypothesis is industry-driven. And so, they didn’t have drugs to affect HDL. It was only LDL. So look, I think that cholesterol ratios are really important and we’ve done advanced and standard lipid testing. I think the standard lipid testing is really good because it tells us about metabolic health. We simply look at ratios and you can predict what the advanced-testing and what the particle size will be based on it.

    In 2017, I’m not ready to say that we should just eliminate LDL cholesterol. Again, I’m try to work in a healthcare system and kind of reached this gap between modern medicine and this approach to nutrition. So, I’m trying to find a happy medium. You know, I could potentially have issues if I were to tell my patients “Oh, just don’t worry about this number or that number”, don’t you think?

Christopher:    I mean, you could argue that maybe you shouldn’t do the test in the first place if it doesn’t mean anything.

Jeff:    In my presentation, I do suggest that. That some people say we shouldn’t even bother with it. And that’s the way it may go in a couple of years. Who knows?

Christopher:    And do you think the same is true of these newer, more advanced tests so the old particle count or LP little A, are you running any of those tests in your clinic?

Jeff:    Right. So, we’ve been doing that for a long time and I always joke that it’s like the movie ‘Matrix’ where the advanced lipid testing is like the upgrades. What do they call the robots where “The stupid guys were the best one?” They were rugged. And so, it’s like standard lipid testing. You get the same information. And so, I’ll do advanced lipid testing if a patient asked for it. The problem is it’s costly and a lot of times the insurance companies won’t pay for it.

Christopher:    Okay. What is the grand truth here? Okay, this is a leading question but I’m going to ask anyway. Can you talk about the coronary artery calcium score?

Jeff:    Yeah so, the coronary artery calcium score… the idea is that all the blood testing that we’ve been talking about here today is really just associational in terms of cardiovascular risk as I see it. If you were an engineer, and I’m friends with several, I probably should have been more myself, if there’s a problem with the pipes you would want to just have a look in and see what’s going on. And that’s the beauty of cardiovascular imaging.

    You know, I’m actually happy to say that in Denver, where I live, the primary care doctors and the family doctors and the interns have actually latched on to cardiovascular imaging. Although, they’re not necessarily looking in the right arteries, we do a lot of ultrasounds of the corroded arteries which isn’t a bad screening tool but they’re not doing it properly. They’re looking predominantly at the corroded intima. And the person that really invented that technology wanted to age blood vessels looking at the intima or the lining. The idea that the ticker the lining, the greater the cardiovascular age.

    And we’ve actually looked at the papers and that doesn’t really seem to correlate with risk it all. Meaning, we have patients that have really thick intima and they don’t have any problems and then we have patients that have thin intima and they do have cardiovascular problem so that doesn’t correlate but we use that as a rough surrogate, looking at the flat burden within the vessel itself as a surrogate to the calcium score.

Christopher:    Right. If the scanner’s the grand truth, do you have all of your patients to be scanned?

Jeff:    Over age 45, I definitely like to do it and in fact, the ones that have the high LDL cholesterol. So, we have these high cholesterol responders that come into the office and they’ve changed their diets and they’ve seen their LDL cholesterol go up or they’ve been on statins for years and they’re sick of taking them. So definitely, over age 45, we start doing scanning or younger if there’s greater concern.

    But the ultimate test as we see it is the heart calcium scan. That’s been around since the 1980’s and the technology, we take for granted all this technology, Christopher. This is an idea that you just take a picture of the heart with a cat scan and it’s a gated image as the heart is beating, you need some more advanced technology.

    So, you take a picture of the heart every time it’s resting in between beats. And they discovered that Cat scans pick up bone and calcium. And so, it could detect the calcium in the blood vessel wall, the small little coronary arteries. And the calcium actually is the disease, you’re actually seeing plaques so there’s different types of plaque but you can see the plaque in particular that has calcium in it and it’s done in slices then you add up the slices and you can determine the calcium score. And then they’ve done this test now on hundreds of thousands of people based on that, they’ve determined risk. And the risk again, is based on seeing the disease process itself. You can have a score from 0 to the thousands. And you can see your risk go up 40-fold. It really gives you a great idea as to somebody’s risk of having an event. And it doesn’t have hardly anything to do with LDL cholesterol at all.


Christopher:    Feel bad now because I’ve known about this test for a while and I still haven’t done one. Do you know if you need a doctor who is sympathetic to your request and is willing to order the scan in order to get one done?

Jeff:    It will be nice to have a doctor that was in support. Again, here in Denver, I’m happy to see more and more doctors are ordering the test. Now maybe, we’ve helped that. You can just order the test yourself. We can get the test for $99 right down the street. Again, insurance unfortunately tends not to pay for it so that’s why you don’t need a doctor’s order. It’s crazy. It just provides a lot of useful information.

Christopher:    And do you know round about how much it is?

Jeff:    Yeah, $99, $200. I mean, those are fair prices these days. You want to try to use a modern machine, original scanner was called an EBCT which actually is a gold standard. So up in Boulder, and you’ve been up to Boulder, Colorado yourself. Front Range preventive imaging. They use the old 64-slice EPCT. That was the original one.

    There’s a very simple machine that has less moving parts to it. So we sometimes send patients out there but we have some local machines here that work this well. And not only does it predict cardiovascular risk, and for instance, if you get a 0 score a paper last year, basically gives you a 15-year warranty that you won’t drop-dead from a heart even and that you don’t need to take medication. This is kind of a mainstream guideline. Also, having a 0 score is associated with reduced all score’s mortality so you can even make an argument that it’s better than getting an anagram in women.

Christopher:    It is the dose of ionizing radiation though? How often do you recommend that your patients get the scan done?

Jeff:    Yeah so, what are the drawbacks to the test? So it’s only a small dose of radiation. Maybe 1-2 millisieverts. And it’s really equivalent to a mammogram and women tend to get mammogram every year. And if you have a 0 score, you can get another calcium score in 5 years. You can get it every 2-3 years but some patients are really anxious when they come in if they have a high score. We have sent the patients the next year to get another test.

    And the other issue with the calcium score of course is soft plaques. It doesn’t see soft plaques. In fact, we have a great email thread where there’s a lot of health care professionals. We talk about this all the time. And I think one of the doctors said “Well, we do a different protocol. So we’re worried about missing soft plaque”. And the first thing I would say about it, if you look at the CAC data, Coronary Artery Calcium data. If you have a 0 score, you’re risk of having an event in 10 years is less than 2%. And that statement is regardless of having a soft plaque or not.

    Now, granted there are people in there that have soft plaque. So, the doctors showed us a particular patient so he’s protocol is he’s actually sending them for CT Angiograms before we send him for CAC. And so, he had a patient he showed us. “Here’s a patient that had CT Angiogram. Now mind you, a little more radiation and you have to do IV Contrast so it’s more invasive”. And the patient had a 50% soft legion in has 0 calcium score.

Christopher:    Right. So, this is presumably some soft plaque that doesn’t contain calcium therefore doesn’t show up on the Coronary Artery Calcium Scan?

Jeff:    Yeah, exactly. So, I would agree that that person is in increased risk. And that the calcium score, it’s missing that. But you have to understand, there’s really a small percentage of individual that’s missing that. I have a comment for a good engineering expression relating to calcium score that says. Don’t let perfect be the enemy of very good. And so, the calcium score is a very good test and you could definitely do the protocol where you send everybody for CTAs but how are you going to convince patients. Well, I have this great screening test that might cost a little more money, it uses a little more radiation and we have to inject the IV to you. To me, that’s not a really good argument. So until the time that we find a better cost-effective and non-evasive screening tool for cardiovascular disease specifically heart disease, I’m going to go with the calcium score.


Christopher:    Can you talk about some of your patients who had very low or 0 scores and what they’ve been doing to achieve their scores.

Jeff:    Right. Well some people are genetically really lucky. And you know, you take individuals who are aged 45, regardless of what they’ve been doing. And you do a calcium score, a third of them or more are going to have a 0 score. And so, those are the lucky ones but you want to address definitely, cardiovascular health in terms of these simple things.

    And so we talked about what causes heart disease. So, we’re trying to tell people to make a 20% change. A simple change that will give them a great positive response. And so, these are things such as eliminating processed food, eating whole foods. We think the sugar grain, the starch, the industrial vegetable oils, and the canola corn soy which are particularly pathogenic.

    Interestingly, these are the air quote, healthy oils that we’ve been told to eat for a half of century because it lowered the LDL cholesterol. It lowered the bad cholesterol. But now, if we go back to what Russell Ross said, we think that they’re driving inflammatory disease so we go back to eating natural fats. And just important to say that not everybody will benefit from a low-carb, high-fat diet or a ketogenic diet.

    So in our book, we actually point that out. There’s a couple of surprises that in terms of longevity, I think it’s important to perhaps keep the carb low but if the appetites control, you want to kind of ramp down the fat intake also, protein’s not a bad thing. So supplements, we tell patients the D3, the K2 supplement. There’s a new one. We like magnesium, we like vitamin C, we like artisans’ salts, the pink salts that have selenium and all that kinds of stuff. As far as we see metabolic disease and heart health, this is the lifestyle approach that we recommend to these patients. Of course, they’re ecstatic when they get 0 scores

Christopher:    Of course, as I head by one day. Do you see people who are eating a high carbohydrate diet but don’t have any type of cardiovascular disease because I think those people are out there. Maybe you don’t see them because you’re so well-known in the low-carb circles but do you see that?

Jeff:    Absolutely. In other words, the patients that walk in off the street and they have the 0 score. They’re maybe something genetic. I can’t recall that I had a patient that actually smoke, drank and they were sedentary and they ate sugar all day. I can’t recall that patient that had a 0 score. But that wouldn’t be a good advice for them. But you regardless, even if they have a 0 score, I would still tell them to clean up their diet.

Christopher:    Okay. Yeah, that makes absolute sense. So, talk about your approach to statins then if we already agree the cholesterol is just on the scene of the crime that perhaps is not causal and insulin is the main player and statins are drugs that lower cholesterol. Do you see any place for them in your practice?

Jeff:    Yes. In 2017, I do Christopher. And so, when it comes to primary prevention that means health patients that don’t have a history of cardiovascular events. We actually look at the statin data, the absolute risk reduction for non-fatal advances somewhere under 1% over 5 years. It’s actually really small and unfortunately, the industry inflates absolute risks calling out relative risks. And doctors don’t quite understand. They played into it over the years and that’s something that we’ve learned that when you start looking at absolute risks, the benefit seems to be quite small for primary prevention if you believe that data at all.

    The Jupiter trial is a great example in 2006 where they were trying to essentially tell doctors, healthcare professionals and people that for primary prevention, we should just put statins in the water to get LDL cholesterol lower and lower.

Christopher:    That’s truly terrifying.

Jeff:    It’s unbelievable and it’s an echo chamber today. When you look at the guidelines, 2013 guidelines in the US. If you look at the nice guidelines in the UK, it’s still the same. It’s all about the focus on bad cholesterol. I am flabbergasted in 2013, when you read through the guidelines, they don’t even talk about the metabolic syndrome. It’s absolutely crazy. So, that’s primary prevention but for secondary prevention and patients that have already been flagged as cardiac patients and there’s some controversies about that like patients who got stents who really didn’t need them and they’re flagged as cardiac patients.


    But there is some mortality data to show a small benefit with the use of statins although I still believe that you get 10 times the benefit with proper diet. And so, in a cardiac patient, it’s a hard argument for me to say “Well, we’re not going to give you statins”. And so, what I try to do is consider a lower dosage of statins as possible, in terms of what the mechanism. Well, it may be working on inflammatory pathways. I think that’s how the statins are working. And when we prescribe it, we’re not trying to lower cholesterol. We’re trying to address inflammation along with the diet.

    So, we work with the cardiologist if you have a high calcium score. Also, that might be… considering a patient is a cardiac patient. For instance, if they have a density score in the calcium over 400. Or if they’re in the 70 or 50% high off a risk. Although I think just having the calcium score might be an indication so I have that conversation with my patients. It’s really interesting that the latest, we’re now looking at calcium volume versus density and it gives us an indication of whether the plaque is salivated or stable. And this is an area that we’re still learning about.

    But overall, I want my patients to be well-informed and to have this conversation. We could decide together what to do.

Christopher:    We’ve seen a couple of papers recently that describes mechanisms by which statins maybe causing calcification and also diabetes. Have you seen those papers?

Jeff:    Yeah, well right. So the argument is that for the statin people, the statins actually raise the calcium score in a good way. And it might be true actually. So, what happens is that the statins might raise the calcium density while the volume stays the same or drops a little bit. And then when you start to look at these ratios, it might be that you’re seeing this consolidation and that’s something we’re looking at as well, regardless of taking a statin. Ivan and I interviewed Matthew Udaf earlier in this year because we’re at one of the conferences in San Diego and he’s one of the founding cardiologists in the technology. He refers to it as “Stable, Old Calcium”. So this is an area we’re looking at.

Christopher:    Talk about the book. ‘Eat Rich. Live long’. I know it’s not ready quite yet but can you talk about the premise of the book?

Jeff:    Yeah so, I think there’s a lot to the title. Eat Rich are perhaps some layer to it. But the idea that diets that are ancestral in nature that are nutrient-dense help us to improve health. And so it’s like Hippocrates told us to “let food by thy medicine and medicine by thy food”.    

    And so, the idea that these ancestral foods will really improve our health. And there’s 3 sections, 3 parts to the book and the first part goes into how we got where we are now and the problems were, what we didn’t understand about nutrition and what we understand now. And what’s funny is that the second part really goes into solutions. So we have the masterclass, we have a 10 step approach to better health, I can’t give it all the way. And then part 3 is for the more technical people that want to look into more details when you’re having problem.

    Very interesting, we talked about four body types. So we have insulin-resistant, the skinny fat ones, thin on the outside, fat on the inside. And then you know, typical type-2 diabetics that are metabolically unhealthy and they have a weight issue. And then we have the more difficult ones that are actually insulin sensitive. They’re healthy on the inside but they have weight-issues on the outside. And the fourth group is just the healthy people. These individuals that are metabolically healthy tend to be females, discriminatory unfortunately.

    We talked about what is the approach to those kinds of challenging patients. But ultimately, we think that the 10 steps apply to a lot of the individuals and then you have to tweak it based on these 4 body types. We’ve like to have some common grounds. It frustrates me Christopher that when we have diet experts out there, fighting with one another, it only serves to confuse people and hopefully, out book will help with that confusion.

Christopher:    So there are differing approaches then, depending on the body types or you’re just going to assess my body type until we do a low-carb diet anyway?

Jeff:    Right so again, low-carb, high-fat is not something that everybody needs to do. From my clinical perspective, when we talked about this in the book is that if I can control people’s appetite, there’s a fundamental approach that we’re going to be making progress. And so, there individuals that are metabolically healthy, it’s not so hard to control appetite. In other words, they get into ketosis so they don’t need as much fat intake. And ultimately, if we control people’s appetite, they’re going to eat less. And we think that that’s really good for the longevity factor. In fact, if we can control people’s appetite, they skip meals because they’re just naturally not hungry.


Christopher:    When will the book be available?

Jeff:    So, February. And this is hopefully right before our low-carb conference that’s coming up first weekend in March.

Christopher:    Ah. And I had such a good time last year in Colorado. I came out for the conference and I saw the talks and then I went off for skiing, snowboarding really, not skiing in Tilly Ride, Silverton and Ashburn, just had an amazing time. Talk about what’s on the agenda for the conferences this year.

Jeff:    Yeah, first of all, we’d love to have you again, Christopher. Come out and maybe give a talk in one of these years but this is going to be our 3rd year in the making. And Rod Teller who’s from Melbourne, Australia is our co-organizer. He’s a skier also but you don’t have to ski. I mean, it’s a great excuse to come see the beautiful Colorado Rocky Mountains in the winter.

Christopher:    Yeah. And if you have sleep apnea, you’re going to have a lot of fun.

Jeff:    Yeah, we do have to warn people. It is based off at 9000 feet. So you do have to prepare. Where we’re staying this year, they have a bar that has oxygen in it. Yeah, I remember you got hit with the altitude sickness.

Christopher:    It goes away after a week.

Jeff:    How about a day or two? Stop discouraging people. But you have to keep yourself hydrated. You have to watch alcohol intake in the first day or two. I mean, if you can get yourself into Denver and slowly acclimate it with help, we try to have a variety of speakers. So this year, some of the new faces; Andrew Mentee who just published the purest study who is really a 7-country killer. We have Erick Kassa and I’d have to check the details. Rod had found him. Rob Wolfe is coming. Yeah, we have Catherine Cross who again has all the Kraft data. We have an interesting endocrinologist- Jake Kushner who’s down at Baylor. He’s the chief of pediatric endocrinology and his putting all the kids on keto diets, they type 1 diabetics. Macon Ross who works with Jason Fung. David Diamond who loves to talk about the controversy with statins and how the pharmaceutical industry inflates.

Christopher:    There was an excellent interview on the stem-talk podcast that I should listen to. That was one of my favorite. So come to the show notes and look for the link for that one.

Jeff:    Yeah, that talk is unbelievable. We’re so happy that David is coming. Yeah, and the list just go on and on. So Steve Finny is coming, we don’t even have them listed yet. It’s going to be another grand one. We’d love to have everybody come. I know it’s time and money but there’s nothing like being at these conferences in person to just be around people that are passionate about all this stuff like you and myself.

Christopher:    Yeah, absolutely. That’s why I love the conferences so much. It’s not really about watching the talks. You can do that offline later. What it’s really about is shaking someone’s hand and making some friends.

Jeff:    Yeah, absolutely. We’re hooked.

Christopher:    Excellent. Well, I will of course link everything that you’ve talked about in the show notes for this episode. You can come to, scroll down to a show and then a particular episode. It might make a detailed time at each episode. And I also make a transcript. Jeff, where can people find you online?

Jeff:    They can look up Dr. Denver, Denver’s diet doctor. That’s the easiest way to find us.

Christopher:    Excellent. And is there anything else that you’d want people to know about?

Jeff:    I want them to teach their other healthcare professionals. I want them to talk to their doctors. And just in baby steps, help exert efforts and everybody’s contribution is important.

Christopher:    That’s an interesting one. I have to ask you a question about that. Have you had or heard about any patients having good luck with that type of activity. I could imagine a primary care doctor when they’ve already got 7 minutes to see a patient. They’re not going to be really wanting to read some review paper, the patient had just presented them.

Jeff:    It’s definitely a challenge. But you know, we’ve heard some nice stories about it. To what you’re saying, it’s frustrating to me when we try to invite local healthcare professionals to the conference up in Brackenridge but that doctors are too busy to learn about nutrition.


Christopher:    That’s very interesting. So, maybe this is a way for us to displace all the dogma, it’s by going to see a local primary care doctor. And then handing them some of the review papers that I will link in the show notes for this episode, how about that?

Jeff:    Yeah, that’s good. Well, we had some fun just last week. We did a rebuttal to a weight-loss surgeon that was not saying very good things about these types of diets. And so, we contacted them to do a rebuttal. Luckily, there are some of nutrition advocates on the news team at the local channel. And so, we got to do the rebuttal last week. And you know, get the message out.

Christopher:    I will of course link to that too. Well Jeff, it’s been fantastic. Thank you so much for your time. I’m very, very excited about the work that you’re doing. And we’re having a baby at the end of January so I’m not hundred percent on the conference. But I will do my very best to look forward to seeing you again in the future.

Jeff:    Good luck with the baby. Thanks Christopher.

Christopher:    Okay, thank you.



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