What if Heart Disease and Diabetes had the same cause? | Ivor Cummins

those would cardiovascular disease not diagnosed with diabetes are simply undiagnosed so essentially Kraft was saying from all those research that most heart disease is essentially insulin resistance syndrome we're here with Ivor Cummings and why don't you introduce yourself all right I'm Ivor Commons also known as the fat Emperor which is a long story and I've been researching metabolic disease and cardiovascular disease root causes for around six years now I get out there a lot to do public speaking conferences like this and many others and I've published a book with dr. Jeffrey Garber eat rich live long which was released in March in the US and Canada and yeah I now work on behalf of a charity to get awareness of the calcification scan of the heart the CAC score out to the wider world in the coming years so that everyone knows about this amazing technology how did you get into or what was the impetus for research in cardiovascular disease for you right well originally I got some blood tests that were way out of whack from the normal one of them was GGT a liver enzyme gamma butanol transferase one was serum ferritin the kind of iron loading in the blood my cholesterol high was also or was also high so I went to several doctors trying to query what are what is the meaning of these high values their way outside the norm and I didn't get any satisfactory answer on aid the causes for them or be the implications for morbidity or disease or death in the future I five kids so you know I was interested in this and I found I had to I'm a master technologist to my corporate role I lead teams and complex problem-solving activity in engineering so it occurred to me I can go to the databases ResearchGate PubMed I have access and I'll research these biomarkers and find out all about them and within a few weeks I understood everything that my doctors apparently did not but why don't we jump into insulin resistance real quick if you could quickly explain the concept right well I discovered pretty quickly I very quickly got onto researching insulin and metabolic syndrome so metabolic syndrome is more properly called insulin resistance syndrome or cardio metabolic syndrome many names but it essentially means that you are releasing too much insulin based on the food you eat and if you're advanced into it your fasting insulin will stay high even when you're not eating so essentially those two ways of viewing it one school of thought is that you become insulin resistant through negative factors in your lifestyle and then the insulin has to be increasingly released hyperinsulinemia to overcome the insulin resistance and that's where the insulin resistance is the cart or is the horse and it hyperinsulinemia is the cart but there's also views and there's merit in bold that eating foods that drive up insulin excessively chronically over time that the high insulin bursts drive the body to become insulin resistant so it's more the hyperinsulinemia that's the driving factor and there's a a kind of a responsive insulin resistance but the key thing people need to know is that when you have both insulin resistance and hyperinsulinemia together that's where you're in a pathological state so for example if you're on a very low carb diet you may have peripheral insulin resistance because your cells want to spare the glucose because you're eating very little glucose and your body wants to spare the glucose through the brain so it develops insulin resistance to hold glucose out of the cells to keep it in your bloodstream for the brain which is fine that's not pathological but a view of insulin resistance with concurrent hyperinsulinemia the metabolic syndrome that's the pathological state I think I've heard in several places people talking about how low carb or ketogenic diets actually increase your insulin resistance but that is not the full picture yeah it's not relevant to pathology or disease so it is this the body's response so if you go low-carb for a significant period you will develop this peripheral and muscular insulin resistance to keep the glucose paired makes absolute sense evolutionarily and that's fine if you certainly then eat a lot of glucose or carbohydrate and you're in that state your blood glucose will shoot or pretty high because you're in a low insulin State the enzymes to deal with fats have been created and maximized and your system is not really ready to suddenly take a bolus of carbohydrate so you hear about the pizza hangover we're a low carb person kind of has a big blowout has a pizza and they feel terrible and that's because their body gets a shock with a sudden influx of glucose the body is coiled like a spring to spare glucose now a massive bolus comes in and the blue glucose goes really high and you can feel pretty bad so if you're on a low-carb diet and you are stabilized and feeling good ideally you should keep cheats to a minimum certainly big cheats that big glucose spike is not going to be good for your physiology so we got on to the topic of insulin resistance but as you were saying your research has been into cardiovascular disease what is the connection between insulin resistance and cardiovascular disease right well there's a huge overlap in fact dr. Kraft who did 15,000 insulin assays on patients back in the 70s I interviewed him before he died at 95 and he essentially said those with care those would cardiovascular disease not diagnosed with diabetes are simply undiagnosed so his suggestion was that most heart disease was essentially diabetes diabetic dysfunction now type 2 diabetes is insulin resistance syndrome so essentially Kraft was saying from all those research that most heart disease is essentially insulin resistance syndrome and there are so many pathways by which if you are in the pathological state of hyper ins an insulin resistance yeah there are so many pathways detrimental to your vasculature it's not funny so your inflammatory markers will be raised your TNF alpha will be raised which attacks the endothelium your and fat cells will be swollen it's called hypertrophy and the insulin signaling in your fat cells with the larger cells will no longer work so well and that will lead to lower lowered adiponectin and increased leptin and it will lead to a whole range of hormones being out of balance which will also contribute to vascular distress then you have the high insulin it itself has been shown to incorporate lipids into the vascular wall into the endothelium the high glucose spikes that are part of living in that world will gleich hate and damage the components in your plasma and your lipoproteins your LDL particles and your blood cells so I mean I could go on but the state of high insulin and insulin resistance is also a high glucose state hyper Ansley Mia hyperglycemia these are some major driving forces towards a thorough squatting disease and they disturbed the whole milieu in the body so many other hormones are going to be rising and their function igf-1 is going to be rising insulin like growth factor and that has concerns for cancer and for heart disease so it's like this he set off this kind of storm in your body but one one interesting experiment by professor even who basically wrote the the story of insulin resistance as being one of the primary drivers of modern chronic disease he did a study in 2002 and they took several hundred middle-aged people randomly take him and he did a steady-state plasma glucose which is the ultimate insulin test so what they do is they infuse glucose to keep it operating 5.5 millimole and then they infuse insulin on the other side to keep it controlled at that level and with a steady insulin bolas they keep the glucose pushing in to maintain 5.5 in your body and if someone whole body is insulin resistant you won't get used much glucose but someone whose insulin sensitive they will be absorbing a lot of that glucose dynamically and you will get putting quite a lot of glucose to keep them up at five so it's a very exotic test with multiple drips to carry it but it gives you an extremely accurate all body insulin resistance value way better than just measuring insulin and he split them perfectly into the upper third of insulin resistance the lower or the middle third and the lowest third and there were an average age of 61 these are middle aged people are a little older but the interesting thing was because he got this amazing measure accurate measure of insulin resistance what he saw was that the most insulin sensitive lowest insulin resistant third of the people 70 they had no disease no death in the next seven years was very unusual for 61 year olds they were incredibly clean the middle group of insulin resistance had 12 instances of death and disease with two deaths and eight cardiovascular disease diabetes severe hypertension couple of cancers and the upper insulin resistance third had 28 disease and death incidents with four deaths cancers diabetes heart disease so he basically had demonstrated it was p zero zero zero zero one because this difference was dramatically statistically significant and he had shown that insulin resistance dominates the chronic disease world not just heart disease but general chronic disease this measure of insulin resistance is more powerful than anything else so the hazard ratio for being high in insulin resistance in that experiment right was 40 X steady-state plasma glucose was a 40 X multiplier of risk just based not experiment and interestingly LDL was measured and it was a one point zero zero one X it had no prediction of anything in the seven years which was a great control the LDL predicted nothing where the SS PG predicted for TX hazard ratio so I thought it was a beautiful little experiment there are countless more that pretty much say the same thing but that one was so dramatic and probably most people have never read it so they said controversial at all the idea that LDL doesn't actually denote anything but hyperinsulinemia is a far better predictor of chronic diseases and heart disease well LDL was easy to measure our way back insulin was extremely hard it's very hard you have to use an immunoassay so LDL and cholesterol was easy to measure and it got ahead and they saw correlations for heart disease and heart disease was a big deal and they said right we've got our boogeyman and it was kind of true LDL does partake in the a thorough scrubbing process but just not in the way they think so basically LDL got ahead and then drugs were found with that would lower the LDL and it became a massive business and now the whole world a doctor said hey we've got LDL bad cholesterol it's the cause we can treat it it was fantastic everyone was happy and then insulin began to come along get measured accurately and yet some paper showing wow this insulin is much more important but the world had moved on and to be honest no one really wanted to say hey we're kind of wrong and cholesterol and you know when cholesterol does predict it's partially because hyper insulin drives up the cholesterol so it's not even the cholesterol it's more the insulin that's extremely embarrassing and would totally upset so many enormous business models no one's gonna whenever part of it so professor even and Kraft were shouting into the void and no one really wanted to know that's the way it looks now earlier in your talk this morning you're talking about non-native LDL so what is the significance of non-native LD yeah so native LDL would mean a native undamaged particle with its full complement of proteins on the outer shell and no electrical negative charge and no decile ation which means it's on its way to becoming a little oxidized it's losing components so in age of LDL is a perfect lipoprotein ball full of cholesterol triglyceride and the current lipid theory is that these native non damaged LDLs are inherently toxic that they get in through your endothelium the single cell layer on the inside of your artery wall that they get into the wall of your artery get trapped there get oxidized become part of atherosclerosis that's the theory and if you have more LDL particles in your bloodstream you'll probably have more diffusion into the wall more will get caught and oxidized and set off inflammatory cascade and it's as simple as that the LDL is the bad boy AB just the LDL now another school of thought which is getting a lot more evidence for it is that the normal LDL native LDL does not really cause those problems it can go into the wall it can go into the endothelium but it does not really cause the vast majority of heart disease this idea is that the vast majority of heart seizes calls call cost by minimally modified LDL which is mildly oxidized and the papers I've been digging up recently the classic Orthodox people would say that's only minimally ox oxidized mildly and that's not a problem and they admit sure we see around 50 times more of that in people with heart disease than healthy people but that doesn't matter it's minimally and it doesn't cause a big problem it's just Eldee alcohols problem but those recent even studies were two of them one of them they took a healthy people and they took people who had issues patients who had bad cholesterol ratios and they took their blood and they'd fractionated it into l1 l2 l3 LDLs which are native and then elf or an l5 which are mildly oxidized minimally oxidized in the in the assay that checks for that in your plasma and they found that the healthy people had no l4 and l5 like a sediment ago and the unhealthy people had l4 and l5 s so they took the L 1 2 & 3 natural from both people and it did not cause any endothelial to stress the endothelial cells incubated with it they were fine no cell death but the l4 and l5 minimally modified mildly oxidized from the dye from the unhealthy guys that killed 40 percent of the endothelial cells in culture so they said wow this minimally modified LDL is a huge deal it's not like people have been saying oh it's only minimal it doesn't matter this is a huge disc could be the primary cause of atherosclerosis and so they then got LDL and oxidized with copper and massively oxidized it and they found out it only killed around 45% of the cells so they demonstrated that the minimally in your blood that was damaged in your plasma by hyperglycemia and by hyperinsulinemia and all the other causes that stuff is as bad as shockingly oxidized LDL in terms of damaging your internal lining of your arteries and when that is damaged you will get more LDL going in oxidized than otherwise so this is the cause of heart disease but the orthodoxy would say no no no no no no don't want to hear that it has to be that LDL is bad not that you make your LDL bad by all these bad things you do in the root causes the LDL hypothesis has to be LDL is bad . so we're gonna see this battle in the coming years because another study did a similar thing with the sally ated LDL which is the step just before it gets minimally oxidized and even that LDL was shown to dramatically cause LDL to quantity and the delial cells compared to all the normal aldea taken from the same people so we've got it from two sides now publish papers 2009 2016 2017 and these guys are demonstrating what I said to you the LDLs damaged in your plasma appear to be the primary driver of atherosclerosis so there's going to be a lot of arguments coming up so so the LDL that is minimally ox oxidized by glycation or hyperinsulinemia is almost as bad as the super oxidized LDL that you oxidize with copper exactly in that experiment looking at endothelial cell death that was precipitated by these particles I mean the bar for the non oxidized completely good native LDL of which the people most of the L they have is native the bar doesn't even rise for death on a naught to 50% death of endothelial and then the L 4 is very mildly and it jumps up to maybe 10% the L 5 is up to 45% I think and then the massively oxidized horrorshow LDLs went up to maybe 50 or 53 they were pretty much so they had a massive understanding there this minimally modified LDL that we get in the oxidized LDL assay which is available now it's not it's minimally oxidized in one way but in terms of the damage it can cause the endothelium it's not really minimal at all that's a chemical term minimally but it's as bad as the stuff that's totally oxidized because the receptors take it up and the cascade occurs so it's gonna be really big I think in the coming years this discussion that's really interesting I'm quite new to this researching the oxidized LDL relative to a lot of the other lipoprotein technology but I've been blown away by the first papers I've got the the other really interesting mechanism was the you were talking about the glycocalyx I don't hear that often mentioned too often can you tell us what that is yeah I'm new to the glycocalyx as well I got a tip off a few months ago by Malcolm Kendrick referred to it in his blog and I had heard of it before and was the way whereas the kind of the nonstick coating on the inside of your artery arterial wall Annie knew was probably important but I had no time to go digging but Malcolm referred to it and he had a nice paper and I said I'm gonna go after that so I got I had 50 60 70 papers around that in the following weeks and I printed them all out reviewed them analyzed them got cross references got two other papers and eventually I pulled it all together so the glycocalyx is its strands of proteoglycans they're kind of amino acid and glucose molecules and kind of hairlike strands they're only around maybe 200 nanometer height and the reason it was only discovered 30 years ago or not before was as soon as you take arteries out of living animals the glycocalyx disappears almost immediately so they're able to in vivo electron microscope see it now and it's a very exotic hairlike structure and they've worked out a lot about as would the hairs get the flow of the blood and they measure of thermal panel sensors and depending on the flow and the shear of the blood they'll trigger the endothelium to release nitric oxide and many other components so they're McConnell sensors they also filter a plat --let's and LDL particles and many other particles s OD superoxide dismutase which is a very important antioxidant well the glycocalyx holds these and manages them and allows them to interface with the endothelium or keeps them away so it's an extremely exotic layer a gossamer layer and it stops blood cells getting too close to rub off the endothelial surface amazing functions but long story short I've series of papers now what destroys the glycocalyx is sugar spikes in your blood hyperinsulinemia CRP you know C reactive protein the inflammasome on across this factor-alpha going up which again insulin resistance diabetes obesity is where you're going to get that and and when they do operations they've noticed that they get a rapid atherosclerosis in the new vessels they put in and they're beginning to realize now in new papers it's because after the ischemia and the reperfusion in the operation the glycocalyx is basically eradicated for a period and they're tying that to the rapid a thorough scroll since after operations the glycocalyx has gone and morphology a thorough Scrolls has happens at the branch points an artery is very specific places and they've now done the work pathologists and they see that the glycocalyx is much thinner and compromised in those zones so it was all a test out and they've stripped the glycocalyx with chemicals and shown that 10 to 20 times more LDL gets into the endothelial cells if you increase in the strip away the structure so I think the realization is the glycocalyx is enormous ly important in LDL saving and in management of inflammatory responses and a lot of modern diets effect on atherosclerosis and problem LDL it probably goes down to the damage of the glycocalyx a lot of and yeah this is an almost like a you know the door into the individual that needs to be protected it is literally yes it's it's a moat or a series of gates yeah protecting the endothelium and I think when you do have genuine damaging problems the glycocalyx does dissipate and maybe in a beneficial way allows monocytes and immune components to get access so it could be very good eeveelution Airy that when you've got a problem going on the glycocalyx gets compromised and allows in LDL four components that the endothelial cells may need allows in inflammatory agents which are needed to to mop up problems or repair or clotting factors so it may have a function where it appropriately gets kind of taken away to allow action to go on but then of course in our modern food supply evolution never allowed for modern foods that would have our our body full of excess of fats and sugars nearly all the time so I think we've got chronic damage to the glycocalyx which means we got chronic disease like atherosclerosis yeah you had you had a really interesting slide showing the effect I think it was six just six hours after a glucose heavy meal or yeah I got that off a company you've been working for 20 years for searching and they got some of the first electron microscope views of glycocalyx and they've also got a and in the mouth probe that can actually see through the tin vessels and assess glycocalyx quality and consistency non-invasively and they were the ones who've been doing a lot of papers and research and that was their image they gave volunteers a high-carb I think high sugar I don't have all details there but a high carb high sugar meal and they watched a jet two hours later the glycocalyx has come down around half four to six hours later to come down to almost nothing so they have demonstrated this that's the effect excessive glucose in the bloodstream is appears to be very damaging to the glycocalyx the problem they highlighted is they saw that it took 8 to 12 hours for the glycocalyx to fully regenerate but the problem is most modern humans on a standard American diet they're gonna dump within 3 or 4 hours another pile of crackers and pizzas and carob and sugar on top of it before it even recovers so I guess yet are gonna have chronically depleted glycocalyx which again is gonna be chronically exposed to to disease and there was one other thing you were talking about how some inflammatory markers would damage the glycocalyx and you're also talking about how pretty much anytime you eat almost as a text of having the process of food your inflammation goes up yeah I've heard it says you know food and digestion is inherently an inflammatory process because the electron transport chain and all all the systems used to render food and into the huge amounts of energy per gram that we take from us involves the creation of free radicals and side products in a healthy body with very healthy food is really manageable so the super oxides and other things that are created by the processing making the energy like a power plant if you have excellent systems working well you will detoxify all the dolls convert them and recycle them and to be very little damage to the to the physiology I think though when you're eating very bad food and too often that process becomes chronically damaging over time you are not dealing with the inflammatory effects well you're eating foods which create excessive inflammatory effects and free radicals and as your health declines your body and you get older becomes less and less able to try and manage that bad food so inflammatory markers rides rise and then kind of all parents of the Machine begin to suffer and then they contribute their own you know acceleration by by by becoming less functional in their own right and I think this is aging and and and chronic disease it's a deterioration of the body because of all of the processes it has to rome to stay alive but if you eat impeccably well on a really good nutrient-dense low carb high healthy fats diet with a range of nutrients like magnesium k2 C again and potassium and you get all the good nutrients to make the machine work well and you eat the right kind of food and it's very varied a nutrient dense and you're not chugging loads of oils that give you nothing and if you do all that and some exercise now you're synergistically putting together things which will make the human machine really home and there you'll get a long-lived excellent stage of repair machine and I think I used the analogy once you see people who have these old cars and they were never restored they were just kept beautifully with many oil changes and waxing to stop roast and they're credible when you see them 60 years old and they're just perfect a human can be somewhat like that or you can treat your car your automobile you can't row in Coke and pizzas not to any exercise put on a big goat and get insulin-resistant and your car is just a piece of crap you know in fact it's a piece of crap long before it should even be one you know that's that's kind of the way it is one last hypothetical question let's let's say someone did have a really high calcium score which as you said earlier is very indicative of heart disease what what should they do about that right so a really high calcium scores is kind of like your a secondary prevention patient because it's almost a heart attack equivalent if you have a really high score so if you huge amount of disease that disease you have was built up over the previous years so for instance you have an irony that you could go low-carb and get suddenly fit and healthy after a bad life a year ago and now get a calcium score today and it's 800 it could have been 820 a year ago or could have been 780 we don't know so all I can tell you is right now you have a lot of disease evidence in your body what do you do a low-carb for anyone who's got heart disease overwhelmingly they will have had some level of diabetic dysfunction so a low-carb high healthy fat diet with fasting is a no-brainer really that's a given and ideally which fasting because you view big disease you want to bring in heavy guns and just eating healthy food now is a great intervention but you've got big disease you want to do big interventions so a lot of fasting will always give you more results so so do that but you need to get fat adapted first get used to your diet then start fasting you want to get magnesium potassium and k2 and all of the critical elements and minerals that being low in them increases your risk of having this disease you've already got it now so you need to assume I don't know exactly what I did wrong but I want to do everything right now to reverse it and exercise and stress training is important to build insulin sensitivity muscular as so you should add in exercise as well because you've got big disease you want to do a lot of things medications I'd have to say my co-author dr. Gerber and people who have a high score or a prior heart attack he does give a low-dose lipid-lowering for the anti-inflammatory effects because he can't take a risk with someone who has big disease they give some benefits they also may have downsides he monitors them carefully and he keeps doses low but he believes that the safe thing is to take a certain amount until you're more sure the person's risk in the longer term maybe they might go off them later if their calcium score was 800 and they'd go back 2 years later to check have I stabilized at an 800 in which case my risk has plummeted you don't need to lower it but let's say to go back and it goes to 720 two years later and they go wow I'm doing really well maybe they could reconsider the medication so so there are personal and doctor-patient decisions there but I think nutrition and certain types of exercise and sleep getting sun access for nitric oxide released in the skin ideally healthy sun exposure and and stressed avoiding excessive chronic stress all of those 3 s's we call them contribute to her morn home ona imbalances which can contribute to the whole heart disease milieu so if you've got a big score you're kind of want to attack every angle whereas someone who has a zero score like me I can kind of just broadly make sure my diet stays nutrient-dense do some fasting do a bit of exercise someone a high score has to take serious action so you kind of do everything or our book each rich live long I'm not selling in here but it lays out all of the science and all of the plays and it's a long story if you have a big score great it's great okay and real quick so how long is a reasonable time to you know you make all these interventions and then you want to check again how much time should you if you have a very high score two years later is fair enough and maybe 18 months with a very high score but you really need to leave time for the interventions to act so a year and a half to two years and you want to see it just stabilizing staying similar level or maybe going up five percent normal people who don't intervene who have high scores it's usually going up 20 to 40% a year until they have their heart attack that's the natural law you can break the natural law stop the disease progressing with the measures that we mentioned and then would you hope to see as the calcification slows down and stops calcifying because the disease is gone there's no need for the calcium to try and repair it that's a safe nearly as having a low score in the first place if you maintain stable over years so let's say two years if you have a very low score it's not a guarantee but you're looking really good compared to most people maybe six seven years later for a middle aged person if they got a zero because you're very unlikely if you've got a zero at middle-age to get a really big surprise score a year or two later I mean when you know you're doing all the right things so six seven years later good to check in case you missed something and in case you have a surprisingly high score or seven years later and what you were doing you're just missing something somewhere and you know what can drive calcification our kidney issues inflammatory diseases like lupus there's a whole raiment amination there's a whole range of inflammatory issues in the body that can drive vascular distress and disease and calcification that are not diet and are not necessarily a mineral insufficiency so you can never say never it's worth checking in six or seven years later even with a zero because something could have happened in the interim and your blood test might not show up at the calcium multiply yeah it could acid reflux be one of those other factors acid reflux and GERD that is it only came up the other day that is being linked to course to a SIF suffered Jia esophageal cancer shortcut and it's been generally linked I believe to higher rates of heart disease and other chronic diseases too but not very strongly but the fix for GERD or esophageal reflux is a low carb diet I mean it almost never fails a low carb well-formulated diet from someone who's eating a lot of high carb and vegetable foods it should resolve GERD really fast within weeks and as a very good book by norm Robillard I think it's an ORM oral-b a I ll Aird made a French named norm Robillard and that is basically the guard handbook but his main intervention is low-carbon he's loads of patients who have transformed their lives and so norm norm was the guy for GERD I met him five years ago and I always remember his name yeah well thanks so much I know we went over a little bit um where can I get everyone to access your stuff oh I'd say if you google Ivar Commons my name I mean you got a bunch of hits my youtube channel Twitter and Facebook and I think a good place to start is if you google Widowmaker CAC those two words Widowmaker CAC you'll get a free viewing of the Widowmaker and learn all about this incredible scan and then my lectures on YouTube we'll talk a little bit about the scan but a lot about what we've been talking about today you know all the fixes for this metabolic disease epidemic we have in the world today and how to fix it

Channel: What I've Learned

Views: 391,293

Rating: 4.8978009 out of 5

Keywords: ivor cummins, what I've learned, keto, heart disease, insulin, ketogenic, health, jason fung, brain, blood sugar, heart, low carb, diabetes, insulin resistance, lchf, glucose, ldl, cholesterol, heart attack, CAC, medicine, cardiovascular disease, diabetes mellitus, type 2 diabetes, interview, keto diet, carnivore diet, science, biology, blood pressure, insulin sensitivity, hdl, atherosclerosis, ketogenic diet, nutrition, fasting, doctor, statin, intermittent fasting, fasting healthy, medical, statins

Id: ofq-8ToY2fc

Length: 36min 51sec (2211 seconds)

Published: Mon Dec 17 2018

Reddit Comments

[u/Zycro]

This is the best health channel on YouTube

[u/vincentninja68]

I dont know shit about the Glycocalax, legitmately new concept for me