Dr. Laureen Lawlor-Smith - ‘Therapeutic Carbohydrate Restriction Working with Cholesterol’

[Music] thank you very much and good morning I'd like to start off by saying that um I'm neither a lipidologist nor am I a cardiologist and therefore this is not my primary area of expertise but as someone who works full-time seeing people who want to undertake either a low carbohydrate diet or a ketogenic diet to achieve their Healthcare goals the issue of elevated LDL is one that I deal with multiple times a day and I've therefore put together some information and some tools that I find very useful and I'm hoping that you might as well so we know that people who undertake therapeutic carbohydrate reduction either in the form of a low carbohydrate diet or a ketogenic diet EXP experience improvements in most of the parameters of cardiovascular disease including uh Improvement in type 2 diabetes if not remission of type 2 diabetes Improvement in metabolic syndrome a reduction in weight and blood pressure reduction in triglycerides small dense LDL LP little a and inflammation and they also usually experience an increase in HDL the only outlier is LDL and when undertaking a low carbohydrate diet LDL L might decrease or it might stay the same or it might increase and in fact there are a group of patients who tend to be leaner fitter more metabolically healthy who experience extreme increases in their LDL cholesterol above five and there is a term been coined by Dave Filman and Nick norwitz which is lean mass hyperresponders to describe this group of people as well as an elevated LDL they also have high HDL and low triglycerides so I just want to do a little bit of a review of cholesterol and its metabolism so as you know cholesterol is an essential element without without which we wouldn't exist and it has a number of functions so it's vital for cell membrane structure and function uh brain structure and function it's involved in the manufacturer of vitamin D and a range of hormones um and it also is important for bile acid synthesis and we require bile acids for absorption of fats and fat soluble vitamins the other fat I'm going to talk about is triglycerides so triglycerides are the way we store and transport fats around in our body and a triglyceride consists of a a glycerol backbone with three fats or three fatty acids attached so neither triglyceride nor cholesterol dissolves readily in water or dissolves in blood and therefore to transport these around in our body we require things called lipoproteins so the lipoproteins have an Outer Perimeter which is consists of phospholipids and the phospholipids allow the lipoprotein to dissolve will be suspended in blood the Outer Perimeter also contains a particular protein and that protein is specific to the type of lipoprotein and helps the body determine what's to be done with this particular lipoprotein and the inner core contains both cholesterol and triglycerides so lipoproteins also have a number of vital functions so they're involved with the transport of all the fat soluble vitamins including ad and K they're really important for our immune system both in preventing infection and treating infection they're involved with the transport of antioxidants such as Vitamin E and co-enzyme Q10 and they're also essential for cell repair so there are three large groups of lipoproteins and I'm going to limit myself to talk about two and these are the two that are largely manufactured in the liver so if we focus on lipoproteins as a way of transporting things around in the body we have low density lipoprotein or LDL and LDL is involved in delivery of cargo to the body including cholesterol and triglycerides so LDL is formed in the liver as a quite a large particle which is called a very low density lipopro prot it's pushed out into the blood and as vldl offloads its cargo it becomes smaller so it becomes intermediate density lipoprotein and this continues to offload its cargo becoming LDL and as time goes on it becomes smaller and smaller and ultimately it's recognized by the liver and is taken up in the liver to be filled up again and recycled the other lipoprotein I'm going to talk about is high density lipoprotein or HDL and HDL is more involved with recycling lipids triglycerides cholesterol and other particles to the liver so it comes out of the liver as quite a small particle empty particle and as it goes along it collects cholesterol triglycerides some proteins and gets bigger and bigger and ultimately it's recognized by a receptor on the liver and it gets taken back up in the liver and it um offloads its cargo and it heads out again so one of the things that um HDL does is allows for recycling of some of the parts of vldl IDL and LDL so as the vldl particle becomes ideal and then LDL and LDL gets smaller and smaller the outer rim of the particle gets smaller and smaller so it needs to offload some things like phospholipids and protein and cholesterol so hdel is involved in picking these up and again recycling them through the liver so low density lipoprotein is just not one particle it's a large number of particles and I just want to talk about three separate parts of LDL so large buoyant LDL is the healthy LDL which is just doing its job it's just delivering its cargo and going back to the liver there is no association between large buoyant LDL and risk of cardiovascular disease the other two are small dense LDL and lipoprotein little a so small dense LDL occurs when the LDL particle is damaged and when it's damaged the receptor on the liver doesn't recognize it and it doesn't get taken back up back up into the liver and recycled so the things that can cause small dense elal are things like glycation from a high blood sugar or oxidation from seed oils or cigarette smoke or air pollution and it's this small dense LDL which is associated with cardiovascular disease and there's a clear relationship lipoprotein a is another subset of LDL and as well as having the Appo lipoprotein B 100 which is characteristic of LOL it also has an Appo lipoprotein little a attached to it so lipoprotein little a is associated with increased risk of cardiovascular disease and it's thought that one of the mechanisms is that lipoprotein little a prevents the breakdown of cloths lipoprotein little a is largely genetically determined but there is an association with diet in that we know low carbohydrate diets reduce lipoprotein little a so why is it that when we decrease our carbohydrates and usually increase our fats that we see an increase in LDL so this is the lipid energy model which has been proposed by Dave Feldman and Nick norwitz and essentially what it says is we are switching from being a carbohydrate burner to being a fat burner and that fat needs to be transported around in our body so vdl particles are manufactured in larger quantities because we have to deliver fat and as that vldl offloads its fat cargo it becomes LDL so essentially LDL is increasing because of the increase process of pushing triglycerides out and using them we also know as I've spoken of before that as the vldl becomes ideal and LDL it needs to offload some of its cargo including things like phospholipids and cholesterol and proteins and these are taken up by HDL so as well as LDL going up HDL goes up as well this is an incredibly efficient system whereby triglycerides are just um delivered through the body and so therefore we get a low triglyceride as well so this system relies upon having both low leptin and low insulin because both of these substances inhibit lipoprotein lipase activity which is what is pulling the drug glyceride out of the lipoproteins so for someone who's lean and fit and metabolically healthy this works well however someone who is overweight or metabolically unhealthy they may have a high leptin or a high insulin and then this tends to switch this process off hence the reason why people who are overweight and metabolically healthy are much less likely metabolically unhealthy are much less likely to see an increase in LDL on a low carbohydrate diet so this whole discussion is based around the diet heart hypothesis and the lipid hypothesis and this has been around for about 50 years and um I think Paul discussed some of this yesterday so first of all we have the diet heart hypothesis which postulates that dietary saturated fat increases the risk of cardiovascular disease or in fact that it causes cardiovascular disease there have been multiple reviews and metaanalysis um of this this is a concept cept and it's essentially being disproven and I quote from the American College of Cardiology own journal says recent recent metanalyses of randomized Trials and observational Studies have found no beneficial effects of reducing saturated fat intake on cardiovascular disease and total mortality and instead found protective effects against stroke so in spite of this it is still considered as gospel in most of the medical and dietetics community that saturated fat causes cardiovascular disease but this has been disproven moving along it is believed that dietary saturated fat increases ldal cholesterol and we've just seen from what I've said to you is that this this it depends so younger fitter healthier people are much more likely to see an increase in LDL cholesterol when they increase dietary saturated fat it's much less likely to occur in people who are metabolically unwell so I want to focus the rest of my conversation on the lipid hypothesis and the lipid hypothesis is that LDL cholesterol causes cardiovascular disease um and we know from large studies that there is an association between heart disease and LDL cholesterol so this is uh a study on lipoproteins and mardal infarctions it's quite a large study of 384,000 residents of the UK um followed up for a number of years almost 12 years and you can see that on the horizontal axis we have ldal cholesterol in Mill moles per liter and on the upright axis we have Hazard ratio for micard infarction or heart attack and you can see up to an LDL of about four there's no association between uh LDL and heart attack but as soon as you exceed four there's an increasing association between LDL and heart attack um and this has led to the conclusion in the medical community that LDL causes cart disease and I quote from the European atherosclerosis Society consensus statement consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally established as that LDL causes atherosclerotic cardiovascular disease but is that true firstly we know that more than 50% of people who prevent present with a heart attack have a normal LDL we know that indigenous Australians have lower ldls and lower total cholesterols than the rest of the population the non-indigenous population and yet indigenous Australians have twice the risk of cardiovascular disease we also know that LDL alone is not associated with cardiovascular disease if HDL is high and triglides are low there is a no association between between LDL and heart disease looking at data from Cory calcium scoring so coron calcium scoring is the best way to predict future cardiovascular disease and mortality if we look at the data from coronary calcium scoring we know that there is absolutely no association between LDL cholesterol and degree of atherosclerosis as evidenced by coronary calcium there's no relationship at all and if we look at groups who are supposed to be at high risk of cardiovascular disease for example if we look at people with a ldo cholesterol exceeding 4.9 almost 50% of people have got no coron and calcium and similar if we look at people with familial hyp cholesterolemia who we expect to have a high risk of cardiovascular disease 49% of them have no coron calcium so are we confusing the arsonist with the fireman so um over the last few weeks I've I've done a lot of research and I've looked at review articles and metas analyses about fires and I've discovered that fires are associated with firemen if you go to a fire there are often firemen there and not only that there's a time and dose relationship in that the longer the firemen are there and the more firemen that are there it is more likely that it's going to be a larg fire so I've made a decision that what I'm going to do is I'm going to arrest all the firemen and put them in jail because I think that that will make a big difference to the incident of fires now as ridiculous as this sounds this is what we've done with LDL cholesterol we have jumped to the conclusion that LDL is the arsonist where it is equally possible that LDL is the fan so what we know about LDL is that it has all sorts of impact on repairing damaged tissues so if you have a coronary artery which is damaged by a mechanical means such as high blood pressure or possibly via oxidation um or infection LDL comes along and it's involved in cell repair it's involved with treating the infection and it's involved in decreasing the oxidative stress on the artery so is it possible that Lal cholesterol is in fact the fan and it's not the arsonist so this is my opinion which is not shared by 99.9% of the rest of medical community but I think we have failed to prove that ldal cholesterol increases the risk of cardiovascular disease and the other problem with driving LDL cholesterol through the FL floor is that low LDL is associated with increased mortality now this is uh quite a a huge study it's almost 15 million Koreans uh followed for a mean of 8.8 years um and looking at the risk of uh mortality associated with levels of ldo cholesterol and so on the upright axis we have the hazard ratio for mortality and on the horizontal axis we have ldo cholesterol in Black we've got milligrams per deciliter and I've just put a couple of figures in milles per liter and you can see that a cholesterol LL cholesterol level of less than 2.6 is associated with increased mortality and the lower the LDL cholesterol the higher the mortality and it's not until we reach an Lal cholesterol of 3.6 that there's Associated increased mortality we also know that low LDL cholesterol is an independent risk factor for poorer outcomes in people who present with a heart attack both for a future heart attack and also for mortality we know that low LDL cholesterol is an independent predictor of mortality in people with heart failure so maybe driving LDL cholesterol through the floor is not such a good thing so next is where does LDL cholesterol rate in terms of its association with cardiovascular disease and this is a great study which was actually only released last week in the New England Journal of Medicine and it's 1 and a half million people followed for 7.3 years for cardiovascular disease and 8.7 years for death and it's a bit of a complicated slide so let me take you through it so the top line is the association between these risk factors and cardiovascular disease the bottom line is association between risk factors and mortality and the columns from left to right uh body mass index blood pressure non HDL cholesterol which comprises LDL cholesterol as well as some other things then we've got current smoking and diabetes and again across the bottom access you've got the age um ranging from 40 to 80 so men are represented as blue and women are represented represented as red and you can see in descending order of importance for cardiovascular disease the most important risk factor for cardiovascular disease is in fact type 2 diabetes rating second is smoking rating third is blood pressure and down at Fourth we have non-hdl cholesterol and if you look at the lower line which relates to mortality the number one risk factor for mortality is diabetes the second risk is smoking the third risk is blood pressure and you can see that neither non-hdl cholesterol nor BMI rates at all so why is it that we are so focused on LDL C rol well when you've got a hammer all you can see is nails so prior to the early 1990s in general practice um the early 1990s saw the introduction of statins into Australia I think Sy Sy Statin was the first Statin in the 1980s we didn't test for cholesterol we didn't talk about cholesterol we didn't try and decrease cholesterol but the data around the association between elal and cholesterol was was there so what happened is in the early 1990s that drugs were reduced introduced on the market and all of a sudden all we could see is LDL cholesterol and why was that and that was because the pharmaceutical industry was involved in pointing Us in the direction of LDL cholesterol so LDL is something that is discussed constantly in general practice and you know the focus is is just not warranted so by now this is how you feel so what the hell do I do now so as a clinician it's a really difficult area my education and my research and my guidelines that I follow are all really heavily influenced by the pharmaceutical industry and also the food industry in addition in order to prevent litigation and in order to maintain my medical registration it's really important that I follow mainstream advice it's really important that I follow the guidelines because otherwise I risk being sued or being deregistered and the final thing I want to talk about is I want to talk about cognitive dissonance so I think cognitive dissonance plays an incredible role um in this area so cognitive dissonance describes the emotion that you feel when faced with two opposing ideas and it becomes much worse if one of those ideas is considered gospel it's something you've believed your whole medical career and here we have an an opposing idea and the emotional response to that may cause the rejection of the new idea out of hand which often happens or may cause an emotional reaction and I think anger is a really common emotional reaction and I've seen that in in professional meetings and you certainly see that with patients when they're trying to talk to their GP or their Specialists about this issue so as a non-clinician as a patient you have all of those problems so you have a clinician that you are seeing who's been adversely impacted by the pharmaceutical industry and has also these pressures about litigation and maintaining their medical registration but I wanted to point out two other things and that is fear and um emotional blackmail so as a clinician it is my job to talk to the patient who's in front of me to work out what their health care goals are and to talk about treatments which are available and talk about the benefits and the risks associated with that treatment and help them to make a decision unfortunately in healthcare that's not what we do we tend to tell people what to do um and we tend to attempt to motivate people by fear and by emotional blackmail so it's common there's a common um tale I come back from patients who've gone to see their GP or the cardiologist and they have been told your uh LDL is horrendous it's going to kill you if you don't take this stat and you're going to die if you don't take the stat and you're going to have a stroke and be permanently disabled and the emotional blackmail often happens as well in that I've had a number of patients who've been sacked by their cardiologist because they won't take a Statin so what is the way forward so first of all I'd like to recommend this uh review article about Staten therapy in people who experience an elevation of LDL cholesterol on a low carbohydrate diet this is written by Paul Mason and Ben bman and David Diamond it's a great article and it contains a lot of uh really useful information which nonclinicians can share with their treading practitioners if a decision is made to um try and decrease LDL cholesterol there's a couple of dietary options that are available and the first of these is to increase carbohydrate so increasing carbohydrate by between 50 and 100 grams a day tends to turn off that drive of triglyceride being pushed through vldl and drops LDL but the problem with that is that may impact on the goal of being on a low carbohydrate diet in the first Place we've already talked about the impact of dietary saturated fat on ldo cholesterol and it's very variable so decreasing dietary saturated fat can also be attempted so for a lot of a lot of us who've started low carbohydrate diets we've enjoyed the saturated fat so we've love putting cream um in coffee and putting butter on our vegetables and maybe having fat bombs and keto treats so it may well be that reducing some of those things might decrease eldo cholester control and you can consider swapping out saturated fats for monounsaturated fats and polyunsaturated fats so moving on to drug treatment I'm only going to talk about statins a discussion regarding pcsk9 in hibit is in banic acid is Way Beyond the scope of this conversation but I want to introduce a couple of Concepts firstly is primary prevention versus secondary prevention so primary prevention is preventing someone from having an event preventing someone from having heart attack secondary prevention is treating someone who's already had an event and trying to prevent a secondary event I also want to talk about relative risk reduction versus absolute risk reduction so relative risk reduction is something that the pharmaceutical IND industry uses constantly to emphasize the potential benefits of their drugs so relative risk reduction presumes that your risk of having something is 100% so for example we've got the relative risk reduction for having a heart attack um when you're on a Statin a Staten reduces your relative Risk by 29% which sounds fantastic but in fact the absolute risk reduction the risk reduction a real person in the community will get is 8% so absolute risk reduction describes what happens in the real world not presuming you've got a 100% chance of something this is a review article by Paula burn and marann Demari which was published in 2022 and they've looked at all of the data surrounding Statin and stroke heart attacks and total mortality so moving down the the chart the relative RIS risk reduction of having a stroke is 14% which sounds fantastic but the absolute risk reduction is only 4% now when we're looking at all cause mortality it only relates to secondary prevention there is no mortality benefit of taking a Statin in primary prevention uh for secondary pre mention with statins all cause mortality has a relative risk reduction of 9% and absolute risk reduction of a small 35% so this would all be very good with you know reducing stroke heart attack and in secondary um prevention we're reducing um death so that sounds great but that what happens if the statins have any side effects now many many cardiologists will tell you statins don't have side effects but let's look at the data so if we look at large trials real world trials looking at Statin adherence we know that between 20 and 80% of patients will stop taking their Statin and a significant proportion of those will stop taking their Statin because they're not tolerating it we know that statins are associated with muscle symptoms and damage and this is suggested to be be between 5 and 10% additionally statins induce insulin resistance and statins also increase the risk of type two diabetes and this is time and dose dependent so the longer that you someone is on a Statin and the higher the dose the more likely that diabetes will ensue so if you look at someone who's been on a Statin higho Statin for 2 years the um Hazard ratio is about 2 and a half so you've got a two and a half times increased incidence of getting type 2 diabetes so again what are we going to do with all that information so I want to introduce you to number needed to treat so this is from the number needed street.com which is available on the internet um and this looks at statins for elevated LDL cholesterol in primary prevention um and what it's saying is basically you'd have to treat 104 patients to prevent one heart attack in primary prevention you'd need to treat 154 patients to prevent one stroke and that one in 50 of your patients would develop uh type 2 diabetes and one in 10 would get muscle pain or damage so if we plot out um 100 patients uh in primary prevention and put them all on a P we will prevent half a stroke we'll prevent one non-fatal heart attack and we'll create two diabetics and will induce 10 lots of muscle pain or damage so let's look that 100 people for primary prevention put on a Statin for 5 years we'll help one and a half people we won't help um 98.5 people and 12 patients will be harmed so the absolute majority of people who are on a stat for primary prevention War will not benefit from being on the Statin let's have a look at secondary prevention um so in secondary prevention again 5 years of a Statin um one in 83 people will uh will not die as a result of being the stattin will prevent death um one in 39 will prevent a heart attack um and one in 125 will prevent a stroke but will create one in 50 of these people get diabetes as a result of being on a Statin and one 10 will get muscle damage so let's take a look at that so 5 years secondary prevention will prevent one stroke will prevent two and a half heart attacks will prevent one death and will create two lots of diabetes and 10 people will have muscle painal damage so 100 people on a stattin for secondary prevention will help 4 and a half people we won't help 95.5 people and will harm 12 people so again in spite of the fact that stattin for secondary prevention are considered sacrosanct and you wouldn't open your mouth to suggest that it was a consideration not to give us patient EST Statin in secondary prevention the evidence is that the majority of people on a Statin for secondary prevention will not benefit and some will be harmed so looking at coronary artery calcium score I just want to give a plug for this coronary artery calcium scoring is a really simple test it takes 5 minutes it's low radiation and it is the best way of predicting both future cardiovascular events and death um and I use this a lot in my practice um and then you can put a coron artery calcium score into a risk calculator this is a multiethnic study of atherosclerosis study which I use so you can insert the coron AR calcium score in there and all of the other risk factors um and come up with an absolute risk of having a cardiovascular event and the Misa calculator uses 10 years and again you can apply roughly if you can work out what the absolute risk is you apply roughly a third reduction in um heart attack um and 1 in 50 to 1 in 100 risk of developing diabetes and a 10% risk of get developing muscle pain so you can get a much more accurate look at what a Statin will do for a particular person or for yourself so finally we don't use coronary artery calcium scores for secondary prevention um however there are cardiovascular risk calculators for secondary prevention um and this is a smart risk calculator and again you know it it is presumed that if you had a heart attack you've got 100% chance of having another heart attack and that's not true at all this will give a a much more accurate idea of what the the risk of having another event is so I'd like to conclude by thanking a few people so when I started out I didn't know anything about cholesterol except LDL cholesterol is bad and HDL cholesterol is good so it's been a really steep learning curve for me so so I want to thank these people Dr David Diamond Dr Paul Mason Dave Filman Dr Nadia Ali and Dr nit Norwick you can find them all by looking for Journal articles um but they all appear on podcasts and on YouTube clips and a little plug um I know Twitter is a horrible uh uh social media platform these days um but however if you want to keep up to date with the latest in statins and uh cholesterol if you follow these people on Twitter all of the latest articles come out so the article that I've quoted from a week ago I picked up on Twitter so thanks very much for [Music] listening

Channel: Low Carb Down Under

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Keywords: Low Carb Down Under, LCDU, www.lowcarbdownunder.com.au, Low Carb Sydney 2023, Low Carb Keto Health, Laureen Lawlor-Smith, Keto and Cholesterol

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Length: 31min 47sec (1907 seconds)

Published: Sat Jan 20 2024