Dr. Paul Mason - 'Saturated fat is not dangerous'

I'm going to present on one of my favorite topics today and that's about that it's a wholly misunderstood topic so we all know the story back in 1977 these Dietary Guidelines were introduced into the United States they recommended a significant reduction in overall fat consumption as well as a specific reduction in saturated fat intake now these guidelines gradually percolated down to Australia so in 1979 they were introduced into Australia as dietary goals and over the years there's been numerous iterations that have resulted in our current Dietary Guidelines the 2013 edition now central to this introduction into Australia was a professor Stuart Roswell Gil's the chair of nutrition at the University of Sydney at the time this institution here that we're at today and in his recollection which he recorded in a 1995 article he acknowledged that there was no background review of the medical literature at the time prior to the introduction of the Australian dietary goals now you'll see this is a recurring theme that's through the iterations that they've undergone there's never really been a substantiative effort to have a look at the science in its entirety so to this very day our guidelines still suggest that we limit saturated fat and the dies now I struggled with this because I said I've read the literature and to the best of my ability I cannot see where it says that traded fats are bad so I said what references were they looking at so I went through their reference list and all the best research that I was reading they didn't read and I thought why is that and I kept reading through them and then buried in the appendices I came across this statement here now I won't read it out but I'll tell you what it means they did not look at any research pertaining to saturated fat and cholesterol during the review period full stop so that explains why the Australian Dietary Guidelines and myself came to quite different conclusions about safety of saturated fats in the diet now when I've had a look at the current Dietary Guidelines I thought well what research did they not look at so I've put up three studies here these are what's called systematic reviews or meta-analyses in medicine medical science we have different tiers of evidence and this is at the very pointy end the top level of evidence of medical science and from these review papers they consolidated all the research from numerous authors and they came to what they considered would be an average conclusion or a final conclusion and the balance of evidence that was available during the period of development of our current Dietary Guidelines says that saturated fat in the diet is not associated with any deleterious health outcomes that is it's safe so following the publication of our Dietary Guidelines I thought well let's have a look and see what the new research is and again the pattern continues the top one there is a combined meta-analysis and a systematic review from the British Medical Journal very clearly demonstrating that saturated fat science associated with all cause mortality or any of the other nasty stuff paper in 2016 showed the same and again more recent paper from this year in 2017 saturated fats are not dangerous in the diet at this point in time you should be getting the message that saturated fats have no evidence of being harmful so let's flip it on its head a little bit then and say well if saturated fat is safe what about reducing the fat in our diet is that safe or as it would seem is that potentially harmful so to do that we're going to come to the most expensive medical study ever performed 700 million US dollars big study lots of dollars so this study the diet arm of the study went for about eight years they had about 50,000 participants and on average there was about a 10% reduction in dietary fat so if you were going to find a reduction in all cause mortality through limiting fats in the diet this study would demonstrate that so what did it show well here's the results table so the first thing to point out here is that all the results on here do not reach statistical significance that's a fancy way of saying we can't trust them they the trends if they show any trends it could be statistical error so in a sense it doesn't show anything on their results table here but you will note that here they talk about all participants and they've got a column for participants without a history of heart disease interestingly for a study that's looking at risk of heart disease and fat in the diet they didn't have a column for participants with a history of cardiovascular disease so I'm just going to pause here for a moment I'm not going to read out that verbose comment on the left but this was buried on page 661 of the article in the text there's several doctors in the audience today so can I just get a show of hands of anybody who thinks they know what that comment would actually mean because it seems of Juicin so it's pretty obscure I'll tell you what it means for those females with a history of cardiovascular disease if they were randomized to go to the low-fat diet group their risk of problems such as heart attacks was it increased by 26% increased now this was the only statistically significant finding from the whole study funnily enough it didn't end up in the results table but we'll just let that one go through to the keeper so the take-home from this if you're sitting there and you're worried about saturated fats in your diet don't full-stop but some of you still probably don't comprehend the connection between saturated fats and cholesterol and I know in the clinic every day I see patients every week and they ask me but what about cholesterol but what about cholesterol we've got this paradigm in our head that cholesterol is terrible so let's have a look at what cholesterol is you can see this here this is a molecule on the left now that's what cholesterol looks like if I take away just one atom it ceases to be cholesterol so when we talk about good and bad cholesterol it makes no more sense than if we're talking about good and bad water molecules it just is that's what it is their cholesterol is absolutely essential most of it is actually made by a body about 75% of it so it's seen in every cell membrane it makes up about 30% of our cell membranes without it we die it forms the basis of a steroid hormones it forms the basis of vitamin D it's necessary for bile acids it really is an essential structure without cholesterol we die now when we're normally talking about cholesterol in common parlance we're not meaning cholesterol we're not talking about this we're talking about something far more complex we're talking about something called lipoproteins now to understand what lipoproteins are we need to understand that fat is essential for life and it has to travel around the body but it doesn't dissolve in the blood fat is insoluble so what that means is that if we just released fat into the body like that which sometimes happens medically you end up with what's called a fat embolism where the fat will pump it'll block the blood vessel and that's bad news bear so to get around this we have these magnificent structures called lipoproteins now you need to think about them as like submarines where they carry their fat cargo around our circulation so you can see on the picture here that we've got an inside cargo it's carrying fat cholesterol triglycerides vitamins antioxidants several things we've also got a very complex outer membrane here where we've got several proteins embedded within it now I want you to take note of the embedded proteins because we're going to come back to that is essential to understanding how they work these are what we call the signaling molecules now there's several different types of lipoproteins and the differences are based on their size the amount of triglycerides and cholesterol that they carry and the type of proteins that are embedded within the walls but the two that I want to focus on today HDL and LDL these are the ones that are commonly thought of as being good and bad cholesterol but now we can think of them as being HDL as being good lipoprotein an LDL well the jury's still out so we can actually analyze LDL far more in depth than what is done on the standard blood tests that's paid for by Medicare so we generally understand that cholesterol is made up of so-called good and bad but the blood tests I do in the clinic I can do what's called lipid electrophoresis and I can separate LDL out into its separate constituent parts and not all of these are harmful so types 1 & 2 which we call pattern ion unoxidized is totally benign it's harmless but as soon as you go and test types 3 through 7 its associated with oxidation and several other things and that is the type of LDL cholesterol that's associated with harm so this is what we call a kaplan-meier survival curve and this derived from about two and a half thousand patients after a heart attack and this was designed to have a look at their mortality based on whether they were that pattern a cholesterol or the pattern B cholesterol now the obvious point to make here is that heart attacks are bad after five years most people had died you can see the mortality here in in the group that had the patent B was almost 90% after five years now what about the group that had the patent a the one that we said wasn't as bad well they had a significantly lower rate of death so more than double the people after five years he had that better pattern of LDL were surviving after five years so this certainly means something so this is a sample one of the tests which I've actually ordered in the clinics are anonymized it and this is an example of what we can actually the kind of data and information that we get on our patients in the clinic now I've just like to point something out here so I'm sure people have heard of the term small dense LDL and they visualize that these these particles are massively small and they borrow into the inside of the blood vessel and that's how they do the damage that is wrong no such thing that is a complete and utter misconception they are smaller but have a look at the size now one nanometer is a millionth of meter tiny the difference in size is in their order of one or two nanometers so it's really not a huge structural difference and in actual fact it just relates to what happens to that protein on the outside of it that makes that small measurement when that small difference when we actually measure it so let's have a look at what the effect of diet is on this pattern of cholesterol so if we assume that pattern B is bad which the data clearly suggests it is what gives us Pat name what gives us a pattern B so we know that if we have saturated fat then a cholesterol goes up now here you can see in this individual here all their cholesterol this is subsection one subsection 2 and in the area here that we don't like it so much nothing high LDL cholesterol but safe LDL cholesterol in this individual so what happens though when we have carbohydrates now saturated fats increase your cholesterol well carbohydrates turn your quest all bad so now we have LDL it's a little bit in 1 & 2 pattern a look at all this awful stuff in pattern B now I could talk about these other aspects of the LDL and HDL but for the purposes of not over complicating it we'll just ignore those for the moment now let's go back and remember those different types of lipoproteins in that how they had a unique protein embedded in their wall now these three lipoproteins in the middle here they're all essentially the same they all have that same mark on them so what actually happens is it begins it leaves the liver with a load of triglycerides starts as a VLDL and then as it moves around the circulation it gets rid of some stuff and swaps some stuff around and it ends up shrinking in size and it progresses through being an ideal to end up as a low-density lipoprotein same molecule but we tend to think about them as being differently it's just a the same molecule on a different pathway now the important thing is here you'll see how we've labeled it with a be 100 the name of the special protein that labels this uniquely is a poby 100 funny name you don't need to understand what it means just remember that C unique signal now that signal allows this bitter cholesterol this LDL particle to be taken up by the liver and removes it from the circulation it's a docking signal now what happens if we damage that docking signal and we can we do it all the time with sugar you've just seen a presentation where this concept of advance quark oscillated end products was presented now that same thing happens to the protein on the outside of this lipoprotein particle so this black strand here represents protein strands then we have sugar that attaches to it and that D functions it that ends up progressing to again what we call advanced glycosylated end product so what happens now we've got this particle going through our circulation comes to the liver and the liver says I don't know who you are there's nowhere to go so the only other alternate pathway is this one we see down the bottom involving something we call a macrophage within a blood vessel and we'll come back to that later but that's essential to know well let's take a closer look now so this picture on the top right is a demonstration of a macrophage you can think of them as little pac-man they just engulf whatever it is that's not they're not meant to be there they've got special receptors called scavenger receptors now the damaged fov 100 is not recognized by the liver but it is recognized by the scavenger receptors on the macrophages inside the wall of the blood vessel so this is basically part of the process of what we call atherosclerosis let's look at it another way the bus it represents an LDL and clearly we can see where it's going heading straight to the liver now if we disturb the signal then remember there's only one of these on each molecule there's only one signal there's no backups here then it doesn't know where it's going it's just going to drive around aimlessly until finally it ends up on this crappy this is what LDL does if we damage the signal molecule it doesn't get taken up by the liver it ends up ganking up the inside of your blood vessels now this is a this is a process this is well-versed in science now other side note those researchers from Nagoya in Japan have actually found that what reduces the size of these particles from pattern a to pattern B is actually the glycation they've found that there's a very very strong Association now if we come back to the role of glycation or sugar damage in this we can see a supporting research here demonstrating that for the same level of LDL cholesterol increasing our blood glucose levels associate higher risk of heart disease so this front column here this is low level of glucose and this is your risk of heart attack or myocardial infarction for the same amount of LDL in your circulation you can see that the risk goes up up up in each of these columns both for males and females the increased sugar is actually what's associated with the damage now having a look at it another way just from the last talk you're all aware that insulin resistance is associated with high blood sugar levels so this is what happens when we when we map it out with insulin we see insulin level very low risk there's very little difference in your risk of heart attack if you have high levels of LDL if your insulin is controlled what happens if your insulin level goes up skyrockets so you can have high LDL but it's only when it becomes glycated and damaged from the sugar which we get from carbohydrates that the damage is done so this leads us to an understanding of how low carbohydrate diet can improve our LDL cholesterol now many people don't realize I'm sure everybody here does but out there in the big wide world they don't realize that complex carbs are chains of glucose molecules and when you digest them they enter the bloodstream and then we know what happens then they're exposed these other products we can have this glycation and then we end up with oxidized LDL so that's why in the clinics when I'm seeing patients I frequently see I do this test on the patients a transition from a pattern B LDL to a pattern a LDL after treating them with a low carbohydrate diet now let's take a brief detour because I know I'm going to get asked questions on this later statins people think statins prevent dying but the better way to think about it is that they might not prevent dying but they just delay dying because we know it's going to happen eventually so this paper set out to answer the question how long does do statins delay mortality so they had 11 studies over 90,000 participants and they'll followed for about 4 hour half years so here's the question if you took a statin for four and a half years and you had a history of heart disease this is a group most likely to benefit how long do you think your life span would be increased by so I want everybody to just answer to yourself here's the answer according to this study [Music] now what happens if you don't have a history of heart disease so this was published in the British Medical Journal a couple of years ago not a bad little Journal very interesting reading now for the final part of the talk here I'd like to focus on a particular interest area of mine and that's to do with vegetable oils and fish oils now if I do my job everybody in the audience here will be out at answer this question what is the nexus between aspirin and vegetable oil I'm hoping that a few people might already have a bit of an idea so we're going to focus on two types of polyunsaturated fats called omega-3 and omega-6 fats now these fats are absolutely essential for life they can't be manufactured in the body every one of these omegas that we get has to be ingested now they're both essential so while we're going to talk about improving your ratio today we're not aiming to absolutely eliminate omega-6 from the diet which by the way is pretty much impossible for if you did that then you'd have some serious consequences they're both essential that they need to be present in balance so to understand this I'm going to introduce you to something that you probably the doctors will remember from biochemistry and the rest of you probably will never have heard it's eicosanoids these are basically local hormones they only act on cells close to the site where they're produced and they regulate several important things including inflammation and swelling fever clotting and the immune system very important little chemicals now of relevance they're only made from omega-3 or omega-6 fats now this omega-3 omega-6 fats so with the three on top here and a six on the bottom here they're actually stored in this fat layer that surrounds the outside of the cells and so when the body wants to make one of these eicosanoid products it reaches up into the cell membrane and grabs out one of these and uses it to make the product so let's have a look at this process in a little more detail so on the Left if the cell grabs an omega-6 we can see what happens it ends up going down through this process and produces something called arachidonic acid now let's have a wee closer look at this side now once we're with arachidonic acid you can see with the action of these other enzymes here arachidonic acid can be converted into the substances which have very very inflammatory in actual fact we frequently use medications to target these enzymes to reduce the production of these chemicals we know how inflammatory they are so the middle one there the series two prostaglandins something like prostaglandin e2 we specifically target that with anti-inflammatory medication now if we come back and have a look at the other side of the coin if the cell grabs an omega-3 that ends up producing something that we call epa and DHA basically these are what's found in fish oil and the products that we have from conversion of these and not that inflammatory very much less inflammatory than on the other side so if we come back to the whole process these two pathways are inextricably linked so it depends on which one they're grabbing from the cell membrane but the processing of it depends on these enzymes have only included two of them but both these dull Sardi such raised enzymes are shared by both pathways so what that means is that if we and they compete for these enzymes if we increase the amount of omega sixes then we reduced the ability of the omega-3 side to convert to the more active forms and we can see this here in this plot here and you can clearly see this is a plot of omega-6 in purple and omega-3 in green increasing levels of one will lead to a reduction in the amount of the other so clearly if we're trying to optimize our ratio it's if we want more omega-3 it's not just enough to pump in the omega-3 we should also follow this up with a correlated reduction in our omega-6 so assuming we can do this let's have a look at what it might mean practically so remember fats that are found in all their cell membranes our red blood cells are cells you have so we can assess this ratio in our red blood cells from a simple blood test so these graphs represent prospective data that was published in two very good journals the Journal of the American Medical Association and their New England Journal of Medicine now the risk of heart attack is depicted by the vertical bars going up and increasing amounts of omega-3 in the cell membrane as shown along the bottom here so what we can see is that the highest level of omega-3 in both of these studies so six point three percent here 7.3 percent here was associated with ten times less risk of dying from a heart attack than the people with the lowest level of the mega three in their cell membranes if there was one blood test that you would do maybe besides insulin to assess your risk of dying from a heart attack this is what I would do and this is what we do do in a clinic let's look at other another way if you had less than four percent omega-3 in your cell membranes and most of my patients when they come in do if we were able to increase you to this range of four to eight percent that would lead to a 42 percent risk reduction in having a heart attack and if we were able to put your over eight percent 69 percent reduced risk of having a heart attack and this is what we try and do when we optimize your fat intake so this graph here just demonstrates a spread of omega-3s in the population and we can clearly see that the people are sort of two or three percent three or four percent they vastly outnumber the people who are over eight percent where we really want people to be well this is an actual patient result so this gentleman here you can see he was already on a low-carb diet when we did this test but then we've started focusing on the fats and oils so you can see he started out with a really good omega-3 level to be with 8.9 here's what he's in that low-risk group already and yet over the course of about 12 months we were still able to get a massive massive improvement this puts him in rarified air this is good off the charts so how did he do it well he reduced the sources of fats in the diet with excess levels of omega-6 and he increased his intake of omega-3 so what you can see here in blue this is demonstrating the amount of omega-6 in some common fat so you see at the top things that we usually like coconut oil and butter not much omega-6 here right it would be easy to offset that with a fish oil supplement what about some of these seed oils down here let's have a closer look at the ratio of omega-6 and omega-3 in some vegetable and seed oils out of this world so if you were worried about those inflammatory products of the omega-6 side of the eicosanoid pathway you're probably not going to be having this healthy grapeseed oil which I dry every time I go to the airport I see this wonderful billboard saying the most healthy grapeseed oil well it's not hard to be a little bit healthier than that but it's also important to take a look at the rest of our food supply this graph here demonstrates the level of omega-3 soon in grass-fed beef on the Left this is about 3 percent here what happens when we start to grain feed them what happens after 196 days of grain feeding previously healthy beef with a very good amount of omega-3 you don't just need to eat your fish to get omega-3 grass-fed beef will do fine 0 and interestingly if we have a look at farm salmon we see something similar not to the same extent but there was one study that demonstrated that farmed salmon had about 17% less omega-3 oils than wild course honey now I'm not going to get into a debate about ethics on that it's interesting tonight though that the farm salmon as well as having all the algae they're often fed a lot of pellets so thank you for your time the questions will come later

Channel: Low Carb Down Under

Views: 237,732

Rating: 4.8948569 out of 5

Keywords: Low Carb Down Under, www.lowcarbdownunder.com.au, LCDU, Low Carb Sydney 2017, #LowCarbSyd, www.lowcarbdoctors.com.au, Saturated Fat, Cholesterol, LDL Cholesterol, lipoproteins, polyunsaturated fats, australian dietary guidelines

Id: NUY_SDhxf4k

Length: 28min 35sec (1715 seconds)

Published: Wed Apr 25 2018

Reddit Comments

[u/dem0n0cracy]

Low Carb Sydney 2017. It's rare for someone to beat me to post this. Good job Alex. :D

[u/unibball]

A very good presentation. Although, at 23:23 he makes the mistake, as many do, using the term alpha "linoleic" acid. That should be alpha "linolenic" acid. See his Omega 3 and Omega 6 slide. Common error. Why did they have to be named so similarly anyway?