Dr. Paul Mason - ''Hard science on the real cause of heart disease - why you should avoid seed oils'

[Music] thank you g'day I'm Dr Paul Mason  and today's lecture is about a fairy tale   the one about saturated fat causing heart disease   the idea that saturated fat in the diet  will increase your LDL level and kill you   and this Fable is easily debunked in  2009 this paper reported that 75 percent   of patients hospitalized for heart  attack did not in fact have high LDL   which leads to the question if LDL doesn't  cause heart disease if it doesn't cause   these atherosclerotic plaques what does do we  have a better alternative to the fairy tale   in fact yes we do this a blood clot I'm going to  argue that your risk of clotting is a key risk   factor in both developing atherosclerosis  and dropping dead of a heart attack   the role of blood clots which can be called  thrombosis in causing heart attacks is both   both well-known and accepted you see fatty  looking blockages like this often exist   without any symptoms at all because there's  still enough room for the blood to get past   a complete occlusion however as can be caused by  a thrombosis or a blood clot is a different story   look on the rise at the thrombosis you can see  it's filling the space where blood once flowed in   the wrong artery this could easily prove fatal  what is less well-known however is that these   blood clots actually cause atherosclerotic plugs  to form in the first place you see atherosclerotic   plaques are basically healed blood clots after  a thrombosis of blood clot forms it heals that   it does not completely disappear and repeated  episodes of thrombosis over time leads to the   progressive buildup of a plaque here you can see  a single plaque with the lipid or cholesterol   core covered by a layer of connective tissue  compare that to this example with two layers of   plaque one on top of the other the more recent  thrombosis is sitting on top of an older one   in fact this cyclical process can occur as many  as four times at a single site within an artery   this still leaves us with the question  though of where do these crystals these   elongated shapes that we see in  atherosclerotic plaques come from   it's been long accepted that they're  made of cholesterol which is released   by LDL particles contained within these  bulbous structures here called foam cells   it is I'm not sure they're even exclusively  made from cholesterol let alone cholesterol   coming from LDL it's quite plausible that what  is thought to be cholesterol is in fact made of   something else entirely different something we're  going to take a closer look at later in the talk   the fine cell that you've just seen are formed  when something called a scavenger receptor on   a macrophage or a smooth muscle cell binds  to a damaged LDL particle and ingests it these foam Styles then store the cholesterol  bounds with fatty acids in droplet form   now foam cells don't like to release this  cholesterol that's what makes them foam   cells in the first place it makes it hard for  them to contribute to cholesterol crystals   furthermore the cholesterol in foam cells is bound  to fatty acids that's what makes it form droplets   and as you know there's a big difference  between a droplet and a crystalline deposit   that you see in atherosclerosis to make the  crystals you actually need pure cholesterol   what then can provide the ingredients for these  Crystal shapes that we see in atherosclerotic   plaques and red blood cells is the answer their  outer membrane contains more free cholesterol than   any other cell in the body and not surprisingly  red blood cells are quite abundant in blood clots   and when we look within atherosclerotic plugs  we see clear evidence of these blood clots   we see the presence of platelets which are  fragments that play a key role in initiating   blood clotting and we see fibrin which forms  fibrous strands that binds it all together this   study for example surgically removed sections of  atherosclerotic plaque and found clear evidence of   all of these ingredients deep within they obtained  further definitive proof of the presence of red   blood cells by using a brown stain for a chemical  called glycophorum a a chemical only found in red   blood cells look at all the brown conclusive proof  of degraded red blood cells deep within a plaque   and further evidence of red blood cells and  clotting in the pathophysiology of atherosclerosis   is provided by this New England Journal of  Medicine paper from 2003 it clearly describes   the central accumulation of red blood cell  membrane within atherosclerosis furthermore the   investigators also injected red blood cells into  animal models of atherosclerosis and found that   this Blood injection produced plaques containing  both cholesterol crystals and foam cells   the upshot of all of this is that thrombosis  or blood clots are Central to the development   of atherosclerosis and so clotting risk  what we call a pro-coagulant tendency must   two be a risk for atherosclerosis so this  raises the question how do the lipid risk   factors for heart disease that we all know  about relate to clotting tendency if at all   now you may have seen one of my previous lectures  where I talk about the validity of triglycerides   and HDL as markers of cardiovascular risk  essentially there's robust evidence that higher   triglycerides and low HDL is associated with an  increased risk of heart disease so I began to   explore whether these metrics had any association  at all with the risk of blood clotting if they   don't then this whole clot Theory goes down the  drain except I do and I didn't have to look very   far literally dozens of papers have been published  on these connections between leopard parameters   in the blood and clotting risk for example  triglycerides associate with the activity of   factor seven a key component of blood clotting  HDL inhibits the clumping of platelets a key   initiating factor in the formation of clots in the  first place therefore a low HDL level removes the   break on clot formation and oxidized LDL promotes  both platelet clumping and also the secretion of   something called tissue Factor the single most  potent stimulus of clotting there is whatever way   you look at it what we consider to be lipid risk  factors are in actual fact clotting risk factors   a high triglyceride level or a low HDL level  is an independent risk factor for thrombosis   now the risk of thrombosis for these blood clots  is manifestly increased when a plaque ruptures   fortunately plaques are often stable and here you  can see one such example the yellow arrow points   to a relatively thick margin of connective tissue  lying over the top of the plaque this on the other   hand is an example of an unstable plaque with only  a thin layer of connective tissue over the top   which leads to the question what causes thinning  or destabilization of this protective cap and one   answer is foam cells those cholesterol stuffed  macrophages you saw earlier they can secrete   enzymes that break down the protective tissue cap  these enzymes are called Matrix metalloproteinases   and high levels have been independently associated  with the tendency of plaques to rupture there's 23   different types of Matrix metalloproteinases in  humans and one which has been consistently shown   to play an important role in plaque rupture  is number nine in fact high levels of Matrix   metalloproteinase 9 has been shown to be an  independent predictor of cardiac mortality   which led me to ask the question do triglycerides  and HL levels have any association with Matrix   metalloproteinase 9. given it plays a key  role in cardiac risk and not surprisingly   the answer is yes both higher triglycerides and  low HDL is associated with plaque destabilizing   Matrix metalloproteinase 9. and more specifically  oxidized LDL the presence of which is indicated   by a poor triglyceride to HDL ratio has been shown  to play a causal role in Matrix metalloproteinase   IX activity of course there's other factors that  are key to the formation of a blood clot besides   unstable plaques and one of the most important  of these perhaps is damage to the inside lining   of blood vessels here you can see hair-like  structures lining in artery and this is what is   called the glycocalyx and it's the first line of  mechanical protection that arteries have against   clotting amongst other things the glycocalic  shields the artery wall from coagulation particles   it secretes A protein that blocks abnormal  clots from forming called antithrombin 3   it mediates the production of nitric oxide which  dilates blood vessels and itself is another potent   inhibitor of coagulation in short the glycocalyx  is an effective defense against coagulation   and again thrombosis it should be no surprise  then that oxidized LDL can damage the glycocalyx   and once this barrier of protection is gone  the risk of thrombosis increases exponentially   now's a good time to get to one of the  key root causes of heart disease oxidation   oxidation is basically an umbrella term  that refers to a chemical reaction that   occurs when an electron is torn away from  a molecule or atoms that's basically what   rusting is and oxidized LDL and other sources  of oxidation in our blood can do this to the   proteins and fats within our blood vessels  you've probably heard the term free radical   this is a term we often use for molecules that  can cause this oxidation damage and when it comes   to oxidized LDL there's nothing magical about  LDL the key factor is the oxidization oxidation   itself is bad not oxidized LDL is perfectly fine  any source of oxidation stress within our blood   vessels can damage the lining if Our arteries  damage the glycogalex it just so happens that   LDL being a normal resident in our circulation  can be a very effective vehicle of oxidation but   only if it is oxidized that oxidation itself is a  major cause of heart disease and I do deliberately   use the word cause is why antioxidant supplements  like an acetyl cysteine have been found to be   protective against heart disease any source of  oxidation which enters our circulation is bad news   and that includes what we inhale after  President Eisenhower's heart attack his   doctors probably shouldn't have overlooked  his two to three pack a day smoking habit   because that was almost certainly a major  cause you see the pollutant particles that   we inhale including from smoking can enter our  circulation a fact that was proven more than 20   years ago and within one minute of inhalation this  particulate pollution is detectable in the blood   and these particles carry with them  oxidation stress and this is why   there is such a strong relationship between  pollution and cardiovascular mortality and   the consequences are clear pollution  is a major cause of death full stop   and what about diabetes after all we know that  diabetes is associated with a tripling of the   risk of dying from heart disease and stroke well  it comes down to sugar in the blood consider this   research from 1962 that demonstrated blood glucose  abnormalities occurred in 73 percent of heart   attack patients this has been known for a long  time and the mechanism oxidative stress it's been   long known that high in fluctuating blood glucose  levels as occurs in diabetes generates this   oxidation which is one reason high blood glucose  levels increase clot risk yes we're back here   high glucose levels also stimulate  Matrix metalloproteinase 9 secretion   remember that plaque destabilizing enzyme here you  can see both type 1 and type 2 diabetics have much   higher levels of this plaque destabilizing enzyme  in their aortas I'd like to now discuss seed oils because of their polyunsaturated structure  characterized by a readily reactive double   bonds these oils are very prone  to oxidation even without cooking   this study found High rates of oxidation within  walnut oil occurred within days and consumption   of oxidized oil leads to oxidation of lipoproteins  within our blood lipoproteins that can deliver   oxidation stress throughout our arteries compare  the blood oxidation levels after consumption of a   low oxidized oil to that of a highly oxidized oil  understand that oxidation within our circulation   is a cause of heart disease and if you understand  that you can see why seed oils could be a problem   but besides their oxidation potential there's  another element to seed oils that makes them   particularly problematic when it comes to  heart disease something which is usually not   considered at all you see they contain something  called phytosterol or plant sterol which you   can think of as fake plant cholesterol as you  can see they're near identical to cholesterol   but not quite similar enough to be absorbed by  the body in place of cholesterol but different   enough to not work the same basically phytosterols  interfere with the normal biochemical processes   that use cholesterol the highest concentration  of these plant sterols is found within seed oils   especially rice bran corn and rapeseed and another  significant contributor of these plant sterols in   our diet simply due to the volume consumed is  cereal and while our body tries to reject plant   steroles some does get through about one percent  of what we consume actually gets incorporated into   our tissues and one of the tissues is fake  plant cholesterol gets into is your arteries   and it's probably no surprise that when it  does it's associated with premature severe   cardiovascular disease proof of that was provided  when researchers performed a biopsy of the aorta   of a 33 year old male with premature severe  cardiac disease and detected plant sterols   and this is not an isolated finding these  three papers from 2005 2011 and 2015 all   reported plants to roles were detected in  diseased arteries interestingly it's likely   that these plant sterols also contribute  to the crystals found in atherosclerosis   they may not in fact be made of cholesterol  understand that you're not looking here at   Crystals directly but rather the space where  they used to be before they were dissolved in   processing and it's entirely possible and I would  argue likely that one source of these crystals is   phytosterol or plant sterol you see being almost  identical to cholesterol plant sterols readily   form crystals crystals which are difficult to  differentiate from those formed by cholesterol   remember these foam cells the supposed supply  of cholesterol well while foam cells don't like   to release their cholesterol they're only too  happy to spit out phytosterol or plant sterols   this makes phytosterol a much more likely  contributor to these crystals observe how   foam cells or macrophages are only too happy  to store cholesterol compared to plant sterols   and plant sterols which may form these crystals  might also be supplied by degraded red blood cells   for not only does the outer membrane of red  blood cells contain more free cholesterol than   any other cell in the body it also contains plant  sterols the consumption of plant Foods especially   seed oils has been repeatedly shown by research  to result in plant sterol accumulation within   red blood cell membranes interestingly  enough at the expense of cholesterol and I think it's very likely that through  oxidation stress and plant sterols seed oils are   quite possibly an even more significant cause of  modern disease than our carbohydrates and sugars   this paper for example after analysis over over  195 000 subjects concluded that seed oil intake   resulted in a greater incident of death than  sugar when it exceeded six percent of energy in   the diet consider them that the average Australian  gets more than 13 of their energy from seed oils   and when we look at the intake of polyunsaturated  fat which is a very good surrogate for seed oil   intake we can see consumption began to rise in the  early 1900s well-timed to have a causal role in   the epidemic of heart disease that followed which  is why three large-scale randomized controlled   trials the gold standard of research have found  that replacing saturated fat with seed oil   led to a significant increase in mortality and to  my knowledge there's no study that shows otherwise   ongoing review of data from the Woman's Health  Initiative for example a study of over 48   000 females has found that lowering  saturated fat intake is associated with   an increased risk of heart disease  of between 47 and 61 percent   findings of another study based in Sydney  which ran between 1966 and 1973 were finally   disclosed in 2013 reporting that replacing  saturated fat with polyunsaturated fat in men   who had a heart attack increased their  subsequent risk of death by 62 percent   and in a very similar story the mortality data  from the Minnesota coronary survey which was   completed also in 1973 was not published until  2016 and when it was published it revealed that   in a population of 7 000 participants increased  seed oil intake increased the risk of death   the totality of these studies provides  compelling evidence of the dangers of seed oils   the plant sterols within seed oils also play as a  role in reducing blood levels of LDL it does this   by inhibiting the normal healthy absorption of  cholesterol from the small intestine that leads to   a reduction in the production of the LDL precursor  vldl and it also increases the removal of LDL from   the blood and this combined LDL lowering effect  to plant sterols is why increased saturated fat   intake is seems to raise cholesterol you see  saturated fat often comes from animal sources   that means it doesn't contain plant sterols and  if you reduce your seed oil intake while you   increase your animal fat intake your cholesterol  levels may be permitted to return to normal levels   not go high because saturated Fat's not making  it go high but it's the removal of the seed oils   that's permitting the LDL to rise back to normal  healthy physiological levels there's one major   exception to saturated fat intake being associated  with increased LDL and it's the exception that   proves the rule that's coconut oil coconut oil  is a plant oil it contains to rolls and that's   why coconut oil drops LDL levels while at the same  time loading your body tissues with plant sterols   indeed this knowledge makes me reconsider  whether coconut oil is actually healthy   to close I'd like to briefly discuss statins as  you may know in high-risk populations that is in   subjects with heart disease statins have been  shown to reduce the number of cardiac events   and the mechanism behind this has nothing at all  to do with lowering of LDL rather statins inhibit   blood clotting Pathways and inhibit the release  of plaque destabilizing Matrix metalloproteinases   and statins can be something of a double-edged  sword though inhibition of clotting can also   have complications this is clear with the  significant increased risk of brain bleeding   known as hemorrhagic stroke that occurs with  Statin therapy I believe that the mechanism   of Statin benefit which include inhibition  of Matrix metalloprotonases and inhibition   of blood clotting likely explains why benefit  from statins is evident basically from day one   the side effects however which include a  71 increased risk of developing diabetes   are likely to attenuate this benefit over time and  perhaps this is the reason why the only study that   appeared to show a mortality benefit of statins  in a primary prevention population was terminated   early by being a shorter trial perhaps the full  impact of Statin side effects was attenuated   food for thought in closing I'd like to  acknowledge the work of Scottish GP Malcolm   Kendrick on exposing the role of blood clots in  atherosclerosis this is well documented in his   book which provides an excellent summary of the  clotting Theory still I wouldn't be surprised if   you'd never heard of him because there's a fringe  figure who had the outrageous audacity of arguing   against the lipid hypothesis as a result he's  been canceled at least by Wikipedia this is true   that's the justification that was provided  for the deletion of his Wikipedia page   in closing the whole story we've been fed  about saturated fat causing atherosclerosis   is nothing but a big old fairy tale  rather than worrying about how much   saturated fat we're consuming we should  be worried about factors that increase our   clotting risk like oxidation pollution Sea Dog  consumption and blood glucose levels thank you [Music]

Channel: Low Carb Down Under

Views: 348,731

Keywords: Low Carb Down Under, LCDU, www.lowcarbdownunder.com.au, Low Carb Gold Coast 2022, Paul Mason, Malcolm Kendrick, Blood Clots, atherosclerotic, triglyceride to HDL ratio, heart disease, Statins, phytosterols

Id: -xCr3mvFCHM

Length: 24min 28sec (1468 seconds)

Published: Sat Jan 07 2023