Dr. Paul Mason – ‘Blood tests on a ketogenic diet – what your cholesterol results mean’

good morning so my mention is dr. Paul Mason and I’m a sports and exert medicine physician from Sydney and today I’m going to talk about cholesterol what it is what performs it good what prepares it bad and more importantly how to translate a cholesterol blood measure to see whether there’s any cause for concern and we’re going to finish our talk by looking at the Feltman protocol where people have been shown to be able to dramatically fell their LDL stages simply by following a high-fat diet for three days but please note this lecture is purely educational and in no way constitutes any personal medical suggestion so I’d like to start by sharing a legend about one of my patients it was a 48 year age-old male and where reference is trod in I did a double-take I actually didn’t know why he was there I imply he inspected rent but as it turns out he had a rather unique problem you interpret he had recently applied for health insurance income protection insurance and he had received this letter from the insurance company apparently they felt that he was high risk this is a recent photo not question Erica solid he’s 48 year olds people this is his DEXA search the blue domains represent lean material the colour expanses represent solid so why did his insurance company refused to enjoy him why did they think he was a bad peril well it was his cholesterol status they were high this is his test result and the insurer located their decision based on this research so down the right-hand side you can see what we call the reference ranges with a lower and an upper quality and if a result falls outside of this comment compas it’s considered abnormal and what I’ve done here is I’ve foreground three of his reactions which falls outside this array his total cholesterol he’s H DL which stands for high-pitched concentration lipoprotein and he’s LDL which stands for low-density lipoprotein but if I was his insurer based on this result I would have signed him up straight off and to understand why let’s take a closer look at exactly what we’re looking at when we look at these lists so the call cholesterol is very loosely but incorrectly used to refer to a number of different corpuscles in our blood that carry fattened around their body and there’s five major class of these particles and their compensate identify is lipoprotein now a little confusingly one of the fattens that these carry around the body is actually cholesterol but to call these lipoproteins cholesterol is a bit like mistaking a horse float for a pony it just really doesn’t make any sense and we can differentiate between these lipoproteins based on their size and the concentration and the lipoprotein on the bottom left the big one that’s the least dense the biggest that’s worded after we eat but by the time we do a fasting blood test the chylomicrons have basically disappeared from our blood so we don’t need to focus on chylomicrons anymore now in yellow you can see three lipoproteins which are linked by arrows VLDL IDL and LDL this stands for very low density lipoprotein intermediate density lipoprotein and low-density lipoprotein and the reason I’ve joined them by arrows is to demonstrate that they are essentially the same particle so they all is the beginning as the largest the VLDL and then as it flows around our form it gifts some of its cargo to tissues that’s what they’re meant to do and as it offloads its merchandise they wither they get a little bit smaller it’s like a deflating balloon but they’re still the same particle and finally up on the top right here you can see HDL which is closely known as good cholesterol with higher levels generally considered positive now you’ve also probably heard of LDL referred to as bad cholesterol but the LDL we’re looking at here in fact is not deleterious in any way I’d be quite happy to have a bunch of that in my flow and I do but not all LDL is good it can turn bad if it mingles with the wrong army and that wrong audience is carbohydrate or more specifically glucose if we expose LDL to glucose it can be damaged in a process called glycation and that then pass that shattered particle to be vulnerable to a process announced oxidation and both of these damaging gradations construct the corpuscle fractionally smaller you’ve probably heard a small dense LDL before that’s what it is it’s been damaged and that damaged as a consequence of exposure to sugar this damaged LDL is what leads to heart disease not the other stuff so now we know what the different types of lipoproteins are let’s have another look at my patients cholesterol panel now you’ll notice one thing where it says cholesterol 8.8 and this is consistent with millimoles liter this is the units that we use in Australia and the UK now the explosion of the cholesterol underneath that doesn’t add up to the total cholesterol and there’s a very good reason for this because this panel is missing some of the lipoproteins that we just ascertained which we know exists and the reason they’re missing is because they’re not actually calibrated on a standard blood test you examine centrifuging the blood to rotate it down so that you can actually bar the specks is a time-consuming and expensive procedure so it’s usually not done so instead some appreciates are calculated which is really a polite period for saying their guests so VLDL we know exists but it’s actually not listed here but it’s is actually forecasted as an integrated part of the planning for old yellers approximated ideology here in actual fact is assumed to be absent determines it a bit easier to do the forecasts if we claim that’s not there right so then we use these presumed qualities to calculate LDL so I said any wonder that accuracy is not ever guaranteed at least the HDL is measured now one alternative to all of this guessing would be to centrifuge the test and actually bar these specks separately and that’s what I often do so “what were doing” we get the sample and we residence it in a gelatin and then we invent the gel down and as we spin it the specks sink into the gel at different proportions and different magnitudes depending on the way in which big-hearted they are and what density they are and you can see here the dark recognises represent peaks of the different LDL people and the results are presented something like this and you can see that the peaks actually correlate with the dark recognizes in the gelatin so we can actually measure this now I only want to focus for a moment where it says LDL when we’ve subdivided it into seven sections and I only want you to have a look at the meridian it’s a nice smooth peak there’s only one meridian and this is because it represents a health population of LDL the fact that there’s only one meridian means that there’s not been any change in size due to damage of the LDL they’ve not been glycated they’ve not been oxidized and this is what we call a pattern a LDL this is healthy now if the corpuscles were damaged I would expect to see more than one crest so well let’s have a closer look at what happens with the LDL when it does hang out with the wrong mob and where reference is does get impaired first of all it gets exposed to sugar glucose and that induced glycation decreases a little bit and then that compiles it very vulnerable to oxidation and interestingly this oxidative process has been shown to be significantly intensified when we have an X of omega-6 fattens the category resounding vegetable and seed lubricants there is a connection so let’s come back to this graph now and up the top we’ll we are currently our single LDL let’s supplement the two detriment people so let’s see if we employed that sample into a gel tube and spun it down what the hell is it look like so have a look at the middle blob where the LDL is represented and now you can see it spread out and you can see in this example two different people of LDL and down the bottom knot of the test here but another one of my patients just for illustrative purposes you can see here in the LDL you have three definite Crests this is patent B LDL this is the dangerous LDL and you need to understand it doesn’t occur because of saturated obesities it occurs because it’s damaged by sugar it’s damaged by blood glucose level so to understand why it’s so injury and can lead to blockage of our blood vessels let’s have a look at the normal life cycle of VLDL once it’s that established from the liver so as it donates its shipment it contracts in width through the intermediate stage and finally ends up at low-density lipoprotein and then the low-density lipoprotein are able to be taken back up by the liver or by cadres in the peripheral tissues and they use something which I’ve shown here in blue-blooded which is called an LDL receptor and these LDL receptors are able to specifically recognize the LDL particles and that’s because there’s a special protein on the LDL particles which we call a PO b1 00 and you can think of this like a protection swipe placard if you don’t have a security swipe card or if you’ve snapped it into it’s broken you can’t get in that door so if we have a look at an LDL in dark-green here is the appo b1 00 protein there’s a very important point here there’s only one of these proteins for every LDL molecule there is no redundancy if you separate it it does not work there’s no backup and if it’s working properly this is the security swipe card that will allow the LDL receptors to recognize it and take it out of circulation now the problem is the sugar damage actually targets the proteins it actually targets this that wants the LDL receptor won’t be able to recognize this particle I don’t know who you are you’re not welcome here persona non grata go away so what happens in that situation well the LDL is coming out of the liver converted to IDL LDL and then the LDL get marred so that implies it’s not recognized at these receptors so then what happens it begins to accumulate their numbers then an increasing number of the flow and this is when we see what’s called a high LDL particle count now one thing you need to know because at the end of their pilgrimage they’ve bequeathed most of their cargo so they’re quite small so the absolute publication of LDL is not undoubtedly going to be that high but the number of members of particles is and this is why the LDL particle count has quite useful predictive evaluate for heart disease because it shows these damaged small-time thick-witted molecules that are small and can’t be taken out of the dissemination so if they can’t be taken out of the flow in a regular health space what happens to them well they end up here they row the inside of our arteries so you can see on top of the deposit there you’ve got a thin layer of cells that seam on top is just one cell thick it’s called the endothelium and this fatty accumulation exists underneath that bed and we can see from this graph now so in yellow here we’re graphing oxidized LDL in the circulation and you can see that an increase in oxidized LDL is what actually precedes the development of this atheroma inside the blood vessel which we can see in red as you make the oxidized LDL out of circulation it points up lodged in the lining of the blood vessels so how does the LDL actually get through this layer that’s one cell thick well oxidized LDL has the effect of increasing the permeability of this layer that’s been shown in a great deal of scientific articles so if you have oxidized LDL this membrane becomes a little bit leaky or porous and the LDL particles are able to travel to the underside of it and then once they’re underneath they come in contact with a cadre called a macrophages so remember how the LDL receptors would only recognize healthy LDL well these macrophages have a receptor called a scavenger receptor that simply recognizes damaged LDL it’s quite convenient they have a very strong affinity for it so what the fuck is do the LDL particle obliges with the scavenger receptor and it engulfs it a little like a pacman and then eventually these macrophages end up so full of LDL that we call them sud cadres and now you can see a sud cadre with all the lipid droplets inside and this is the way in which damaged LDL ceases up lining the inside of our blood vessels and this is the end result this artery here is called the left anterior descending artery it’s the primary artery giving the heart muscle and it’s been injected with dye so you can see the internal lumen the diameter of the lumen and you can see here that’s a significant narrowing and that is caused by LDL that’s been damaged by sugar and that’s why hba1c is such a brilliant blood test for predicting congestive heart failure because hba1c looks at how sugar shatters the ret or attaches to the red blood cells it correlates with high-pitched blood glucose levels and we know that high-pitched blood glucose levels are what will likewise detriment our LDL and that’s why diabetics have a significantly higher rate of her affects now for the good news we can often tell if your pattern a or motif be based on the standard blood test despite the limitations of it and the inherent inaccuracies within it we still get a lot of very important information and we often might not was also necessary do any further testing so we’re going to look at two things and the first thing we’re going to look at is called the triglycerides so in this patient now you can see they’ve got an abnormal triglyceride and exceptionally low-grade triglyceride which forms me question the invoke collections but they’ve got a high total cholesterol so let’s have a look at how triglycerides relate to pattern a and blueprint B so in this paper here you can see the green strand represents pattern a and the maroon word represents pattern B the highest the lettuce string is the more likely it is to be a pattern a cholesterol the higher the red thread most likely it is to be pattern B and along the bottom you can see the triglyceride degrees in yellow are the units for the UK and Australia and in off-color they’re the human rights unit is set out in the US and in Europe now we can see if we’re looking at the scarlet pipeline that if our triglycerides are lower than 0.5 million miles later then you’re almost certainly going to have a pattern a phenotype but if we go down the other side if your triglycerides are over 2 your chances are having a bad fellow type a awfully very high and remember this example we just looked at they had a level of 0.4 so they’re going to be very very comfortable the other factor that’s really useful on this blood evaluation is the HDL level this is another patient high total cholesterol and a high HDL cholesterol let’s have a look at the similar kind of graph for this patient so again we have the good phenotype in dark-green and the pattern B in ruby-red except this time as the multitude goes higher it glances better so we can see that if your HDL cholesterol and I use the term loosely is less in about 0.4 0.5 you’re almost certainly going to have a bad profile however if you have over 1.5 you’re singing easy and the one example we just examined 2.6 doesn’t even register on this flake that’s what a kidder genic diet can do so let’s have a look at my patient who was denied guarantee and let’s have a look at his outcomes on each of these and see how informative that can be so his triglycerides is 0.9 that’s certainly down the good end but would you sign off on it I don’t know there’s a gray area but have a look at his HDL 1.7 clearly in the Green Zone I didn’t need to do any further testing on him I wasn’t worried about his cholesterol levels even without doing a sub fraction I was confident that he was patent a now there’s one more metric that we can use to assess for patent a and B and that’s when we use the power of triglyceride an HDL together and that’s when we calculate what’s called the triglyceride to HDL ratio we part the triglyceride by the HDL now in his event millimoles manager he’s came out at 0.53 so let’s see where this fits on a same kind of graph so in green in yellowed retain the Australian forces if it’s under 0.8 it’s good so if his is God of 0.5 again he can rest easy if it was over 1.8 then would approximately be certainly had a pattern B and if it’s in the intermediate zone well that’s when we need to think a little bit harder so just for the benefit of some of our international public so these are very conservative lists the latter are how I interpret the data and I’m sure there’s a lot of other people who could interpret it slightly differently and I’m probably a bit more conservative than most people I don’t like to leave a lot of apartment for indecision but in Australia if you’re under 0.8 in matters of millimoles a chairman well in the u.s.If you’re under 1.8 with milligrams then you can probably remain easy so if I’m interpreting a blood experiment I’ll usually look at the triglycerides if they’re good happy days if not try the HDL if that’s good excellent if not we move on to the triglycerides HDL ratio and almost every one of my patients who has been on a ketogenic diet for a sustained period of time will end up having at least one of those figures typically two or three looking excellent and if it’s not then we have to have a bit of a think then and that’s an independent individual decision do we do an hba1c do we do a coronary vein calcium compose do we do lipid sub fraction there’s a lot of other tests we can do inflammatory markers which are also highly predictive and we look at the whole picture but what you do next should be discussed with your doctor now we’ve all heard about the Feldman protocol so essentially what happens is if you have a very high LDL level on a ketogenic nutrition it’s been demonstrated quite nicely that if you go on a very high fatty nutrition for about three days and have a blood test at the end of it your LDL degrees will significantly drop some would even say plummet and this is why it comes down to these LDL receptors now these LDL receptors are what actually takes healthy LDL out of the bloodstream it doesn’t work for damaged LDL remember it simply works for the healthy LDL and the amount of LDL in the blood has an inverse relationship to the number of receptors if we have more receptors which are capable of take the LDL out of the circulation then we’re going to have reductions in our circulation it’s only logical and interestingly increasing the amount of calories in our nutrition which increases our insulin actually increases the genetic saying of these LDL receptors in actual fact rather than doing a high-fat diet as with the Feldman protocol a lesser amount of carbohydrates would probably do exactly the same thing because of much stronger insulin response now why does it take three days well just because you increase the construction of a gene doesn’t mean that you get an instant result there’s a lot of steps that you need to go through before you end up with the final product which in this case is the LDL receptors and it’s this process between genetic upregulation and the final protein synthesis that likely lag explains the three-day delay between when you increase the amount of energy in the food and the LDL actually Falls now in addition to increasing the number of LDL receptors insulin also increases the affinity that each of these approachable has for each LDL particle so it’s an extra benefit and the reverse of “hes also” true-blue we participate LDL receptor construction reduce with fasting because it lowers your insulin status and this explains why so many people have an heightened LDL compared to regular if they fast for longer than the usual eight or ten hours before their blood measure fasting will be enhanced your LDL level because your insulin stages will quit and the number of LDL receptors take LDL out of the circulation will likewise lower that’s how it handiworks now as a little aside one of the terms and conditions of statins those medications which lower your cholesterol they actually increase the idiom of LDL receptors and that’s something a lot of people don’t know about and that’s one of the major mechanisms by which they actually reduce the amount of LDL particles in the dissemination and it’s probably understated so to finish I’d like to conclude a few things so having a high LDL is not ever a bad thing having injured LDL is and remember it’s not damaged by fat it’s damaged by sugar high carbohydrate nutritions and having a high blood glucose level is what will lead to these pathogenic detrimental LDL particles you can use your triglyceride or you could use HDL to evaluate a blood experiment to estimate whether it’s likely to be patent a or patent B and if you have patent a then it’s not doesn’t have any significant association with any increases in cardiovascular likelihood and finally as far as my patient was concerned if I as the insurance company to sign him up he appears superb expressed appreciation for[ Applause]

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