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 athletics and rehearsal prescription specialist from Sydney and today I’m going to talk about cholesterol what it is what draws it good what clears it bad and most importantly how to translate a cholesterol blood experiment to see whether there’s any a matter of 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 descent their LDL tiers 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 advice so I’d like to start by sharing a narrative about one of my patients it was a 48 time aged male and when he stepped in I did a double-take I certainly didn’t know why he was there I represent he inspected ripped but as it turns out he had a rather unique problem you witness 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 query Erica solid he’s 48 year olds people this is his DEXA examination the blue places represent lean tissue the red-faced fields represent solid so why did his insurance company refused to enjoy him why did they think he was a bad risk well it was his cholesterol ranks they were high this is his test result and the insurer located their decision based on this test so down the right-hand side you can see what we call the reference wanders with a lower and an upper appreciate and if a decision falls outside of this invoke range it’s considered abnormal and what I’ve done here is I’ve highlighted three of his results which fell outside this range his total cholesterol he’s H DL which expressed support 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 right away and to understand why let’s take a closer look at exactly what we’re looking at when we look at these figures so the word cholesterol is very loosely but incorrectly used to refer to a number of different molecules in our blood that carry fattened around their body and there’s five major years of these particles and their compensate refer is lipoprotein now a little confusingly one of the paunches 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 horse it just really doesn’t make any sense and we can differentiate between these lipoproteins based on their size and the density and the lipoprotein on the bottom left the big one that’s the least dense the biggest that’s organized after we eat but by the time we do a fasting blood test the chylomicrons are essentially 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 circulates around our torso it bequeaths some of its cargo to tissues that’s what they’re meant to do and as it offloads its baggage they shrink they get a little bit smaller it’s like a deflating bag 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 circulation and I do but not all LDL is good it can turn bad if it mixes with the wrong horde and that wrong gang is sugar or more specifically glucose if we expose LDL to glucose it can be damaged in a process called glycation and that then makes that shattered molecule to be vulnerable to a process called oxidation and both of these damaging steps obligate the particle 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 carbohydrate 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 outage 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 witnessed which we know exists and the reason they’re missing is because they’re not actually calibrated on a standard blood test you appreciate centrifuging the blood to revolve 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 ethics are calculated which is really a polite call for saying their clients so VLDL we know exists but it’s actually not listed here but it’s is actually approximated as a part of the forecast for aged yellers forecasted ideology here in actual fact is assumed to be absent represents it a little easier to do the computations if we impersonate that’s not there privilege so then we use these accepted appreciates to calculate LDL so I said any wonder that accuracy is not always guaranteed at least the HDL is measured now one alternative to all of this guesswork would be to centrifuge the sample and actually evaluate these corpuscles separately and that’s what I often do so which is something we do we get the sample and we sit it in a gel and then we spin the gelatin down and as we invent it the specks sink into the gel at different rates and different profundities depending on the way in which big they are and what concentration they are and you can see here the dark discerns represent meridians of the different LDL populations and the results are presented something like this and you can see that the tops actually correlate with the dark distinguishes in the gel so we can actually measure this now I really want to focus for a moment where it says LDL when we’ve parted it into seven the articles and I precisely require you to have a look at the crest it’s a nice smooth top there’s only one heyday and this is because it represents a healthful population of LDL the fact that there’s only one pinnacle 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 particles were damaged I would expect to see more than one flower so well let’s have a closer look at what happens with the LDL when it does hang out with the wrong populace and where reference is does get shattered first of all it gets exposed to sugar glucose and that justification glycation shrivels a little bit and then that stirs it very vulnerable to oxidation and interestingly this oxidative process has been shown to be significantly accelerated when we have an X of omega-6 flabs the species voicing vegetable and seed oils there is a link so let’s come back to this graph now and up the top we’ll we are currently our single LDL let’s include the two marred populations so let’s see if we leant that test into a gel tube and spun it down what would it look like so have a look at the centre blob where the LDL is represented and now you can see it spread out and you can see in this example two distinct people of LDL and down the bottom knot of the sample now but another one of my patients just for illustrative purposes you can see here in the LDL you have three different Tops this is patent B LDL this is the dangerous LDL and you need to understand it doesn’t appear because of saturated fats it occurs because it’s damaged by sugar it’s damaged by blood glucose level so to understand why it’s so injuring and can lead to blockage of our blood vessels let’s have a look at the normal life cycle of VLDL formerly it’s that started from the liver so as it bequeaths its payload it contracts in sizing through the intermediate stage and finally aims 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 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 certificate swipe placard if you don’t have a security swipe card or if you’ve snarled it into it’s broken you can’t get in that door so if we have a look at an LDL in lettuce here is the appo b1 00 protein there’s a very important point now there’s only one of the following options proteins for every LDL molecule there is no redundancy if you divulge it it does not work there’s no backup and if it’s working properly this is the security swipe placard 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 represents 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 comes marred so that aims it’s not recognized under 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 journey they’ve donated most of their cargo so they’re quite small so the absolute magnitude of LDL is not necessarily going to be that high-pitched but the number of particles is and this is why the LDL particle count has quite useful predictive value for heart disease because it reflects these damaged big thick-witted specks that are small and can’t be taken out of the flow so if they can’t be taken out of the flow in a ordinary healthful nature what happens to them well they end up here they line the inside of our routes so you can see on top of the deposit there you’ve got a thin layer of cadres that stratum on top is just one cell thick it’s called the endothelium and this fatty deposit pass underneath that bed and we can see from this diagram now so in yellow here we’re graphing oxidized LDL in the dissemination and you can see that an increase in oxidized LDL is what actually predates 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 outcomes up deposited in the lining of the blood vessels so how does the LDL actually been through this layer that’s one cell thick well oxidized LDL has the effect of increasing the permeability of this blanket that’s been shown in a good deal of scientific articles so if you have oxidized LDL this layer 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 cell called a macrophages so remember how the LDL receptors would only recognize health LDL well these macrophages have a receptor called a scavenger receptor that simply recognizes injured LDL it’s quite convenient they have a very strong affinity for it so what they do the LDL particle obliges with the scavenger receptor and it engulfs it a little like a pacman and then eventually these macrophages be brought to an end so full of LDL that we call them sud cadres and now you can see a foam cell with all the lipid droplets inside and this is the way in which damaged LDL aims up ordering 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 route supplying the heart muscle and it’s been injected with stain so you can see the internal lumen the diameter of the lumen and you can see here that’s an important 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 foreseeing heart disease because hba1c looks at how sugar shatterings the ret or attaches to the red blood cells it correlates with high blood glucose levels positions and we know that high blood glucose stages are what will likewise impairment our LDL and that’s why diabetics have a significantly higher rate of her criticizes now for the good news we can often tell if your decoration 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 need to 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 excessively low-spirited triglyceride which realizes me question the note straddles 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 lettuce course represents pattern a and the red argument represents pattern B the higher the lettuce cable is the more likely it is to be a pattern a cholesterol the highest the colour wrinkle more likely it is to be pattern B and along the bottom you can see the triglyceride positions in yellow-bellied are the units for the UK and Australia and in blue they’re the human rights unit used in the US and in Europe now we can see if we’re looking at the pink 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 friend type a highly 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 same kind of graph for this patient so again we have the good phenotype in lettuce and the specific characteristics B in crimson except this time as the count disappears higher it ogles 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 discovered 2.6 doesn’t even register on this proportion that’s what a kidder genic diet can do so let’s have a look at my patient who was disavowed policy and let’s have a look at his causes on each of these and be seen to what extent informative that can be so his triglycerides is 0.9 that’s certainly down the good end but would you should be signed on it I don’t know there’s a grey 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 elevations 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 segment the triglyceride by the HDL now in his instance millimoles manager he’s came out at 0.53 so let’s see where this fits on a similar kind of graph so in light-green in yellowed remember the Australian measurements 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 nearly 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 figures these are how I understand 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 chamber for indecision but in Australia if you’re under 0.8 to its implementation of millimoles a ruler well in the u.s.If you’re under 1.8 with milligrams then you can probably rest easy so if I’m interpreting a blood test I’ll typically 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 food for a sustained period of time will end up having at least one of those figures generally two or three ogling excellent and if it’s not then we have to have a bit of a visualize then and that’s an independent individual decision do we do an hba1c do we do a coronary vein calcium score do we do lipid sub fraction there’s a lot of other tests we can do inflammatory markers which are also terribly predictive and we look at the whole picture but what the hell are 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 food it’s been demonstrated quite nicely that if you go on a very high solid diet for about three days and have a blood test at the end of it your LDL ranks 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 healthful LDL out of the bloodstream it doesn’t work for impaired LDL remember it merely 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 that are able to take the LDL out of the flow then we’re going to have less in our circulation it’s only logical and interestingly increasing the amount of calories in our food which increases our insulin actually increases the genetic face of these LDL receptors in actual fact rather than doing a high-fat diet as with the Feldman protocol a lesser amount of carbohydrates is very likely do exactly the same thing because of much stronger insulin response now why does it make three days well just because you increase the phrase of a gene doesn’t mean that you get an instant aftermath there’s a lot of steps that you need to go through before you be brought to an end 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 retardation justifies the three-day delay between when you increase the amount of energy in the nutrition and the LDL actually Precipitates now in addition to increasing the number of LDL receptors insulin also increases the affinity that each of these responsive has for each LDL particle so it’s an extra benefit and the reverse of “hes also” genuine we ensure LDL receptor showing abbreviate with fasting because it lowers your insulin stages and this explains why so many people have an hoisted LDL compared to normal if they fast for longer than the usual eight or ten hours before their blood measure fasting will increase your LDL level because your insulin heights will lower and the number of LDL receptors do LDL out of the dissemination will likewise droop that’s how it labors now as a little aside one of the mechanisms of statins those prescriptions which lower your cholesterol they actually increase the phrase of LDL receptors and that’s something a good deal of parties don’t know about and that’s one of the major mechanisms by which they actually increase the amount of LDL particles in the circulation and it’s probably understated so to finish I’d like to conclude a few cases things so having a high LDL is not always a bad thing having impaired LDL is and remember it’s not damaged by fat it’s damaged by sugar high carbohydrate foods and having a high blood glucose level is what will lead to these pathogenic damage LDL particles you can use your triglyceride or you could use HDL to evaluate a blood test 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 case was concerned if I as the insurance company to sign him up he inspects magnificent thank you[ Applause]

athletics and rehearsal prescription specialist

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