Dr. Paul Mason - 'Blood tests on a ketogenic diet - what your cholesterol results mean'

good morning so my name is dr. Paul Mason and I'm a sports and exercise medicine physician from Sydney and today I'm going to talk about cholesterol what it is what makes it good what makes it bad and more importantly how to interpret a cholesterol blood test 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 drop their LDL levels 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 story about one of my patients it was a 48 year old male and when he walked in I did a double-take I really didn't know why he was there I mean he looked ripped but as it turns out he had a rather unique problem you see 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 ask Erica fat he's 48 years old people this is his DEXA scan the blue areas represent lean tissue the red areas represent fat so why did his insurance company refused to enjoy him why did they think he was a bad risk well it was his cholesterol levels they were high this is his test result and the insurer based their decision based on this test so down the right-hand side you can see what we call the reference ranges with a lower and an upper value and if a result falls outside of this reference 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 stands for high density 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 numbers so the term cholesterol is very loosely but incorrectly used to refer to a number of different particles in our blood that carry fat around their body and there's five major classes of these particles and their correct name is lipoprotein now a little bit confusingly one of the fats 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 formed 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 linked them by arrows is to demonstrate that they are essentially the same particle so they all start out as the big one the VLDL and then as it circulates around our body it donates some of its cargo to tissues that's what they're meant to do and as it offloads its cargo they shrink 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 favorable 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 crowd and that wrong crowd is sugar or more specifically glucose if we expose LDL to glucose it can be damaged in a process called glycation and that then leads that damaged particle to be vulnerable to a process called oxidation and both of these damaging steps make 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 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 in millimoles liter this is the units that we use in Australia and the UK now the breakdown 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 saw which we know exists and the reason they're missing is because they're not actually measured on a standard blood test you see centrifuging the blood to spin it down so that you can actually measure the particles is a time-consuming and expensive procedure so it's usually not done so instead some values are calculated which is really a euphemistic term for saying their guests so VLDL we know exists but it's actually not listed here but it's is actually estimated as a part of the calculation for old yellers estimated ideal here in actual fact is assumed to be absent makes it a bit easier to do the calculations if we pretend that's not there right so then we use these assumed values 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 measure these particles individually and that's what I often do so what we do we get the sample and we place it in a gel and then we spin the gel down and as we spin it the particles sink into the gel at different rates and different depths depending on how big they are and what density they are and you can see here the dark spots represent peaks of the different LDL populations and the results are presented something like this and you can see that the peaks actually correlate with the dark spots in the gel so we can actually measure this now I just want to focus for a moment where it says LDL when we've divided it into seven sections and I just want you to have a look at the peak it's a nice smooth peak there's only one peak and this is because it represents a healthy population of LDL the fact that there's only one peak 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 peak so well let's have a closer look at what happens with the LDL when it does hang out with the wrong crowd and when it does get damaged first of all it gets exposed to sugar glucose and that caused glycation shrinks a little bit and then that makes 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 fats the kind sounding vegetable and seed oils there is a connection so let's come back to this graph here and up the top we'll now to our single LDL let's add the two damaged populations so let's see if we put that sample into a gel tube and spun it down what would 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 distinct populations of LDL and down the bottom knot of the sample here but another one of my patients just for illustrative purposes you can see here in the LDL you have three distinct Peaks this is patent B LDL this is the dangerous LDL and you need to understand it doesn't occur 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 damaging 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 created from the liver so as it donates its cargo it shrinks in size 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 cells 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 b100 and you can think of this like a security swipe card 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 green here is the appo b100 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 break 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 means 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 gets damaged so that means it's not recognized at these receptors so then what happens it begins to accumulate their numbers then increase in the circulation 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 volume of LDL is not necessarily going to be that high 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 small dense particles that are small and can't be taken out of the circulation so if they can't be taken out of the circulation in a normal healthy way what happens to them well they end up here they line the inside of our arteries so you can see on top of the deposit there you've got a thin layer of cells that layer on top is just one cell thick it's called the endothelium and this fatty deposit occurs underneath that layer and we can see from this graph here 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 take the oxidized LDL out of circulation it ends up deposited 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 lot 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 cell 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 only recognizes damaged LDL it's quite convenient they have a very strong affinity for it so what they do the LDL particle binds with the scavenger receptor and it engulfs it a little bit like a pacman and then eventually these macrophages end up so full of LDL that we call them foam cells and here you can see a foam cell with all the lipid droplets inside and this is the way in which damaged LDL ends 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 main artery supplying 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 heart disease because hba1c looks at how sugar damages the ret or attaches to the red blood cells it correlates with high blood glucose levels and we know that high blood glucose levels are what will also damage our LDL and that's why diabetics have a significantly higher rate of her attacks now for the good news we can often tell if your pattern a or pattern 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 here you can see they've got an abnormal triglyceride and abnormally low triglyceride which makes me question the reference ranges but they've got a high total cholesterol so let's have a look at how triglycerides relate to pattern a and pattern B so in this paper here you can see the green line represents pattern a and the red line represents pattern B the higher the green line is the more likely it is to be a pattern a cholesterol the higher the red line more likely it is to be pattern B and along the bottom you can see the triglyceride levels in yellow are the units for the UK and Australia and in blue they're the units used in the US and in Europe now we can see if we're looking at the red line that if our triglycerides are less 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 very 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 test 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 green and the pattern B in red except this time as the number goes higher it looks 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 saw 2.6 doesn't even register on this scale that's what a kidder genic diet can do so let's have a look at my patient who was denied insurance and let's have a look at his results 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 divide the triglyceride by the HDL now in his case millimoles leader he's came out at 0.53 so let's see where this fits on a similar kind of graph so in green in yellow remember the Australian units 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 almost 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 audience so these are very conservative numbers these 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 room for doubt but in Australia if you're under 0.8 in terms of millimoles a leader 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 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 usually 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 artery calcium score do we do lipid sub fraction there's a lot of other tests we can do inflammatory markers which are also very 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 diet it's been demonstrated quite nicely that if you go on a very high fat diet for about three days and have a blood test at the end of it your LDL levels 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 only 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 circulation then we're going to have less in our circulation it's only logical and interestingly increasing the amount of calories in our diet which increases our insulin actually increases the genetic expression 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 expression of a gene doesn't mean that you get an instant effect 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 delay explains the three-day delay between when you increase the amount of energy in the diet and the LDL actually Falls now in addition to increasing the number of LDL receptors insulin also increases the affinity that each of these receptive has for each LDL particle so it's an extra benefit and the reverse of this is also true we see LDL receptor expression reduce with fasting because it lowers your insulin levels and this explains why so many people have an elevated LDL compared to normal if they fast for longer than the usual eight or ten hours before their blood test fasting will increase your LDL level because your insulin levels will drop and the number of LDL receptors taking LDL out of the circulation will also drop that's how it works now as a little aside one of the mechanisms of statins those medications which lower your cholesterol they actually increase the expression 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 circulation and it's probably understated so to finish I'd like to conclude a few things so having a high LDL is not always a bad thing having damaged LDL is and remember it's not damaged by fat it's damaged by sugar high carbohydrate diets and having a high blood glucose level is what will lead to these pathogenic damaging 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 risk and finally as far as my patient was concerned if I as the insurance company to sign him up he looks fantastic thank you [Applause]

Channel: Low Carb Down Under

Views: 546,900

Rating: 4.9284821 out of 5

Keywords: Low Carb Down Under, LCDU, www.lowcarbdownunder.com.au, Low Carb Gold Coast 2018, lipids, lchf, low carb high fat, ketogenic diet, low carb doctors, #LowCarbGC

Id: DXKJaQeteE0

Length: 26min 8sec (1568 seconds)

Published: Sat Dec 08 2018

Reddit Comments

[u/unibball]

Excellent presentation from Dr. Mason as usual.

I only suggest that the mechanism for atherosclerosis might be different from his interpretation. See, for example, Subbotin:
https://www.sciencedirect.com/science/article/pii/S1359644616301921?via%3Dihub

Which shows that the endothelium is more than one layer thick, and that particles are found in greater concentrations farther from the lumen.

I would be interested to read Dr. Mason's "a lot of scientific articles" showing the increased permeability by oxidized particles.

[u/Ricosss]

I think he's oversimplifying things a bit with edging on wrong statements but the conclusion in the end is still valid. High LDL is ok if you have high HDL and low TG.

For example

1. LDL doesn't increase because of oxidized LDL, otherwise how do you explain the super high LDL levels seen by Dave Feldman's LMHR while they are not representing highly oxidized LDL levels?
2. If you looked at Ivor Cummins explanation then you'll also see that it is not the oxidized LDL that increases permeability of the endothelial layer but the common factor of high glucose.
3. He doesn't address the point why the macrophages would not engulf the oxidized LDL in the bloodstream. He doesn't say they don't but by not mentioning it he gives the impression that it doesn't happen in the bloodstream. But if it does happen in the blood stream, you'll have to explain more things... inconvenient.

To me that shows he has put some effort in to understand the whole thing, enough to get the essence right but not enough to correctly understand everything.

I got the high LDL factors explained in my articles so if you really want to know what causes high LDL then have fun reading. Unfortunately there is no easy TLDR version. Insulin is the biggest player but the effect is different when you get to insulin resistance:

https://www.reddit.com/r/ketoscience/comments/a2t1nl/vldl_secretion_rate_in_lmhr_consuming_a_low_carb/