Cholesterol - Beyond Good or bad

Dr. Parr, WhatsApp audio.

Hi, good morning, Dr. Kaur. No, no, once you join as an attendee, then only I'll be able to make you a panelist. I can't see you. I can see Ruhi Agarwala, Ananda Kumar. Are you here from Ananda Kumar KS name?

A little bit of time. So what happens is it's not like, okay, instead of statin, I'm just going to give red yeast rice. No, that, that is, that is not functional medicine thinking. Functional medicine thinking is thinking from a perspective of the whole patient and thinking in terms of systems of systems. All the systems are interconnected. Whether it is you're talking about the heart, the heart is related to the gut. The heart and gut are both related to the brain. And all these different interconnections, those are very important to keep in mind when we look at a patient. A patient doesn't come with only a heart problem, only a lung problem, only hypertension, or only diabetes. It is never, never really only one problem. So that thinking in terms of network of networks is actually what is most important in terms of a functional medicine way of thinking. So this is Dr. Mark Houston's, you know, slide. What he says, if you've heard him speak, you will know that there are infinite insults to the vasculature. So according to him, you know, the cardiovascular disease is a problem which occurs at the level of the vasculature. In fact, so often I have, you know, I talk about cardiovascular disease being a diabetes of the blood vessel. And many people make fun of that, saying, oh, for you everything is diabetes. I said, yeah, it is true. It is actually insulin resistance at the level of the endothelium. So that is one of the factors. And for most of us, you know, who are taking care of patients in India, we cannot get away from managing insulin resistance. Well, insulin resistance, type 2 diabetes, both of them. So infinite insults to the endothelium. But the endothelium has 3 finite responses. One is inflammation, oxidative stress, and immune response. So the problem is, you know, immune— the immune system is involved with everything. So it's not that the vasculature is very independent of immune system problem. Every disease is an immune system problem. It's just that it's the type of, you know, problem and the type of response, immune response that we come across. You look at cancer, that's an immune response problem. You look at the ongoing coronavirus pandemic, that is definitely an immune system problem. So there are all these different things which are extremely important to look at. And in the interest of time, I'm going to go to the questions right at the end. So if you, if you have any questions and you chat, uh, typed in the chat box, uh, I'll get to that later. So, uh, overview of cholesterol. As you can see, there are, there are many things to talk about cholesterol, and I don't think I'm going to have time because it's already, um How much time have we, have we, uh, I think already about 20 minutes. So one of the most important messages, which I think is okay in this group, I don't think I need to reiterate that, but I'm sure most of you, all of you are aware of that, is cholesterol from food does not raise blood or brain cholesterol levels. So what do I mean by that? You'll find even today many doctors will tell, you know, their patients don't have coconut oil, don't have eggs, don't have too many eggs, and if you have eggs, don't eat the yolk, eat only the white. That cholesterol does not raise blood cholesterol. Our bodies have the inherent ability to make cholesterol. And even more interesting is brain cholesterol synthesis. The brain has its own independent ability to make cholesterol. The fact is, if cholesterol is something so important, nature does not create redundancies. So that is the reason, and nature would not want to depend on only dietary cholesterol to get all the cholesterol for the body because cholesterol is so vital. So that is the reason the body has an inherent ability to make cholesterol. The problem comes when we can't always figure out why the cholesterol has gone up. Now, in some places you'll find that, you know, in functional medicine we talk about, oh, in functional medicine we are you know, root cause resolution. We look at the root causes. Sometimes we cannot always determine the root causes, but we definitely try very hard. So the next thing is atherogenic dyslipidemia is one of the 32 modifiable risk factors for cardiovascular disease, and we— there are 31 others that we can focus on. Cholesterol is only one of them. Next comes brain cholesterol synthesis, why that is significant, and lab tests. I'm just going to cover a few brief ones. And then of course the important question is, should you recommend a statin medication for your patients? And you'll understand that I don't provide yes or no answers. I'm just, it's my job to provide the information. It's for you and your patient to decide what is the best path forward, because in functional medicine we practice what is called patient participatory medicine. So we have a conversation with the patient to ask, you know, do you think this is something that you would like to do? And that was not something I did. So I was an OB-GYN in Mumbai for many years. Back in those days, I just write a prescription and there was no question about are you going to do this, you're not going to do this, so you just have to do this. So that is the type of medicine that is not going to work long term. So this is, uh, and the other important thing is unless you are yourself in primary care and in India, or you are a cardiologist or an internist, most Most of the time, as a functional medicine doctor, I am almost never anyone's primary care doctor. So I am not the first person they will come to when they have a problem. And most of the time when it comes to statins, they are either already— they have been put on a statin or they have been asked to get onto a statin. And that is when they look for someone like us. So the diet-heart hypothesis, unfortunately, this has been debunked a long time ago, but the message has not reached a lot of doctors and it has not reached a lot of patients. Obviously, doctors have not been giving the right message. How can we expect patients to know anything different? The sad thing is the recommendation to limit dietary saturated fatty acid intake has persisted despite mounting evidence to the contrary. Now, if you haven't read one book called The Big Fat Surprise, Nina Teicholz, or if you are following Dr. Zoe Harcombe, or Dr. Asim Malhotra, who is a cardiologist in the UK. You will know about the saturated fat and the diet-heart hypothesis has been completely debunked a long time ago, actually. In fact, if someone is still talking about the diet-heart hypothesis, they haven't upgraded the knowledge in a long time. I would say that, of course, you can't say that to many of your colleagues, but this is a good paper to read and The other thing, let me warn you, Dr.

Kaur, we can always think that and know that.

Yeah, for sure. Another important thing is, though you may be ready with a whole lot of literature and, you know, everything, your colleague may not be interested at all in reading them. So don't feel that just because you sent a paper that they've read it. And when it— before, in case I forget later on, there's a very good book by Dr. Asim Malhotra, My Statin-Free Life. It's available on Kindle, and I'm sure the paperback is available in India as well. If you haven't read that, that's a good one to read. But again, if you are expecting your cardiologist colleagues to read that, if you hand the book over to them, well, good luck with it. Some will, most won't. So why is cholesterol synthesis in the brain very important? One of the things that happens is if someone is on a statin medication, and statins are very often given as a primary prevention or as a secondary prevention. So primary prevention is someone who has not had any cardiovascular event, no angina, no MI, no, none of that. They just went to the doctor, they found the LDL was high, and the doctor said you need to be on a statin medication, or you have hypertension, you have diabetes, you have blah, blah, blah. Versus secondary prevention is a person who's already had an MI or had any event like that. That person is put on a statin. Now, secondary prevention is a different world altogether. Statins do have some role, but in primary prevention, you will realize, like I said, I'd like you to decide what you want to do. Now, why is cholesterol synthesis in the brain important? So there are two different pathways of cholesterol synthesis. The block and the other one is, I call that the KR pathway. It's difficult to pronounce it. So the block pathway, the B for brain is how I remember it. That is the more important pathway for the brain cholesterol synthesis. Now you can see that desmosterol is one of the major, you know, major things that are manufactured in the brain in this pathway, in the block pathway. And studies on people with Alzheimer's disease have found that there has been lower levels of brain desmosterol concentrations. And on the other hand, these were not the same studies, so we cannot interpolate one between one and the other. There have been studies which have shown that there are statin medications which can cross the blood-brain barrier, and statins can reduce desmosterol. But these have not been in the same study. So this has not been in a study of patients with Alzheimer's who have been on statins and shown to have lower levels of desmosterol in the brain. So we cannot say that statins caused that. But in general, in patients with Alzheimer's, they have found that there has been less desmosterol. So this is, this is an important factor to keep in mind when you are— when your patient is on a statin. And your patient says that I don't feel my brain is working the best. So at that point in time, you might need to switch to a different statin. That is for another conversation. I'm— I don't think we'll have time to go over that.

So Dr. Kaur, in my practice, what I've seen is that a lot of these patients have very low cholesterol and the doctor writes a smiley there, and the patient comes to me because the patient says that they have anxiety or they are not feeling good.

Yeah.

And the only thing you do is stop the statins and the client starts to feel better in a matter of time. But I think this pathway explains it perfectly.

Yeah. So that is the, that is the point. You have to listen to what the patient is saying and what the, what you need to do. So basically, I'm going to rush through this. Now, the reason I brought this up is So cholesterol is not water-soluble. So, and if you've heard, and again, I'm not a lipidologist, and lipidology is something that I find very difficult. And if you want to know more about lipidology, if you're following Dr. Peter Attia, P-E-T-E-R-A-T-T-I-A, he has a very good podcast and his newsletters are excellent. He has a series on cholesterol, and I would definitely suggest that you go through that. Because he explains it way better and he understands lipidology much more than I do. All that biochemistry, I keep saying I must have been asleep in my biochemistry class in medical college. So yes, going back to where does, you know, where do apolipoproteins come in. So, uh, you know that nowadays I find many of my patients come with a, with a blood report of ApoB100 and Lp(a), or those things are already done even if I have not recommended. So one of the things is the ApoB is a much better proxy of total atherogenic lipid lipoprotein particle concentration than what you can see on a standard lipid panel. So standard lipid panel is total cholesterol, triglycerides, HDL-C, LDL-C. And you might find sometimes that some of those numbers like VLDL and all those are calculated. So not actual measured numbers. That is important as well because calculated may not always be very correct. So there are many different nuances, but at the same time, a standard lipid panel is very cheap. Everywhere it is done, in every little village in, in, in the world, I think, can get a standard lipid panel done. So important thing to remember is what is the information you can get from a standard lipid panel. But if you are already doing ApoB, or like your patient has gone to this lab and they gave, they gave them a package of, you know, which was relatively cheaper, and they've already come with these reports. What can you do? So I will go over some of these tests a little bit in detail because that is what is applicable for you in your day-to-day practice. So from a standard lipid panel, the most important information to glean from that is not— so LDL is considered to be the bad cholesterol and HDL is supposed to be the good cholesterol, but very often you'll find that your patients have high triglyceride levels. And they don't report the triglyceride by HDL-C ratio. So studies have shown that if the TG by HDL-C ratio is greater than 2.5, that kind of implies a more atherogenic dyslipidemia. So that information is available on a standard lipid panel. And the other important question is, what should we consider as a normal triglyceride level? Now, unfortunately, we don't have a lot of studies based on South Asians in India which are looking at longitudinally. They're looking at what the triglyceride levels were, and out of those people, how many survived, you know, without cardiovascular disease until old age. We don't have that data as far as I know. If any of you know anything different, please let me know. But going by the, you know, data in the West, So most people in the functional medicine world and in the, you know, the preventive cardiology world consider a normal triglyceride level as less than 120. On the lab reports, you'll find it's less than 150, but less than 120 is what we would like. Some people here are going even lower. Now, I found that in patients, in my patients from India, going super low is not very easy. Because we have a lot of people who are vegetarians, and for them to eat super, super low carb is not going to be that easy. And many of them are not going to take an omega-3 fatty acid supplement because it comes from fish oil. So the most important information to glean from a standard lipid panel is the triglyceride by HDL-C ratio. And as you can see, if the ratio is high, very likely it's the triglycerides which is high. So once you bring the triglycerides down, this ratio will come down. And this number applies to both men and women. Now I'm Asian, so obviously I love free stuff. So this ApoB app, just maybe just want to make a note of this. It's a free app available. Dr. Alan Smiderman has made that available to everyone. So what you can do is you put in the patient's ApoB, the total cholesterol, the triglycerides, and it comes up with an interpretation. So I won't have time, otherwise we could have gone through an actual patient case right now. And in that interpretation, he will tell you what are the possibilities. The only thing is, and I have not had an opportunity to ask him, he looks at a triglyceride level of 133, not 150, but not 120 either. But that is an important, you know, important thing to remember. So the ApoB will correspond to risk determined by an LDL particle number. And I will briefly talk about particle number and size because the test is not available in India. I don't want to spend a lot of time on that. The other big area, which I'm sure many of you have been reading up, is about non-HDL-C. So non-HDL-C is obviously anything that is not HDL. So that is, that is considered to be important nowadays because that has decided many people's risk factors for cardiovascular disease. Another important thing is, I'm sure this is information which is not seeped down everywhere. People think, oh, HDL is supposed to be your good cholesterol. So if you have high HDL, it's fantastic. Like, oh, that's awesome, you need to congratulate. Just as Dr. Preeti, you talked about cholesterol being super low and the doctor putting a smiley next to it. So I'm sure they've put a smiley next to high HDL-C as well. Well, it turns out that high HDL-C may not necessarily be good news. So that is new, fairly newish information in the last several years. So in medicine, when we say new information, it's the last 6 to 7 years. Sometimes it was back in the days, actually, I think it used to take about 20 years for any research to be translated into clinical practice. But now, for people who are aware, it can take much less time because we read up a lot. There is a lot of online resources available. We get access to journals, things that we— so I am middle-aged. Back when I was a medical— in medical college, we didn't have access to journals or anything. For our MD thesis, we had to actually go to Delhi.

So Dr. Kaur, I remember my time, for any research we had to go to the AIIMS library. So there is this government library which has all medical journals next to AIIMS. And we had to actually go alphabet-wise, look at it, get it Xeroxed, come home and read through those papers.

Dr. Preeti, you were in Delhi, I was in Guwahati. So for us, it was two MD students going with a list of all the references and sitting in the dusty library and finding out. So anyway, I'm so happy we are not in that world anymore. Next is a CAC score, and then of course my 32 modifiable risk factors for cardiovascular disease. So HDL-C is not— high is not always protective. So this is a very good paper to read in case you want to— maybe you want to take a screenshot of this. So what did they find? That there is a J-shaped curve when it comes to HDL-C. So there is something called dysfunctional HDL. Now, as far as I know, in India we don't have the test available where we can look for the HDL and LDL functionality. There are some research papers. I've asked those researchers, but I've not received a response to my emails. So just important to remember that if you see a high HDL-C, it's not— it may not necessarily be a cause for celebration, because if it is not functionally healthy, then that is not going to be the thing. So infectious disease, autoimmune conditions, lung disease, cancer, diabetes, kidney disease, the stuff that you're dealing with every day. There are all those different factors which can, you know, change your— change a patient's HDL levels. Lp(a), I don't want to spend a lot of time in it except for saying that because your patients are going to come with reports and with reports of high Lp(a). Now amongst South Asians, South Asians have a much higher number of people of South Asian ancestry have high Lp(a). So in the Western world, Lp(a) is considered to be a marker for premature familial cardiovascular disease. But like I said, in Indians, we don't have a definition of prematurity because almost all cardiovascular disease is premature. Hypertension, you know, developing in young people as young as 18 to 19, and even type 2 diabetes. So Lp(a), your patient may already come with it. The fact is Lp(a) is actually— it's a genetic marker. So there isn't a lot you can do with Lp(a), and lifestyle changes may not change. But at the same time, I have— Dr. Mark Houston has presented on this, and I have also seen in my practice— this is anecdotal, not based on evidence— where once we have— I have fixed the rest of their blood, gotten the blood glucose levels down, inflammation down, blood pressure at a normal level, their Lp(a) levels have changed. The other important question which today we don't have an answer is because in addition to statins, I'm sure many of you are familiar with, a lot of cardiologists are using PCSK9 inhibitors for patients now. The thing is PCSK9 inhibitors are very expensive and many cardiologists will say, okay, your Lp(a) is high, you need to be on a PCSK9 inhibitor. The data has still not shown whether reducing Lp(a) in someone whose levels are high, whether that has translated to lower mortality or lower number of cardiovascular events. So Lp(a) is important for you to know because your patient is going to ask. So this is something important to remember. Next is lipid particle number and size. If you have heard anyone from the functional medicine world, you will find them talking about this very often. And I'm just mentioning it so that, you know, you know what it is. But even in our practice in Canada, actually, because in Canada healthcare is covered by government and I work with a physician who is in private healthcare, even here we don't always do lipid particle number and size for every patient because we have to send it to the US. It's not available here in Canada. So basically what happens is you can see from Dr. Tara Abdaal is actually a fantastic lipidologist. She does quite a lot of the lectures on the A4M. On lipidology. You can see here the large LDL are supposed to be the better and the small dense are supposed to be the worst. Now usually the analogy we give for patients is this is a tennis net and that is a tennis ball. So a large buoyant LDL particle cannot— so if you imagine that the net is the endothelial and is the endothelium. So a large buoyant particle will not get in between the endothelial cells and cause problems. Whereas on this one, you can see that the small dense particles, they are small and they can easily get in between the endothelial cells. So this is a simpler way to explain the difference between large fluffy and small dense. So large fluffy, big fluffy, whatever you want to call them. And Dr. Tara Dahl does a very nice demonstration of using actual balls showing that. But this is a simpler way and easier way to remember that. So again, I'm not going to go over this. This is from LabCorp. It's a report of NMR lipid profile. Now remember that NMR lipid profile, which shows the lipid particle number and size, is a much better test. There are other ways of doing lipid particle number and size, but NMR is considered a better one. The reason I'm showing this is there are numerous instances where your patient's, you know, lipid profile in a standard lipid panel may be very good, but when they go through a lipid particle number and size and NMR, they find that those numbers are not really as healthy as they— as it is imagined. Because obviously, unless you do the right test, it's not going to show up. But I'm just showing this. This is This test is not available in India yet. Next is a CSE score. Now this test is available in India and unfortunately it is quite expensive. I think it's about ₹15,000 to ₹18,000 to get it done. Yes, the patient gets exposed to CT scan, so that is radiation, but CSE score worldwide has been considered to be a better, you know, way to know whether, you know, if you have a patient who you feel that the LDL levels are out of range and ideally should be on a statin, but the patient doesn't want to be on a statin. How do you decide whether the patient should be on the statin or not be on the statin? Doing a CAC score is a very good option. So a CAC score of 0 means the, the, the patient's risk for the next few years— I think it's 10 years usually— is not high at all. So in such a patient, you can probably withhold the statin. But one very important thing is you need to remember, and I'm assuming all of you use electronic medical records, but if you don't, even if you're writing on pen and paper, make sure that you make a note of what you had suggested, that based on your, you know, your lipid profile, I think you need, and your other risk factors for cardiovascular disease, you probably need to be on a statin. But at the same time, note that if the patient says, I don't want to be on a statin, I was last time I was on a statin, I felt terrible. All those things you need to record in your chart so that when your cardiologist colleagues sees your notes, knows that you did put a lot of thinking into it. It's not just like, oh, statins are bad, so you should just stop them. So CAC score, I wish the test was cheaper in India because in India patients have to pay for every possible test. So there is no healthcare to cover this. In Canada, we have healthcare covers this test. So it's easier, but it has to be recommended by a specialist. When it comes to statins— now, Dr. Preeti, how am I doing for time?

Okay, I think I have another 7 more minutes, 7 more minutes for the talk, and then maybe—

okay, so I'm going to rush through this. This is again, what are the important questions when it comes to statins? So LDL is actually a surrogate endpoint. And most of the time when you read papers, you will find that, oh, this medication reduces LDL by 50%, by 25%, by whatever percent. But the question you want answered is, does that translate to lower morbidity and mortality? Now that does— most of the studies are not designed for that long because obviously you cannot do a 2-year study or a 3-year study to know what is going to happen. You need long-term studies, and long-term studies are extremely expensive to do and not always possible. Now statins, when it comes to statins, of course, all of us are familiar with the LDL lowering effect of statins, but statins also have some other effects. One of the major ones is lowering C-reactive protein. In fact, I'm sure many of you have read this— sorry, years ago when they came up with these papers where they found that probably the CRP lowering effect of statins is more important than the LDL lowering effect. And you can see here where exactly. So statin is an HMG-CoA reductase inhibitor. So this is where it functions. And in the other slide, when I talked about brain cholesterol synthesis, I went from acetyl coenzyme A to farsenyl. So these are the three in-between steps. So this is where statins act. And the important factor to remember is when a patient is on statin, obviously this enzymatic pathway is blocked. Everything downstream from that is also blocked. So obviously the effects can be— and many of these things we don't know all the effects. Like I was talking about desmosterol, we didn't know about desmosterol early because a lot of the research is still— a lot of the research is being done, but it does not reach the clinician very often. So what are the other effects of statins? Plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity. So when it comes to lowering CRP, you know, I always tell my non-functional medicine colleagues that, you know, you all have only one tool in your toolbox— a statin. That is the only thing that's going to reduce CRP. As a functional medicine doctor, I have a whole lot more tools in my toolbox. So the thing is, if it is only CRP lowering effect that you're looking for, then maybe there are all these other things you can try first. And then either the patient can be on a much lower dose of a statin if it is the CRP lowering effect you're looking for, or if the patient chooses, they can decide that, okay, I want to give it a shot. I want to get off the statin for some time and see how I do and how my CRP does. So for us, you know, managing higher levels of inflammation is not just putting the patient on a prescription medication. We have a whole lot more tools. Then the next, this is a slide when I showed to some, you know, there was a cardiologist and so I was talking at an event. And the cardiologist said, I don't believe this. I said, where does belief come into this? I'm quoting an actual paper. So most of the time what happens is we live in, you know, a caterpillar world. Like if statin is supposed to be recommended when LDL is high, then we just recommend the statin and not think about what am I really doing for the patient. And this is just one paper. There are numerous other papers as well. And if you want to read Dr. Asim Malhotra's book that has a whole lot more about— so you can see in secondary prevention it is just 4.1 days, and in primary prevention it is 3.2 days. So maximum number of days you're saving a patient could be just 4.1 days. Now again, everything has to be in context, because if the patient is not someone who's going to make therapeutic lifestyle change changes and their CRP is very high and LDL is out of range, they have diabetes poorly controlled, they have hypertension, then it is possible that a statin can be one of the solutions. But it's not necessary that's going to be the only solution, of course. But you need to choose which patients you need to prescribe that for. Again, I'm not going to go over this slide in the interest of time because this is something very important. This is a fairly new paper came out in the JAMA. So statins and worsening diabetes mellitus. So what did they find? They found that insulin treatment initiation was faster. Hyperglycemia was, you know, significant hyperglycemia after starting statins. You can see that all the different— so diabetes essentially got worsened. When it comes to women and cardiovascular disease, February is Heart Disease Month. And I was telling Dr. Preeti, I'm wearing this. 13th February is Women and Cardiovascular Day in Canada. So her heart matters. And women and cardiovascular disease, a lot of other additional risk factors are present which many people are not aware of. And I'm not going to talk about them today because we don't have time. But diabetes and high triglycerides and particularly hypertension are much bigger risk factors for women than in men. So a woman and a statin is, is, and if it raises their blood glucose levels, may not be a great idea because the other thing is Women and statins, there is no data. The, the bold is mine, so I have accentuated that. And this is a very good paper to read. So again, the same cardiologist told me, oh, this could not be true. I said, you know, doctor, this came out in your journal, in Circulation, so I'm not making it up. So although an optimal lipid profile is a measurable objective in the prescription of lipid-lowering therapies for women, We don't have data supporting, you know, using a statin for women. And so it still remains elusive for women, but we are still going to give them statin and still going to make sure their brains don't function anymore. And then we're going to say, oh, you're menopausal, you see. So that is why this has happened. And just deal with it, you know, you're just getting older. So anyway, this is a very good paper to read as well. So what are the causes of abnormal lipids? Again, I'm going to rush through this a little bit. Back in the days before the pandemic, I used to have hypothyroidism before infections, but now in, uh, the coronavirus pandemic has taught us about a lot of different lipid abnormalities. And as you can see, I think one of you had a question about very low LDL or low HDL. So patients who had very low HDL and low LDL at admission, they, they were much more severely ill. And interestingly, LDL and HDL had a, you know, had a relationship with CRP. So the higher the CRP, the lower was the HDL and LDL. Now what we don't have information on is, can artificially changing these LDL HDL levels, would that impact, you know, prognosis? We don't know that because pandemic is very new and no one has really actually looked at that yet. But this is important to remember because you are going to get lots of patients now who have already recovered from a coronavirus infection and their lipids may be abnormal. So recently a paper from, I think this was a paper from Wuhan, where they looked at lipid abnormalities 3 to 6 months later and they found that many of these abnormalities went away without doing anything for them. So obviously the question arises, why do these things happen? Now, I don't know how many of you are familiar with immunometabolism. This is a very interesting topic. And in fact, I had done a video more than a year ago with some clinical immunologists from SGPGI Lucknow about immunometabolism in the COVID pandemic. So basically, what does immunometabolism mean? Every— it's not just the immune cells. Every cell in the body needs energy to function. Now, the energy substrates, as you know, for different things, there are different substrates. Glucose forms one of the substrates, then proteins can be substrates, and fatty acids can be substrates as well. In the coronavirus pandemic, we have found that numerous studies telling us that the patients' prognosis was very often decided by the blood glucose levels at admission, and these were not even people who had diabetes. So higher the blood glucose on admission, worse was the outcome. And the unfortunate thing is many of those patients, if they were put on insulin in the ICU— now that is a standard practice, how are you going to bring blood glucose levels down in the ICU— those patients also did not do very well. So bottom line is we need to maintain blood glucose levels as low as possible before any infection develops. So when it comes to immunometabolism, and that is where a lot of the cholesterol abnormalities come in, you can see that, you know, each cell has a different pathway which it uses. So one question which no one has, of course, the answer is not there yet. Maybe we will have the answers in the future. Hopefully. That's what I was telling these immunologists. I said, just as in the, you know, in Western medicine world, people are always looking at drug targets. In the functional medicine world, we are always looking at, can I treat it with any lifestyle changes, particularly food? Or next, this thing would be, can I treat it with, you know, any supplementation? So for example, one of the things— again, no answers for that yet. As you know, a failing heart or a failing brain or even a failing liver uses more of ketones. So is it possible that we could provide ketones from outside, either nutritional ketosis or exogenous ketones, and make that particular organ function better? In brain, there is some research, and I think heart, probably one or two papers where they use exogenous ketones. But when it comes to an infection, does it mean that at the beginning of the infection we need to give them more proteins so that those particular immune cells which are going to build the immune resilience, they can utilize the amino acids as a fuel versus having more of glucose in the bloodstream. And then by default, it's the glucose that gets used. So we don't have answers for that yet, but maybe a time will come when our dietary recommendation is going to become much more specific where we can say, okay, These are the parameters, and that can come from— I'm being a little, you know, futuristic in my thinking— in the worlds of metabolomics, proteomics, transcriptomics, all those things will come in the next 10 to 20 years. Medicine is really going to change a lot. It's already changing. So maybe we're going to do a metabolic, metabolomic assay and find that these are the metabolomics, you know, pathways which are affected, and maybe using a higher protein diet here versus a lower carbohydrate diet will help. Or in this situation, maybe adding a little bit more of carbohydrates which are not fast carbohydrates, a little slower digesting carbohydrates will help. Maybe in this situation it's going to be fat which is going to be better.

So we've exceeded a few minutes. If we can, we'll have to quickly finish it.

Yeah.

Yes.

So now going to your questions, so these were the questions that you sent me, Dr. Preeti. Now the first question was about the high triglycerides. Now this is just— these are— this is one slide that I'd like you to take a look. Most importantly, first rule out all the possible reasons, and the commonest ones I have found is people think they are on a lower carbohydrate diet than they actually are on. So that would be a big one. And uric acid and fructose consumption is very important. So that is something important to check. And sometimes people are having a lot of fruit smoothies thinking that it's very healthy. That is not healthy. And for uric acid, that is a much bigger problem. But all of you had a lot of questions on omega-3. So the omega-3 question was— there are quite a few of them. One is, okay, low LDL optimal to be maintained. I think you can answer that. Total cholesterol is high with high LDL, that also you need to see if there's particularly— what are the reasons? Hypothyroidism is a common one. So what are the good sources of fat for vegans? It would be avocado, nuts. Vegan sources for fat on a keto diet would be same because fat doesn't raise blood glucose levels. A keto diet is carbohydrates less than 20 grams of carbs a day. Seed oils in autoimmune conditions? Yes, Many of the seed oils can be very inflammatory, but again, it depends on the processing. So some of the traditional oils as well. So if you look at, for example, mustard oil, mustard oil, which is in India, I think it's called the kachighani mustard oil, which is minimally processed. That is very different from what comes in Tetra Paks. A lot of the problem with these oils is in the processing, and sometimes you don't know where the processing is, like what the processing is. Interpretation of fatty acid profile report. I usually go by what the company— the recommendations the company comes up with. There is nothing. So just if you read that report well in detail, spend some time on that, you will understand. This was— these were the next few questions were about omega-3. So that is where I'm going. So this was fish oil and bleeding. Now in the OPERA trial, they used this very high dose of EPA/DHA, 8 to 10 grams. And you can see that these— and these were cardiac surgery, not just any old surgery. They were given this very high loading dose and nothing happened to their bleeding. On the contrary, they required less blood transfusion. And these were surgeries like CABG and all those. So that is one. But the other important question, which I won't have time to answer today, is many of you have probably Read recently that the STRENGTH trial report came out where they talk— they found that risk for AFib had increased in people using omega-3s. Now for omega-3s, just write down the name Dr. Bill Harris. He is the founder of the test OmegaQuant, and he's been in the omega-3 world for many, many years. Lots and tons and tons of research papers. So just watch his videos. Those give you a lot of information. So that Brings me to the end.

Thank you.

My presentation—

I have two more questions for you.

Go ahead.

How do we increase HDL?

Uh, okay, how do you increase HDL? One of the ways is, of course, you have to find out what is causing it. Is it an infection? Already I've talked about all those things. Exercise can increase HDL, but exercise, again, the The problem is just a walk in the park is not going to raise HDLs. It has to be moderate-intensity exercise. Moderate-intensity exercise means exercising at a level where you can speak but you cannot sing at that level. So when you are, let us say, when you're doing weights or something like that, so moderate-intensity exercise is a good one. But why would you want to increase only HDL? And, you know, it has to be— everything has to be in context. And one, someone had a question, uh, how do we decrease a high HDL? Again, my answer is the same for all of them. First, find out the reason why. And if you can't find out the reason, sometimes what happens is when you have fixed everything else, you've managed their inflammation, you've managed their blood glucose levels, you've gotten their blood pressure down Sometimes you will be surprised to see that all the other parameters which you are not really looking at have also changed. One question is about a book for laypeople. So, and everyone is Ruhia Agarwala here, so I don't know whom I'm addressing. Dr. Asim Malhotra's book, My Statin-Free Life, is a good one. And Zoe Harcombe has written quite a bunch of books. Then Nina Teicholz's The Big Fat Surprise is a good one as well. So those are, you know, for educated laypeople. When you are on in this webinar, I am sure you know more than the average layperson. Dr. Malhotra's book is actually just 250 pages. I think it's quite a good one, and it's a very simple and—

sorry, very simple and a nice one.

Yeah, perfect.

So last question, um, Dr. Kaur, I know your time is also, you know, you have another things to do. Your morning has just started.

Yes, almost 7:30 in the morning here, so it was like, right, post-COVID vaccination, you know, patients are getting high triglycerides.

Do you recommend anything in those patients?

See, other than recommending lower carbohydrate diet and omega-3 fatty acids. So my recommendation for higher triglycerides does not change because it is post-vaccination. So it's very likely because of some immunometabolism problem. So in autoimmune conditions, many of them have, you know, abnormal lipids also, and most of those patients, the lipids are fine once the autoimmune condition is dealt with. So one is give the patient more time But the other thing is, was there high triglyceride present even before they got the vaccine or they got the COVID That is also one possibility. So in such a patient, I would definitely look at a lower carbohydrate intake because, as you know, higher carbohydrate, more of, uh, more of problems with blood glucose and insulin resistance. And so another question is, okay, omega-3. Now the question is Omega-3, I don't use any supplement company in India because it affects my brand, because most of those companies available on Amazon, you don't know the quality at all. So what I do for many of my patients is there is one company available in India now, and it's very new. It's a liquid omega-3 called Balance Oil. They also have an omega-3 testing, but it's quite expensive. It's like ₹7,500 for one month supply. Yeah, and so it's not sustainable for a lot of people because 7,500 is not easy. So what many of my patients do is when they have relatives or friends visiting from the US or Canada, I ask them, I ship it to them and then they take it there. And sometimes patients are traveling back and forth too, so they can do that as well. One was a question on uric acid. So, um, oh, where did that question disappear? So uric acid is actually— I don't have time to talk about uric acid today. So uric— high uric acid is a risk factor for cardiovascular disease, hypertension, and most of the time the commonest relation is higher carbohydrate intake, more sugar intake. But uric acid is more related to fructose intake than any of the other carbohydrates. And if you want to know more, you can just Google Dr. Richard Richard Johnson. In fact, Dr. Johnson is coming up with a book very soon. Dr. David Perlmutter is coming up with a book very soon called Drop Acid. So high uric acid is not just about gout, it is way more than that.

And most of the time, a lot of times it's telling you that the body is inflamed, and the moment you settle the inflammation, I've seen uric acid dropping dramatically without doing anything else. So I've seen cases from 13.2 to 6.2 in a month's time.

Yeah, it can do that, but 6.2 is also on the higher side.

On the higher side, but from 13.2, I was surprised myself. What have I done? I didn't know, but in fact I think the cause—

and the other important thing that a lot of people are not aware is high uric acid levels are also related to higher blood pressure levels. So they found that when you drop the uric acid levels, blood pressure has gone down by 2 to 3 millimeters. And sometimes 2 to 3 may not sound like a lot, but some medications can reduce it by just 2 to 3. So if by just dropping uric acid, this has gone down, so, and it also reduces one more risk factor for cardiovascular disease. High uric acid is also related to bipolar disorder. Yeah, so in patients with bipolar have been found to have higher than normal uric acid levels.

One thing which you had spoken in your session was high CRP and dyslipidemia. Um, anything, uh, you do in patients where, you know, you've tried a lot of anti-inflammatory and everything but CRP is not coming down?

One of the reasons we find is, number one, of course you need to rule out acute inflammation. Because chronic inflammation does not have any markers. It's just that if the CRP persists long term, that is when we look at it as a chronic inflammatory marker. Likewise with ferritin, just ferritin without iron studies will not tell you whether the ferritin is high because of iron or is it high because of inflammation. Now obviously anti-inflammatory lifestyle is what we talk about. So you need to do a review of their lifestyle. Are they sleeping well? Are they moving enough? Are they sitting continuously? Food is the biggest source of problems. Then comes periodontal disease. So gum bleeding is an easy way to ask, do you have gum bleeding? And send them off to a dental dentist. Now unfortunately in India, a lot of the tests that are available here where they look for, you know, oral cavity is extremely important when it comes to the microbiome. So there are tests available here. Those tests are not available in India, but that does not mean you cannot send the patient to the dentist to at least look for periodontitis. That is a common underreported and falls below the radar. Periodontal disease has been associated with Alzheimer's, with cardiovascular disease, with as a trigger for rheumatoid arthritis. So oral health is extremely important as well.

Right, perfect. Any other questions? If somebody has, you can write in the chat box.

Otherwise, We will have to, you know, yeah, or maybe you can even unmute yourself and, you know, ask. And I would—

so there is one more question, Dr. Kaur. How can we decrease a high HDL of more than 85?

Yeah, I've already responded to high HDL. Okay, I've said the same answer. It's like, go back and look for the causes, and if you don't find the— and if you don't Find a specific cause, fix everything else, and sometimes you'll be surprised to know that, you know, these other things change.

Anybody wants to unmute themselves and ask any questions, please feel free to do that. You can raise your hand.

I wish I could see all of you, and maybe sometime in the future I'll be able to meet you all in person.

Definitely, Dr. Gaur. I think we all can switch on our videos if, uh, That's okay.

Yeah, so someone has raised her hand. Now thing is everyone is really—

please unmute yourself and talk. I have allowed all of you to talk. Uh, liquid omega-3 is zinzonia oil.

Zinzonia is the name of the company. Yeah, the name of those— this thing is Balance Oil.

Balance Oil.

Yeah, Dr. Shabnam.

Yes.

Okay, I'm Dr. Sandeep here. I don't know whether you can see me or not.

I can't see— I can't—

anyway, I can't see the camera button here, but nice, uh, listening to you. Uh, I think that triglyceride is a more major problem for cardiac events rather than the cholesterol. Maybe I joined a bit late in between you.

Yes, I did talk about that. It is, you're right.

So the— my thing is that lipoglycan— I know how triglycerides are linked with carbohydrates. So like, besides lifestyle management, reducing your carbohydrates What about drugs like, um, saroglitazar, etc.? How comfortable are you with them, or not comfortable with them, in lowering your triglycerides? Because I see saroglitazar is a good drug. It lowers not only the triglycerides, it is very good for many other conditions also, decreasing insulin resistance and all that.

Dr. Sandeep, I'm— what is the medication you're talking about? What is the generic name?

It is coming in India with the name of Lipoglin.

What class of drugs is it? I'm not familiar with it. So for me, the best— this thing for triglycerides, first is of course food, the next is higher dose omega-3 fatty acids. And today I didn't have time to talk about all the different preparations. And so most of the papers have looked at, which have looked at reducing triglycerides with omega-3 have been with higher EPA. And in India, you don't have too many options because you don't get different EPA and higher EPA, higher DHA. But ideally, the best way to find out how much omega-3 is to be given would be to do an omega-3 test. That would give you way more information. One of you had a question about higher dose of omega-3s. So, seraglutide— sorry, I'm just trying to Google it. Can you just give me the spelling?

Uh, it is coming with the name of Lipoglin. The generic name is Lipoglin. Yes, somebody has typed it. It is a very good drug because I find a lot of positive actions with this medicine.

It is, uh, which is a PPAR inhibitor. Okay, I, I have no idea about this.

It is PPAR agonist, not inhibitor.

Okay.

And it has also been used for preventing fatty liver also. It is one of the medicines that is being approved for the use of fatty liver also. That's coming.

The thing with fatty liver is there is no approved treatment for fatty liver pharmaceutically. It is still lifestyle management. And there are some studies using semaglutide. So semaglutide, again, the basic— this thing is the weight loss benefits from semaglutide which have helped fatty liver more. But Dr. Sandeep, if you have had good experience with this, maybe next time you can tell us about it. I have no idea about it.

Yeah, I find it very good because it has multiple roles of action. It lowers the insulin resistance, and I have not come across any major side effect. I've been searching very intensively in the literature also. It is comparatively very safe. And when we look at the PPAR agonists, they have many benefits. Lowering inflammation, decreasing insulin resistance, lowering triglycerides, improving your fat liver. So many, many conditions it has got a good role.

That is what I said. I always believe in a combination of pharmaceuticals as well as lifestyle, because lifestyle changes are not easy, number one, to start and maintain. Because if lifestyle changes are not maintained, they are not going to maintain those benefits.

And they take time to show results, and the client is not ready to wait.

Sorry, Dr. Preeti, someone else had raised their hand. Now everyone is Ruhi Agarwala, so I don't know.

So there is another question, is how to decrease very high ferritin?

So number one is find out what the cause is. Is it high because it's an inflammation marker, or is it high because of high iron? High iron is very uncommon in India because most people are actually deficient in iron. So again, how you would look at inflammation, you know, how you are going to take care of inflammation, use the same method. So is it only ferritin that is high? There is one entity called the hypoferritinemia of autoimmunity, but in those cases ferritin is like more than 500. That is a different story. That then you have to look at the autoimmune conditions and deal with it like you would with any other autoimmune condition. But if it is an inflammatory marker, definitely you need to look at How to reduce inflammation? Where is the inflammation coming from? Is it an acute inflammation? Is it acute? It's an— is it an UTI? Is it a recent COVID infection? So just go back and check what are all the, like, sort of checkboxes.

Sorry, please rename yourself, everybody. All of you are appearing as Ruhi Agarwala, and somebody has raised the hand, so you can just—

that's That's me. My name is Dr. Kohli. Yeah, hi, Dr. Vascular Surgeon. And first, I must compliment you on your excellent presentation. And thank you, Dr. Kohli. Well, you're welcome. As a cardiovascular surgeon, I've learned a lot today. So, Dr. Kohli, if you're really interested in this, I would suggest that you, uh, read up on the books by Dr. Mark Houston. He is the metabolic cardiologist And if you listen to Dr. Mark Houston, you'll feel, oh my God, I'm— am I ignorant? Okay, I'll certainly take your advice. Well, I had one question, and the question is that what is it there in South Asians, uh, in their lifestyle which prompts them to develop CAD? As you mentioned that it is a non-modifiable risk factor. Anything specific? Dr. Kohli, that's a very good question. Now, we don't have a specific answer in the sense that Everyone says, oh, it's genetics, it's genetics, but we had the same genetics for so many years. We didn't have this high cardiovascular disease earlier. One of the factors— there are numerous, so, and I can't say which specific one would be more important. One is air pollution. That has been found to be a recent, fairly recent, in the last several years. And you know that in India, air pollution is extremely high. The other is the sedentariness. Because if you, you know, I often say 1982 television came to India and brought with it cardiovascular disease. Because before television, I think a lot of the older people particularly who retired, they didn't spend so much time watching TV. So sedentariness is another one. And again, you know, just instead of— we have this tendency to blame the patient, they don't move, they don't— but where are they going to move? So We have to find ways of doing that. So sedentariness and also a lot of the work we do nowadays, like my son calls me a laptop doctor because I do teleconsulting. So I make it a point to stand when I'm doing my consults because this is again, most of us, the way our work is designed. Now as a vascular surgeon, of course you're standing in the OT, but for a lot of doctors, that's also not— not only doctors, it's even in the corporate world, they don't have the way to Use a 60Hz.

Sitting all the time and blue light exposure is another thing which is adding to.

Yeah, so sedentariness is another one. The other important factor is the food. You know, essentially, if you look at Indian food, people have not changed what they are eating. Essentially, they are still having roti and rice and, you know, all that stuff. But the roti and the wheat and the rice, the grains have changed dramatically. Like, if I always give the example of, I come from rice-eating part of India. So back when we were kids, our rice used to have those little husks. They were not this ultra-refined, each and every grain is exactly the same size. So the metabolic response to that minimally processed rice or wheat, for, you know, depending on when, where in India you are, is very different from what it is today. Today it is ultra-refined metabolic responses. If you are using CGM in your patients, you will find how different that is. Many of the grains can be very inflammatory, raise blood glucose levels very high. So those are some of the factors. And another important factor, Dr. Kohli, is, uh, I'm sure you're familiar with the MASALA studies. Uh, it is— I forget the acronym, but that is basically cardiovascular disease in South Asians. So this is being done in the US. And they have come up with quite a few of the— so one more thing is there is a polygenic risk score, and I'm not sure how much time I have. I can keep talking until kingdom come. So there is a polygenic risk score which they came up with, and that is a genetic test. It's available. There's a company in Bangalore who does it. It's ₹7,500, I think, for the test. But the fact is, even if that test shows something specifically abnormal, What the solutions are, again, everything goes back to lifestyle. Another important factor is sleep. People sleep a whole lot less today than they did before, and the easy availability of very poor quality food that is like, oh, it's so much easy to just pick up the phone and order some. And some of the other big ones are the poor quality oils that is used in street food. So a lot of people will order a samosa or something like that. So many offices I go, it's like, why can't you have just plain tea? Why do you need biscuits with it? Biscuits are the other big ones that are killing Indians.

How hard you try, we are not able to stop it, means at least a lot of us. So Dr. Kaur, the discussion has been very, very interesting, but we've exceeded our time and we would have to end the session here. Of course, Of course, if you have any questions, you can always share and I can request Dr. Kaur for her insights into it. Thank you, Dr. Kaur, and we will share the recording of this session. Uh, initial 10 minutes were not recorded. Somehow I forgot to press the recording on. I'm extremely sorry about that, but most of the session is here for us to re— you know, so that we can get more insights when we listen to it again.

Thank you, everybody. Thank you for investing your time with us here today, and I look forward to maybe meeting you all in person in India, or maybe if you're coming to Canada, definitely visit. Bye now. Bye-bye. Thank you. Thank you.