Welcome to Dr. Warrick's podcast channel. Warrick is a practicing cardiologist and author with a passion for improving care by helping patients understand their heart health through education. Warrick believes educated patients get the best health care. Discover and understand the latest approaches and technology in heart care and how this might apply to you or someone you love. Hi, my name is Dr. Warrick Bishop and welcome to my podcast and videocast station. Today I'd like to talk about the so-called statin and cholesterol conspiracy. But before I do, there's a couple of definitions or concepts I really want to get across so that when we come to talk about the crux of the issue, you understand the context in which we will be putting it. So first of all it's really important to understand the difference between primary and secondary prevention. Now historically we've only known people to be at high risk of a heart attack when they've had a heart attack. We haven't been able to identify someone before that event. Stopping someone having another heart attack Having a second event is called secondary prevention. Stopping someone having an event in the first place is called primary prevention. Well, of course, if you've had a heart attack, you've defined yourself as someone who's at high risk. So clearly secondary prevention intervention will pay the greatest dividends. if we, because we know who we're dealing with, whereas primary prevention intervention is a much harder thing to get a dividend from because we're looking at a large population pool and wondering who within that population pool is going to be at risk, therefore potentially treating all and therefore the costs associated and side effects associated or treating none. and therefore having people in that cohort having an event. So primary prevention, stopping the first event occurring in the population. Secondary prevention, occurring a second event in the individual. Really, really important that you get that. It's also really important to understand the difference between association and causation. Now we get that confused when we're talking about all sorts of things and it gets confused when we talk about the role of statins and cholesterol and diet and coronary artery disease. Let me use an example outside of medicine to define or give you the distinction between association and causation. If we were to think of speeding and alcohol we would all agree that speeding and alcohol in association with motor vehicle accidents is clearly an association. It clearly increases risk of car accident. But we'd also all agree that people can speed or people can drink and drive or they can drink and speed and not have a car accident. That means that alcohol and speeding are associative, they increase the risk, but they're not causative. Because if they were causative, then every time someone drank, they would crash. Every time someone sped, they would crash. Very important to understand the difference. They are associative, increase the risk of something happening, but they are not causative. They do not immediately make it happen by a direct link. It's also really important to understand the difference between individual risk and population risk. This is really reflected in risk calculators and we might put ourselves through a risk calculator process. We might find that we're at low risk. We're considered, for example, a 5% risk of a coronary event or heart event in the next 10 years. could be reframed and described in a different way. And the way that I would put it is to say a low risk tells us if we take 100 people with the same characteristics, for example my risk is 5% in the next 10 years, if we take 100 people with the same characteristics as me and follow those 100 people for 10 years, that 5 of those people will have an event, 5% in 10 years. Because the event rate will be either 100% or 0% depending on whether you're implicated with a heart attack or not. That is the individual risk versus the population risk. The population has an event rate of 5% for 10 years, but the individual will have an event rate of either 0% or 100%. So there is a disconnect. between a population-based assessment and what happens to the individual. It's important to understand that. There's also in association with, sorry, in conjunction with association and causation, it's also important to understand that we need to discern absolute versus contributory because some of the conversations around particularly cholesterol and statins have been polarized to absolute laws if you like or absolute rights when really they should be in the context of contributory. So one factor in regard to coronary artery disease is unlikely to be the full explanation within an individual. So absolute versus contributory. And this also ties in with single versus multifactorial. And I think we'd all agree one would have to be fairly short-sighted to think that coronary artery disease is a single factor process. Of course, it's a multifactor process. And so to try and get an absolute truth, talking about only one aspect of it, suddenly doesn't seem to hold water if you think it through. The problem is that the debate has polarised people a bit and we've moved to concepts of good and bad, right and wrong, rather than relative risk and relative benefit for an individual. And it's really important we get that as well because while we're standing looking to be polarised, we're missing all the subtlety, all the variation in between. So with that said, and hopefully you've got that behind you, let me kick off with where this controversy started. And it was around about 2013. There were two main papers put out in the British Medical Journal, one by Abramson and one by Malhotra. probably shouldn't be taking cholesterol tablets routinely. So individuals with less than a 10% risk over 10 years, he put that the cost effectiveness and quality of life impacts meant that this was just not worth doing. Basically looking to treat the 100 to help the 10 or less. And that's a pretty fair premise. Of course, in my own practice, I'm interested in imaging the arteries of that 100 to try and find the arteries that look unhealthy so that I can actually be more targeted in my approach, more precise for the individual. So a pretty reasonable position to offer. The second paper by Malhotra was titled Saturated Fat Not Major Issue. And he pushed back on the Ancel Keys 7 countries observational data set and really started to make the point that maybe saturated fats were being blamed and maligned unfairly in coronary artery disease. But really importantly what he pointed out was that if we reduce fats out of our major food groups something else tends to go in. And what tends to happen is that because most of our food is driven by commercial entities, if we take fat out of a food, then as a commercial entity producing that food, you have to look at what to put in. And with three macronutrients, which is fat, protein and sugar, one then has to ask if we're taking the fat out and we've got to put protein or sugar back in, which will we put in, protein or sugar? And if I were to ask a very simple question, what do you think is more expensive protein or sugar? I think that's the answer. So Malhotra was making the point that if we drive reduced fat consumption, we inadvertently drive increased sugar consumption. And this is an area of interest for me. I think that sugar will turn on insulin. Insulin is a storage hormone. If we are storing energy, we tend to store it as fat. And so the consequence of reduced fat in our diet can be increased sugar in those food products, can be increased insulin stimulation, can be increased fat gain, and the consequences of fat gain, obesity, are as detrimental as the fat in the first place. I think a really valid point and one that's certainly worth continuing to talk about. Mahotra also made advocacy of the PREDIMED trial which was released around about the same time and the PREDIMED trial was a primary prevention study taking Spanish predominantly men at high risk and subjecting them to A Mediterranean diet either enhanced with olive oil or enhanced with nuts compared to a low fat diet and this clearly showed us that the Mediterranean diet either with olive oil or nuts was superior to a reduced fat diet for those men. So a really nice reminder that all fat may not be bad. extra virgin olive oil and the nuts and nut oils may well be beneficial and that low fat of its own didn't seem to confer any significant benefit or at least it was not as beneficial as the Mediterranean diet. Well when this information came out there were some back and forth letters some correspondence which really started a debate and a bit of a heated debate at that and a professor Rory Collins who is professor of medicine and epidemiology at Oxford and a member of the cholesterol treatment trialists collaboration a group of uh trialists who had had really an interest in cholesterol management reduction of cholesterol to prevent coronary artery disease, wrote back and really looked to take apart some of the aspects of Abramson's and Malhotra's papers. Well, the back and forth from that led to the request for exposure and openness of the data that formed the basis of the Cholesterol Treatment Trials Collaboration. positions and that meant that different trials needed to be offered up and data sets collected and to be honest to a large degree as far as I can read the conversation or the discussion got somewhat waylaid in the detail of trying to get this information which had been scattered difficult to track down and it moved into a space of conspiracy now Marianne Damacy, who is an Australian scientific reporter and scientist, has covered this very eloquently and allows a recognition of some of the shortfallings in that data collection and the difficulty in obtaining it. But to my mind, that's a little bit of a sub-issue, and I'd like to take that controversy out of it. And let's stick with the facts rather than the to and froing. accusatory defensive remarks between Collins, Abramson and Malhotra. So 2016 saw Ramsden release a re-evaluation of some data from a trial called the Minnesota Coronary Experiment which had run over five years, looked at over 9,000 patients who were residents of nursing homes or mental institutions. There was some unpublished data and Ramsden went back and looked through that. Really specifically looking at the association with serum cholesterol and event, the Minnesota coronary experiment looked at reducing saturated fats in the diet by putting in a vegetable oil linoleic acid and they obtained that from either corn oil or corn oil margarine. Now there was no benefit in the Minnesota coronary experiment by replacing saturated fats with linoleic acid. Now I'm not sure exactly how we can interpret that of its own and apply it to what we would do on a daily basis. Where I think it leaves us is telling us that using a polyunsaturated fat derived from corn, which is linoleic acid in large amounts, to replace saturated fats doesn't really affect outcome in terms of cardiovascular disease in people who may be at high risk for other reasons, mental institutions and nursing homes. What it doesn't help us with is the replacement of saturated fat with extra virgin olive oil or nuts, which would be oleic acid and a mono unsaturated fat. So the Minnesota coronary experiment is really important and interesting. It gives us some insight that linoleic is probably not the fatty acid to replace saturated fats. It's not the polyunsaturated fatty acid to replace fats, but it doesn't help us with the mono unsaturates. But the significant primary prevention trial which was first released in 2013 and then with some corrections released a number of years later was the PREDIMED study. This really looked at over 7,000 high risk individuals who had not had an event. There was no question that a Mediterranean diet in hearts with olive oil or nuts was beneficial for this group over and above. a controlled or low fat diet. And I think this is a really important starting point. We know in the secondary prevention space that the DART study and the Spokane study, both of which took individuals who had had an event and put in place really predominantly Mediterranean style diets, generally enhanced with either olive oil or fish oil, clearly both showed benefit as well. So I think this concept is one of let's think about the Mediterranean diet, let's think about enhancement with particularly oleic or monounsaturated fats, nuts and potentially also omega-3 oils. In summary, remembering primary prevention. probably it doesn't make sense to put statins in the water. So I'm a bit supportive of that initial work that Abramson put out. I think reducing fats in the diet at the expense of increasing sugars is problematic and I agree with Malhotra in that space. We know that lowering LDL cholesterol with linoleic acid as per the Minnesota Heart experiment is really not beneficial for cardiovascular outcome. So maybe we shouldn't be doing it. I think the PREDIMED study stands out powerfully with extra virgin olive oil, nuts, sensible Mediterranean diet with lots of leafy greens, garlic, grains, makes a lot of sense and certainly over and above a low fat diet and certainly given the benefit over a low fat diet. points away from that of its own being an absolute or singular cause. I think we can also sidestep the conspiracy theory. I think there's been issues in the back and forth with regard to the data that's been produced, but personally I'm closely associated with a number of leading researchers in Australia. I know that the ethics of these individuals is beyond reproach. know that myself, following their lead, their guidance, we are really undertaking therapies that we believe truly to be the right thing for individual patients based on those individual patients' specific needs. In terms of secondary prevention, I think the DART... trial and Spokane again reassure us that the Mediterranean diet enhanced with fish oil nuts and olive oil is got to be the right thing to be doing. So remember we're talking about associations. We need to think about the individual. This is not a conversation about good or bad. It's a conversation about contributory and multifactorial. Well, I hope I've been able to answer a substantial amount around the cholesterol and statin conspiracy for you. As always, if you have any queries or questions, drop me a note. You know the email address. Thank you for listening. That was a long one. I do wish you the very best, as always. And until next time, look after yourself, laugh a lot, and please don't die from a heart attack. Goodbye. You have been listening to another podcast from Dr. Warrick. Visit his website at drWarrickbishop.com for the latest news on heart disease. If you love this podcast, feel free to leave us a review.
