David Stokes 0:15
Hello, and welcome to the latest episode of the Doctor family podcast. In this episode, we are lucky to be joined by a chemical pathologist who is a specialist in the diagnosis and management of a number of medical issues. They range from metabolic bone disorders to inborn errors of metabolism. However, for today’s episode, we’ll be concentrating on a major area of their work, which is the management of high cholesterol. We’ll be describing what cholesterol is, what it’s for, how having too much of it affects you and your body and what you can do about it. It was interesting to note that this interview was carried out both of us wearing masks. I suspect however, you won’t notice that but you may notice some of the noises of a busy hospital as well as the local seagulls causing a bit of mischief. So today I am joined by Dr. Kate Shipman who is a chemical pathologist, which is a specialty you may not have heard about, and we’re very lucky to have her sharing her expertise with us today. So perhaps just to start with that, you might be able to tell us a little bit about the area of your specialty and the sorts of things that you tend to look at within medicine.

Kate Shipman 1:15
So chemical pathology, I think will be most people have heard of specialties like haematology, and microbiology. So is similar in the way we share the pathology discipline. But when haematologist looking after patients who have blood problems and the microbiologist look after people have infections, we tend to focus on people with biochemical problems. So those are things that are either caused by enzyme defects and so are detected by biochemical tests or monitored or managed by biochemistry primarily. We tend not to have impatient workload, like our specialties because our rest of the time, we look after the laboratory services. So that’s the test we offer. How test is selected. Have a reported We help people interpret the results.

David Stokes 2:03
Fabulous. And in terms of the tests, there are so many tests available now, I think we could probably devote an entire episode to biological tests that are run in laboratories and the other areas such as sensitivity, specificity, that the things that people don’t tend to know about, they tend to think if you have a blood test, it’ll tell you an answer, which is definitive. And that’s the end of things. And we know things aren’t as black and white as that. But in terms of the sorts of patients that you might very well often see, and certainly the interactions that we as GPs have with you and your specialty, it’s largely around cholesterol and lipids. I think that’s that’s the vast majority of the stuff that I’ve seen.

Kate Shipman 2:40
Yeah. And I think you’ll find that’s what most chemical biologists do because most of our don’t have any lipids specifically in their curriculum, but also trained in diabetes nutrition inborn errors of metabolism, like, lysosomal storage diseases and phenylketonuria and and also metabolic bone diseases. So we have five main areas, but you’ll find that most people focus on the lipid clinic.

David Stokes 3:03
Excellent. So I think the other ones are very interesting. But in terms of today’s podcast, I think we’re going to focus a little bit on the cholesterol and the lipid side of your work, which I know is something I’ve been asked about by a number of my patients. So perhaps if we just started, we talked about cholesterol and itself, it’s something which is obviously out there in the media a lot. A lot of people are worried to know what their cholesterol levels are and how that will affect them. versus just give us a little overview of the role of cholesterol within the body normally, and then perhaps what the problem is with having too much of it.

Kate Shipman 3:38
Yes, cool. So if we talk about fat in general, probably the easiest way to start fats are defined as being insoluble in water so they are a group of compounds and there are two major groups of in fats and those are triglycerides and cholesterol, triglycerides actually, but dietary fat and they’re long chains and we break the ends of a chain off sequentially and that releases energy. So that’s for dietary fat. And that’s what we store as energy. Cholesterol is a subgroup of a type of fat but looks very different structurally actually little carbon rings, and they form cell walls and the basis of hormones like testosterone and oestrogen and vitamin D, every cell in our body actually synthesises for cholesterol we require. And so I think the first confusion that people get is when they talk about dietary fat, they think about cholesterol, was actually cholesterol hijacks and sort of sneaks in with the rest of dietary fat, but really is a very minor component of absorption and diet. I think that’s the first confusion.

David Stokes 4:42
It is and I certainly remember from my days of biochemistry, drawing out the, the chemical pathway to the synthesis of cholesterol, and you could see how very easily the body can make cholesterol from carbohydrates, the sugars within the diet. So it’s obviously an important factor which is which is necessary. What’s the problem when there’s too much of it.

Kate Shipman 5:03
So the issue is that because there’s a bit of cholesterol that sneaks in with the dietary fat once all the dietary fat has been removed from these lipoprotein particles, and we put the fat in particles because fat is insoluble in water, so it can’t to be transported around blood without being wrapped up, I think easiest ways to imagine it like people in a bus. So the bus collects all the people from a gut, and it’s almost all entirely triglyceride and a few cholesterols sneak in. And then the bus goes around depositing with triglycerides everywhere, and you’re left with the naughty people in the back of the bus. And this is the cholesterol that causes us issues. So it’s not the stuff that’s being made within cells, the production of hormones or the cell wall. It’s the stuff that’s stuck in the dietary fat. We have receptors that allow us to pick that up a bit like bus stops recognising the bus number which changes when it’s entirely cholesterol. But if you’re less efficient at sneaking, always buses up and clearing the arteries, your lack of small dents particles, which can go in between the cell walls and cause deposition there, which pushes the cell layers in narrowing the blood vessels, and that’s part of a process called atherosclerosis, which results in heart attacks and strokes.

David Stokes 6:14
But that’s very, that’s very interesting. Actually, the fact that it is a dietary cholesterol seems to be causing a lot of the problem there, the packaged cholesterol within these buses, as you described, getting lodged within vessel walls, causing this atherosclerosis, that the damage to the cell wall. Does it trigger an inflammatory response as well?

Kate Shipman 6:35
Yes. So we believe it. inflammation is a larger component to this and this is why you do see or we used to see increased rates of heart attacks and strokes for example, people rheumatoid arthritis, with the advent, all the excellent immunosuppressive drugs, including biologic agents that people now take, we found that almost obliterated the increased cardiovascular disease in people with inflammatory condition.

David Stokes 6:58
So you were saying the inflammation Just generally within the body predisposes or increases the risk of damage to the cell walls sorry the the blood vessel walls. Yeah. So I was just wondering does does the cholesterol itself trigger an inflammatory response or is it just caught within the cell wall and then there is an inflammation. Yeah associated with it.

Kate Shipman 7:18
So fat also can cause inflammation and particularly, so some of the particles do it more than others because you can get deposition with triglycerides as well. So all our fat in our diet we should absorb immediately after eating a bit like sugars, you should see more come down quickly. So people have remnant dyslipidemia as of that triglycerides and cholesterol floating about for longer, more risk of the getting that deposition. And then within that the different particle type buses, some of them are more oxidative and cause more inflammation reaction than others. So small, dense LDL, are probably the most dangerous from that point of view. And they are associated people when you do a biochemical blood test. If you Low HDL, so that’s less than one in a man and less than 1.2 and a woman. And triglycerides are at a high greater than 1.8 greatful 1.7, so 1.8 and above, and that’s associated with the atherogenic lipoprotein phenotype, which is since discovered to be due to smaller, dense LDL, which are more oxidative, and therefore cause more of a reaction that atherosclerosis. And that pattern is caused entirely by obesity. So if you see a low HDL and a high triglycerides, anyone, even if their BMI is within normal limits, that person is storing fat around the middle, which is causing the particles to become smaller and denser, much more atherogenic. And this is why HDL got a reputation for being a good cholesterol, but actually having more HDL is not protective at all. Just having a low HDL is bad. It’s not because HDL, it’s good. It’s because when HDL is low, that infers the LDL particles have got worse.

David Stokes 8:56
Okay, that is very interesting because certainly it’s something that a lot of people Have clung on to for a long time, I might have a high cholesterol, but it’s okay because my HDL cholesterol is high as a ratio. So that thinking is changing.

Kate Shipman 9:10
Yes.

David Stokes 9:12
Okay. Now, the other thing that brings me to the patients often come in and talk about is when we’ve identified that they’ve raised cholesterol. In practice, we’ll be looking at people’s risks of heart attack and stroke over the next 10 years to make to allow us to have a discussion with them about the risk benefit of taking a medication, for example, a stat into reduce their cholesterol. And I very often find them coming in a little bit like they’re trying to bargain. They’re saying, Well, how about I just try and sort my diet out first, before we consider taking a medicine because clearly, we don’t want to take medicines if we can avoid it. What are your thoughts on diet versus pills or is it not something mutually exclusive?

Kate Shipman 9:53
And so you’re right such as, whatever your problem is, if you are fitter and thinner. Particularly if you didn’t know exercise in a slightly obese, then changing that has a as big a cardiovascular protect protection and prevention as taking a tablet, because if you take both together then you’ll get double the reduction. And it also slightly depends upon what your dyslipidemia is. So if you have a pure hypercholesterolemia, which means that your total cholesterol is high because your LDL cholesterol is high, that is almost entirely genetic or hormonal. So, it’s quite common in women after menopause for cholesterol shoot up. And also it’s things like familial hypercholesterolemia. If you have a mixed dyslipidemia, where the triglycerides are high, and because both triglyceride rich buses also contain cholesterol, the total cholesterol looks higher. So you have a higher total cholesterol but it’s being driven by triglycerides which particles that is extremely amenable to lifestyle modification. And if the HDL is low and you’ve got a high triglyceride, the only way really to fix that is with weight loss. So if those are the patterns that you have, then weight loss is significantly beneficial and you can return your cholesterol to normal. But if it’s a pure hypercholesterolemia, then it usually makes very little difference.

David Stokes 11:14
Interesting. Something else that struck me while you were describing these, these different patients who’ve got different lipid fat profiles, you described some people who even are not in the overweight or obese category who sort of, unfortunately do have this collection of lipids, which is, which is unhealthy, they store the weight in the wrong place. Are they the same patients who would go on to have for example, fatty liver, so the non alcoholic fatty liver which we see more and more these days

Kate Shipman 11:43
indeed, so and we call it this, we even described it ages ago called the metabolic syndrome or syndrome x. And so if you have a, you have also been this theory called the theoretical thigh compartment, which is what you’re born with this space where you can store extra weight Once you filled that space and the rest of the fat goes in bad places like your liver, some people space is very large and some is tiny. And I’ve seen great difference in BMI as at when people present the metabolic syndrome including people at BMI as of 20, or 21. So once you’ve got that fat going in wrong place as you get hypertension, gout, diabetes, fatty liver, and PCOS, dyslipidemia, all of which associated vascular disease, and all of which are extremely easy to fix if you lose weight, but that might be one kilogramme in someone who’s already quite thin to a stone or two and someone who’s quite overweight. And it’s both as ethnic differences that Caucasians can eat more and do less exercise and almost every single other ethnicity described. Within each ethnic group. There’s variation within families, and they’re just some people who can’t really eat.

David Stokes 12:50
That’s fascinating and depressing at the same time. In terms of the other the other treatment that we’ve talked about for cholesterol, which is statins, which I think we’ll talk a little bit more about in a minute. Is there a significant role for statins in people? Who are for example, storing fat in the liver? Is that something that helps at all?

Kate Shipman 13:06
Yeah, so it will, you’ll still get the same benefit from whatever the condition is if you look at people with heart disease because of diabetes or heart disease because of high cholesterol, or heart disease for any cause, if you reduce the cholesterol by one millimole everyone gains the same reduction in CVD risk, cardiovascular disease risk doesn’t actually matter what the problem is. So if you’ve got a risk, because you’ve got a metabolic syndrome, the status will still reduce your risk. It doesn’t mean however, of course, this one risk can bring back even better if you then lose the weight on top were somewhat of a genetic dyslipidemia wouldn’t have that ability to change or dyslipidemia, but they would also gain cardiovascular benefits of being fit and trim, but it just wouldn’t cause you a biochemical resolution.

David Stokes 13:48
So I think the other the other the other part of that, obviously, is that we’re seeing in these people who are storing fat in their liver, that liver function is decreasing and they are at risk of developing. cirrhosis of the liver down the line. Obviously, losing the weight is going to be the biggest part of that. But does does a stat in make any difference as far as you’re aware to the to the lipid within the liver?

Kate Shipman 14:11
Not that I’m aware we don’t build it as a preventative for cure for that. There are some interesting stuff in but really, I think at the moment, its weight loss,

David Stokes 14:19
just gonna lose the weight. Okay. Yeah, again. So another sad, depressing story there. So if we come back to the main treatment that we have for our patients who have got a raised cholesterol, particularly the ones who’ve got the, the more dangerous for which is likely to form these atherosclerotic plaques, these lesions within the walls of the arteries. What was the role of the static, what do we know that’s doing?

Kate Shipman 14:47
So we’re statin basically blocks part of a cholesterol synthesis pathway, so blocks an enzyme called HMG co A reductase, which is rate limiting step. So it slowed down your cholesterol synthesis, which means that you have to Put more of those sort of bus stops those receptors on your cell membrane and take up more of those naughty buses going past because you can’t make as much as you could before. And you still require some cholesterol. So it clears out the blood vessels by slowing down your own production of cholesterol. And it’s nice and safe. We’ve shown even in in vitro experiments, but actually, your steroid hormone production, for example. So cortisol, the stress hormone, if you put a an HMG co A reductase inhibitor, such as the Staton into the salesman stimulate the sales to make the steroid hormones from cholesterol, all of these pathways continue in the presence of the status because there’s so much capacity, so just slowing it down a bit. So you have to clear the cholesterol that’s knocking about out of the blood,

David Stokes 15:40
taking it from the wrong place where it’s causing mischief. Yeah, great. So the other problem, obviously, is that statins have got a terrifically bad press. There are a lot of enemies of the stat out there. What’s your take on that and how do you express that to the patients that you’re seeing?

Kate Shipman 15:57
So generally the risk has been is very low. So you do have a lot of people talking about joint aches particularly. So the problem with statins is but one in 10,000 people can get rhabdomyolysis, which is head to toe muscle breakdown. And it happens if you have a flu, for example, and everything hurts, you can’t move out of bed. It’s not a permanent thing. The muscles regenerate quite quickly. If you were doing perhaps gardening or something like digging up your hedge when you’re not used to it, you know, but the back hurts next, and your legs hurt next in your arms hurt the next day. That’s rhabdomyolysis. So it’s quite a common sort of normal phenomenon, but this is just being caused by a drug. So we want people have it and I think a lot of people have therefore misinterpreted joint aches, etc, to rhabdomyolysis. So if you had rhabdomyolysis and statins, all your muscles should be painful and tender. It’s not joints, and you’ll see a nice raised. CK, which is a blood test of the contents of muscle cells being released into the blood. So the vast majority of people I see with issues tend to describe joint aches and their CK are completely normal. So there’s no objective evidence tool of any functional problems. Often you see that there’s a background of having joint aches long term anyway. I think there’s some confusion also that if you look at the trial rates of muscle aches always high, but it was high whether you had a sugar tablet or the Statin. So I think part of it is that the population groups are generally tweeting or people who’ve had heart attacks and strokes, and therefore are older and more likely to have musculoskeletal complaints. And we also know there are quite a few problems say, for example, after stroke often people feel really tired for about a year and it takes them years suddenly of any lack a new person again, and they don’t understand why they feel so bad for such a long time. And there’s probably a real argument or something to that brain injury but makes people feel ill and achy. Also, we start things like beta blockers, antihypertensives, all of which can have real side effects. So I thinkstatins get attributed to a lot of these and actually, they’re not the agent of problems. And then you’ve got the converse of people who haven’t got any disease at all. We’ve been starting to Staton and don’t really want to be taking a tablet. So then I think they attribute aches and pains but they’d normally just ignore to this new medication because they’re not particularly keen on take it in the first place. And so it’s not saying that you can’t get rhabdomyolysis, I’ve seen one case of it. And I do nothing really but statin to pedal. But it’s quite obvious and it’s quite distinct condition. So generally they’re very safe and they’ve actually studied on women children now for quite a long time and children have never had a documented side effect and the safety data so overwhelming that they actually got ethics to do trials in pregnant women and have completed the safety trials and pregnant women and even the foetuses are fine. So as a class of drugs, extraordinarily safe in comparison to, hypertensives, which have common side effects,

David Stokes 18:40
yes, those are fascinating. I often go down the route of showing them the benefits that they will have in terms of the reduction in risk of death or disability from a heart attack or stroke and then allow them to sort of make their own decision but often I will say have a try. And then if you do run into problems, then stop it. The problems aren’t permanent

Kate Shipman 19:00
But I think that’s a good point is that the stat in side effects if they are, it’s temporary. Whereas, you know, a dense hemiplegia from a stroke is permanent. And so if you can avoid that with a tablet, no side effects, it’s worth it. And if you have side effects when you just stop it.

David Stokes 19:13
The other thing, which I think is come out fairly recently is the benefit of statins. For the older adults, there’s been a lot of pressure on general practice, particularly, but I suspect in hospitals as well to Deprescribe to stop prescribing medications to people when there’s an uncertain benefit. And that’s often the case later in life. Now, I believe there’s been some recent data, which suggests that there is potentially even more benefit in older adults as well.

Kate Shipman 19:39
Yes, and I think part of the problem with the data is that you want to people, probably the benefit increases with time off. So if you’ve got someone with familial hypercholesterolemia, then starting it at the age of 10, may give them 70 years of life as you’re starting at someone and 82 is always going to die at 88. If you get them to 86 and a half, then the benefit looks smaller. Also, if you’re starting to treat In older groups, often they are the people you whittled out the undiagnosed genetic dyslipidemia is the type one diabetes, the other problems, of course, premature vascular disease, you already got a group of people who’ve probably got genetically excellent arteries , and they’ve got a good genetic hand of cards. And so therefore, the benefits look smaller. But we know that economically and also clinically, there is benefit. And now because our populations are so healthy and have a really good and healthy retirement if you’re healthy, and fit, and you don’t want a stroke, because if you have a stroke, Well our medical care so good, we’ll keep you alive for another 10 years, you can’t guarantee that that will be your final event. So if you can prevent it to the time when you’re Fair enough, it is your final event, sort of play hedging your bets, really. But yes, there is and it’s particularly if you’ve got diabetes now out of age that there are benefits even more because that’s another vascular risk factor.

David Stokes 20:53
Excellent. We’ve discussed a lot there about about the risks that the statins pose or in this case, don’t pose The benefits that they confer on patients in terms of reduction in risk of heart attack and stroke. We’ve also talked a little bit about why some people might start on them. So people who’ve had a heart attack or stroke, they will be started on one is what they call secondary prevention to try and prevent further episodes where there’s a very clear and obvious benefit to the patient. Then there’s the primary prevention, so the people who we’ve just identified as potentially having a slightly increased risk of heart attack or stroke over the next 10 years, using various risk calculators that we might use in practice. But there are another group of patients for whom the calculators might not be quite so good. And those are these people with what we call familial hypercholesterolemia. I wonder if you tell us a little bit about that.

Kate Shipman 21:44
So familial hypercholesterolemia is quite a common monogenetic condition, which means there’s one gene view and have it from either parent, which gives you a high cholesterol from birth. And the problem is there’s a mutation in either the bus number or a bus stop for those LDL particles which are ones which happened remnant The cholesterol left in the Dutch particle and these ones that caused the atherosclerosis. So it means that part of your so half of your system that recognises it is blind and cannot see the particles so you don’t think you’ve got any and you can’t take them up. It’s completely asymptomatic. Having the high cholesterol doesn’t really do anything doesn’t make you feel ill until you have your first event, which can be heart attack or stroke or peripheral vascular disease. And this can occur as early as in childhood and late teenage years. And there are you can sometimes see collateral deposition around the eyes. So which is yellow stuff on the eyelids called xanthalasma, or corneal arcus, which is a white ring around the iris. You can see tendon thickening, so lumps in tendons, but only the lumps and tendons are pathognomonic, which means it’s that’s the only condition it really causes it for cholesterol manque around the eye can occur of anyone but cholesterol greater than three. But usually we say that if they’re older than 40 we’re less suspicious for younger than 40 we’d be much more suspicious for them. Underlying genetic condition. It’s very common. There’s more than 2000 mutations described at every single population around the world. And we think that the cholesterol mutations confer benefit against gastrointestinal illnesses. So it saved you from dying of cholera in childhood. And of course, in the old days, no one lived to see a pension. So dying at 40 of a heart attack wasn’t a problem if you could survive childhood. So I think that’s why it’s so common that people have so much high cholesterol. But if you look at some of the hunter gatherer tribes, collaterals tend to be out free or lower. And our LDL receptor is only designed to work up to a level of 1.8. And most people’s level is about 3. It shouldn’t go any higher than that. And in the new PCSK9 trials, he got people down to LDL cholesterol zero, and we just get better quicker. So we don’t actually need that cholesterol set plating we’ve been there’s so many mutations pushing it up because of that gastrointestinal illness protection.

David Stokes 23:51
So you mentioned this, this new treatment. This is something that you might have read about in the tabloid newspapers. It’s an injectable treatment to lower cholesterol. Yes. And I think There’s some quite favourable evidence coming out from that standpoint. So

Kate Shipman 24:02
it supports us in the theory that reduction of LDL cholesterol is good and that there was no lower limit. So this is the first time we’ve been able to render people have an LDL cholesterol of zero. And indeed, they showed tremendous benefit and the benefits were linear. So there’s no it doesn’t get less benefit when you have a lower values. One milimole reduction, whether you’re starting level was 14 or two, still has the same benefit. It’s fascinating drug actually, because they discovered a some families who have zero cholesterol, and have always had zero cholesterol, and seem to live forever have no heart attacks or strokes. They found that they had a mutation in the PCSK9 protein. And so they may have produced none that didn’t circulate. So they created an antibody to take it out as a sort of theory to see if they could cause the same and they did. And from discovery of this genetic mutation to drug being on the market took 10 years which is the fastest ever feminists Coverage genetic mutation a family to a drug being on the market. So basically cholesterol reduction works at any form, it doesn’t actually matter what drug you take, it’s just a PCSK 9 inhibitors tend to reduce LDL by 60%. Maximum dose sasin does about 50%. And primary prevention day stat in does about 40%. ezetimibe probably there’s another 5% on top. So I would add it into other medications or use it by itself, but it’s basically doing exactly the same thing as statins do so there’s nothing magic about it, except it’s a bit more effective. And it’s a different status agent.

David Stokes 25:32
And I understand it is likely to be brought into use within the NHS within a year or so. Is it using

Kate Shipman 25:38
the PCSK9 ? So we’ve had it for a couple of years. Okay, phenomenal,

David Stokes 25:42
okay. And then what are the criteria for being able to prescribe that

Kate Shipman 25:46
so for so we have to do it in secondary care, because it’s a new drug is expensive, but they negotiated a deal with the NHS so that if we provide our secondary care would be cheaper, and I think it was just to make sure that the right people got it then it’s limited to primary prevention only for familial hypercholesterolemia, if the LDL is still greater than five, which means their total class will be about seven. And then it’s for secondary prevention. If your LDL is greater than four, which means your casual six, or if you’ve had more than one event or in more than one place, so like a stroke and a heart attack, or to heart attacks, then it would be an LDL greater than 3.5, which gives you an LDL of 5.5. And ideally, though in secondary prevention, our target is an LDL of less than 1.8. So this is a big group who are higher than 1.8, but less than 3.5, who in whom we cannot escalate therapy. They also say you have to try all the standard things first. And if you don’t tolerate them, it doesn’t matter if you’re still not on anything. You have to have tried things. So large number of patients are actually already on maximum dose data in ezetimibe, and then get the pieces can i as well, because I’ve got genetically high cholesterol to one or two who are intolerant to medications, who’ve had multiple heart attacks or strokes.

David Stokes 27:00
Fascinating and it is administered as an injection I appreciate so

Kate Shipman 27:04
if you get prescribed it, you do it yourself at home, it’s once every two weeks, it looks a bit like an epipen. Okay, so it’s a single use pen device. And everyone’s actually got on really well with it.

David Stokes 27:14
That’s that’s, that’s very, very exciting and new news to me. So I’m looking forward to taking that back. I think the last thing I’d really love to cover and I think it’s another big question that people are going to ask. We mentioned that exercise is excellent for both losing weight but also maintaining a healthy balance of your lipids and cholesterol. That’s correct. Diet. Yeah. What is the diet for managing people’s cholesterol and keeping it healthy or assorted

Kate Shipman 27:40
depends, if you’ve got a mixed dyslipidemia, something associated with weight. If your triglycerides are high, you have to look at alcohol because that’s liquid triglyceride. If that weight and obesity related, then you just want calorie restriction. So if you eat nothing but chips and you eat less chips, you’ll lose weight. So there everyone markets, lots of different diets and then It doesn’t really matter, you just have to pick one that works for you. And diet is so socially or culturally influenced. But some people just can’t make big changes and do something dramatic and so it’s much better to try and cut down the foods that you’re eating what you like, or substitute different varieties. So for example, instead of frying your potatoes, you have been boiled because that automatically halves your calories. And so for example, toast potato 320 calories, Boiled 160 and a portion of carrots 12

David Stokes 28:30
excellent knowledge.

Kate Shipman 28:30
Yeah, thanks. So if you swap your potatoes for vegetables, then again, you can remove the carbs. So all of that weight loss is great, and our cholesterol lowering plan so some foods like plant sterols and oat fibre etc, can absorb some of your cholesterol. That tends to be my a minor change. So for example, if you take plants sterols, first of all, only 10% of people with the right genetics respond. And if you take them every day, you get a 4% reduction in cholesterol, and say a standard dose of statins 40% so Tiny in comparison was just being fit and thinner gives you a significant benefit. So I’d say careful about spending too much money on a lot of these supplements. And if you are, you can check in two weeks if it’s reduced your LDL. So if you can ask someone to give you two forms, you do one perform and after two weeks if it hasn’t dropped, don’t bother. Just be fit and thinner.

David Stokes 29:21
Lovely. So it is just that losing weight and getting getting the lipids and the fat tissue down to what is your own individual personal safe level. Yeah. Okay, much. Lovely. Really, very, very grateful for your time today. Thank you so much. I’m afraid that’s all we’ve got time for this episode. We hope you’ve enjoyed it. I’ll be putting a glossary of some of the terms that we’ve used in this episode on to our website, in case you want to learn more about them. As always, we’d love it when you get in touch with us and interact. Please do get in touch and let us know how we’re doing. Please share this episode with your friends who you think will enjoy it or get something out of it, subscribe and review us either on pod chaser or on your podcast app. Until next time, goodbye.