Transcription
Statins are often talked about as the solution or or the answer for things, but are they just really treating some numbers? And what's the big picture on all this? Let's unpack the data.
Hi, I'm Dr. Eric Westman and welcome to my channel where I review and debunk nutritional misinformation online. In this video from Dr. Alex, who is a pretty good evidence-based medicine source. He's going to talk about statin medicines, the good, the bad, and and then uh have some recommendations for you. Wait till the end where I give you my final thoughts, kind of zooming out a bit from this whole discussion.
>> Hi, I'm Dr. Alex, emergency medicine doctor in the UK. And people ask me about statins and cholesterol a lot. The thing is, if you ask most people what statins actually do, they'll tell you they clean out your arteries. They fix your cholesterol and maybe even reverse heart disease. And that's exactly the problem because statins don't do any of those things in the way that most people imagine. And that gap between what people think statins do and what they actually do creates confusion, frustration, and sometimes genuinely poor medical decisions.
Yeah, I have to say we have a lot of discussions in my clinic about the use of statins and cholesterol levels and fat in the food. In fact, that one's kind of fading a little bit, but the LDL cholesterol and it gets a lot of attention and statins address the LDL cholesterol and have an anti-inflammatory effect. We think so. Let's see what they actually do. what they cannot reliably change and why understanding that distinction matters far more than most people realize.
Now, before we dive into what statins actually do, I need to address something that comes up a lot. I know what a lot of you are thinking right now. Alex, why should I even care about lowering my cholesterol if high LDL isn't actually dangerous? Well, that's a completely fair question and it's one that I get constantly in the comments. So, towards the end of this video, I'm going to tackle that question head on. I'll explain what the evidence actually shows about whether high LDL increases cardiovascular risk because if we can't answer that question first and none of this conversation about statins matters at all.
>> Yeah. You know, I obsess a little bit about the language used and I don't like it when people say dangerous like like you're on the edge of a cliff when we're talking about a risk factor that might be a problem over the years. But that's how doctors and and health professionals persuade people to go on to a medicine, for example, by saying it's dangerous like you're on the edge of a cliff. But let let's talk about it in a less polarizing internet extreme sort of way. It's not dangerous like the edge you a cliff.
Let's start with what statins genuinely do because once you understand the mechanism, everything else makes a lot more sense. Satins work by blocking an enzyme in your liver called HMG COA reductase. That enzyme is responsible for producing cholesterol. When you inhibit it, your liver makes less cholesterol. Simple enough. But the second effect is actually more important. When your liver detects that cholesterol levels are dropping, it upregulates LDL receptors on its surface. Those receptors pull more LDL cholesterol out of your bloodstream and into the liver for processing. The net result is that circulating LDL cholesterol goes down.
Now, here's where the misunderstanding starts. When LDL cholesterol in the blood drops, people assume the cholesterol that's already causing damage just disappears. Well, it doesn't. Statins don't scrub out your arteries. They don't reliably reverse established plaque in a dramatic way. What they do is reduce the exposure that your artery walls have to LDL cholesterol going forwards. That means
>> I think that's a great distinction that a lot of people do think that statins will will clean out the arteries. But even before we get to that effect, let's dwell just a moment on the cholesterol reduction, the HMV COA reductase inhibition in the liver. Cholesterol is such an important thing to make. The liver makes a lot of cholesterol. And in diet studies where you limit cholesterol in the diet, the liver makes more cholesterol to make up for the cholesterol missing in the diet. So I like to come at this from the fundamentals of cholesterol is a essential hormone and actually an essential component. it. It can be turned into other hormones, but it's a component of every cell wall. And if we didn't have cholesterol, if we didn't have the ability to make it, we would die. So, let's just say we need cholesterol.
Now, how much of it? Well, and where do we need it? So, this is where it gets confusing. The LDL particle is actually necessary for life. So, that if people don't have LDLs, they don't do well. LDL particles carry lipid soluble, fat soluble substances through the water soluble aqueous bloodstream. So if you have something coming out of the liver that is fat soluble, not water soluble, it's put on an LDL particle. A lot of triglycerides are put on there. It becomes a VLDLDL. And then that progresses, the triglyceride is taken off. It becomes an LDL. And now the thing about LDL is there's the large LDL and the small LDL. And so that story is ever more complicated and and studies now that compare the small LDL even and LDL not calculated but the actual measurement of it in studies that compare the the power of both of these factors or or paradigms if you will. the insulin resistance score or the metabolic syndrome or type two diabetes is much more of a risk factor than the LDL cholesterol. So point number one is there are many other factors to consider. We'll get he'll get into that in just a minute. And these other factors actually dwarf the effect of a statin medicine, which is kind of interesting because the current state of medical care dwells and focuses on the LDL because I think they think that's the only thing they can do. But what about changing the diet? What about using a medicine to help reduce the weight and to reduce metabolic issues? So now we have other alternatives. Hang on, let's stay in there. Let's keep following this.
>> That means less new damage, slower progression, and in many cases, greater stability of plaques that are already there. The critical line to understand is this. Statins don't repair damage, they reduce future damage. That's a fundamentally different proposition, and it changes how you should think about what these drugs are actually offering for you. That said, statins are genuinely very good at what they do. If your goal is to reduce LDL cholesterol exposure over time, well then statins are one of the most effective tools that we have. The evidence base is strong. In people with established cardiovascular disease, statins reduce the risk of heart attacks, strokes, and cardiovascular death. In people at sufficiently high baseline risk, they reduce the likelihood of a first event. The numbers are real and meaningful. Depending on the population and the baseline risk, we're talking about roughly a 20 to 30% relative reduction in major cardiovascular events that matters. Beyond lowering LDL, statins also appear to stabilize existing plaques like we talked about earlier.
>> Yeah. And I have to agree that there is effect, but it often is overblown or or this difference between the relative risk reduction and the absolute risk reduction is not apparent in most discussions. And in a one-on-one session with somebody, I can pull up a personalized assessment of risk and show you how much that would change if you did take a statin. But now enter in a medication that helps with weight loss. There are now studies showing that the GLP1s these the weight loss shots actually reduce cardiovascular events as well. So but they don't lower the LDL cholesterol as the formal mode of of and target of treatment. They target a different factor. And now clinical trials show that using GLP1s can lower cardiac risk as well. Not quite as high as in the statin trials, but there aren't as many studies done to show the GLP1s lower cardiac risk. But then what about diet change? What doctors pretty much always underestimate or don't even appreciate the effect that diet change can have. And in the Verta Health study, the estimate of the risk factor reduction, it's not they didn't show the outcomes changing, but the estimate of what would be likely to change was about 20 to 40% relative risk reduction based on just lifestyle alone. So this is where I introduced the idea of the statin is not the only tool in the tool chest and uh most people focus on the good, not the side effects. And there are other treatments that lifestyle alone may turn out to be as important or potent as the drugs all of the drugs combined. We just don't know yet. But the early results that I see in and in the clinical trials suggest that the diet alone has similar or better reduction in cardiac events or might in future studies as good or better than these medications. So, it's not the only tool in the tool chest.
>> Plaques aren't static. They can rupture. They can trigger clots that cause heart attacks or strokes. Statins seem to reduce inflammation within those plaques, making them less likely to rupture. That's an important additional benefit beyond cholesterol reduction alone. So, when people say that statins save lives, they're not wrong. In the right population, at the right dose, statins clearly reduce cardiac events. The problem is that people expect them to do more than they were ever designed to do.
Now, I know some of you will have seen the comments or articles claiming that there's no clear link between LDL cholesterol and cardiovascular risk. And look, it's true that if you cherrypick individual studies, especially in very specific populations or over short time frames, you can find results that muddy the waters. But when you zoom out and look at the largest meta analyses where research has combined data from dozens of studies, often involving hundreds of thousands of people followed over many many years, the signal is still very consistent. Higher LDL exposure over time is associated with higher atheroscllerotic cardiovascular disease risk and lowering LDL reduces events in higher risk groups. Until stronger evidence emerges that Curley overturns that consensus, I'm still largely in favor of following the bulk of the data. It's the most sensible approach that we have right now. And it also makes physiological sense when you understand how LDL particles infiltrate the artery walls and trigger the inflammatory cascade that drives plaque formation. The mechanistic story aligns with the epidemiological evidence. That consistency matters a lot.
And this is where we need to be very clear because the list of things the statins don't do is longer than most people realize. The statins do not reliably reverse existing atherosclerosis. There are imaging studies suggesting modest regression in specific circumstances, particularly highintensity therapy, but it's not the norm and it's not something that you should expect. Statins also don't fix insulin resistance. In fact, there's good evidence that they slightly increase the risk of developing type 2 diabetes, particularly at higher doses and in people already close to the diagnostic threshold.
So if there's a study that is a prospective study of first heart attacks in women which there is that says that the metabolic syndrome is more of a risk factor than an LDL cholesterol and type 2 diabetes is even more of a risk predictor than any of these other things even overweight and hypertension. Why do doctors focus on just lowering the LDL and they're not reducing the metabolic syndrome or or they're using a medicine that might even increase the metabolic syndrome the insulin resistance side of things. So there really two competing paradigms here that it does the cholesterol is that the only factor the most important factor or is insulin resistance and metabolic syndrome and type 2 diabetes the the glucose metabolism is that the more important thing or are they both important? What's going to be fascinating is the use of the GLP-1 medications is so widespread and it's helping people lose so much weight independent. You know, people aren't looking at the cholesterol. Thankfully, when people are losing weight on the GLP1s, we're going to find that there's another medicine that dwarfs the effects of statins. The early studies on cardiac risk are pretty clear. The GLP1s lower it almost as well as statins. So, could you combine them? maybe. But the idea is that again, the statin isn't the only tool in the tool chest.
>> They also don't lower blood pressure. They don't improve your fitness. They don't eliminate cardiovascular risk. And they certainly don't make up for poor diet, but inactivity for smoking, chronic stress, or poor sleep. The reason this matters is that cardiovascular disease is a multi-lane highway. LDL cholesterol is one lane, but there's also inflammation, insulin resistance, blood pressure, endothelial dysfunction, oxidative stress, clotting factors, and metabolic health in general.
>> Well, as an obesity medicine doctor, I'm I would like I'd like him to also insert weight, overweight, and obesity in there.
>> Statins operate mainly in one lane. If the other lanes are still wide open, your risk is still there. That's why someone can be on a statin, have excellent LDL numbers, and still have a heart attack. It's not that the statin failed, it's that the statin was never designed to address the other drivers of disease.
Well, I guess another way to say that is don't expect the statin to do everything. And certainly people do have heart attacks on statins. If if the this even gets back to the bigger picture of the hypothesis that the LDL and the saturated fat in the food lead to the LDL the LDL elevation leads to the heart disease that if this really were the only factor or the most important factor you would be able to eliminate heart disease. Well, that's what was predicted in the 1990s. It didn't happen. Now it could be that the metabolic syndrome has become more prominent and the major driver of cardiovascular disease inflammation and metabolic syndrome major driver has changed into something new. It's not cigarettes anymore. It's the metabolic syndrome and diabetes. That is another way to kind of explain both of these being right.
When people don't understand this, they either lose faith in the medication entirely or they assume the medication is enough and neglect everything else. Both outcomes are problematic. And this leads us on to the idea that cholesterol going down doesn't always mean that your risk goes away completely. This is one of the most important concepts to grasp.
>> Yeah. And that has to do with that relative risk reduction. And now the absolute risk reduction. If the absolute risk reduction goes from five to three, a 2% reduction, it doesn't go from 5% to zero. So, there's really no method of intervention that eliminates your risk. It just lowers it a bit. And that's another important point that statins won't eliminate the risk. I had a patient recently who was seeing a preventive cardiologist and she said, "I went to my preventive cardiologist after I had a heart attack and asked him, why didn't you prevent my heart attack because you're a preventive cardiologist and it was not a easy discussion although the cardiologist didn't feel totally responsible for the heart attack because I guess preventive cardiologists can't totally prevent heart attacks. I think that's a pretty true statement. They maybe they've reduced them, but they haven't totally eliminated them.
When you take a statin and your LDL cholesterol drops from 5 mill moles per liter down to two, that feels like a success, and it is progress, but progress is not the same as protection. Lower numbers don't mean zero risk. If you still have metabolic syndrome, if you have high blood pressure, if you have chronic inflammation or poor glucose control, your cardiovascular risk remains elevated. So he's not saying the actual thing to look for in the blood. Uh metabolic syndrome in the blood work focuses on the triglyceride and the HDL. So you want the triglyceride to be low and the HDL to be high. That's the good cholesterol, healthy cholesterol. So the metabolic syndrome doesn't focus on the total and LDL. It focuses on triglyceride and HDL in the blood. Cholesterol reduction lowers risk, but it doesn't eliminate it entirely. What often happens in practice is that people see their cholesterol improve and they assume they're now protected. I've seen this in my own family. They relax on their diets. They stop prioritizing exercise. They don't address stress or sleep. And then when an event happens, they're shocked. But my cholesterol was fine, they say. Well, the answer is that cholesterol was never the only problem. Statins reduce LDL exposure very effectively, but they aren't a shield against all cardiovascular disease.
So, let's talk about the side effects and the trade-offs with statins. Every medication comes with trade-offs, and statins aren't an exception. The most commonly reported side effect is muscle pain or weakness. The exact mechanism isn't really fully understood yet, and it likely varies between individuals between doses and specific statins. Switching statins or adjusting the dose often does help, but some people simply don't tolerate them well. There's also a small increase in diabetes risk. As I mentioned earlier, the absolute risk is quite modest, but it is real, particularly at higher doses and in people with existing insulin resistance. For someone at high cardiovascular risk, the benefit usually outweighs this. For someone at low risk, that tradeoff deserves some discussion. Some people report fatigue, some people report brain fog or digestive symptoms. The evidence here is mixed and not everyone experiences these effects, but subjective experience still matters.
>> Yeah, there is a another study that needs to be replicated and I think over and over again if it's true. the fact that the the GLP-1s now are becoming more used and more people are more aware of them. Statins have an effect that work against GLP-1 hormone. And the the magnitude of it, I'm not really clear on, but if if you're being given a drug that can cause diabetes and also make you gain weight because it works against the GLP-1 system, that that these are other side effects that you don't want and may outweigh any other risk protection that there might be. I guess you might say that in the clinical trials those factors must have been balanced. But I think the current population that I see is uh perhaps different than the population where these first studies were done in the '9s 2000s.
If a medication makes you feel worse, then that's a legitimate reason to reassess whether it's the right choice for you. Statins are a trade. you get a reduction in cardiovascular risk in exchange for small increases in other risks and the possibility of side effects. For high-risisk individuals, that tradeoff makes sense, but for low-risk individuals, it may not. And for a lot of people, this is where the statin debate becomes polarized. One camp treats statins as miracle drugs that everyone should take. Another treats them as harmful and unnecessary. Both missed the point. In my opinion, the conflict isn't really about the science. It's about expectations. When someone is told that a statin will protect their heart, they expect safety. They expect certainty. And when they still have an event or develop a side effect, they feel betrayed. They lose trust in their doctor. And what that does is it fuels anti-statin sentiment. On the other side, doctors see statins reduced in cardiac events in trials and much patients refuse them. based on misinformation which fuels the frustration in the opposite direction. Both reactions stem from the same issue, unrealistic expectations. If you understand that statins reduce risk but don't eliminate it, that they address one major driver of disease but not all of them, and that they have tradeoffs, then you can make a rational decision. But if you expect statins to make you healthy or replace lifestyle change, which is super super important, then you're going to be disappointed. In medicine, managing expectations is often more important and much more difficult than managing numbers.
>> Interesting. I I like that kind of middleof the road approach there. And it's important to if you're using a statin to use the other tools. I liked his metaphor of a multi-lane highway where all of these different factors are in different lanes and the blood pressure reduction isn't going to be achieved by a statin, for example. The insulin resistance isn't going to be reduced by the statin. That's a different lane. But what about a metaphor where actually the the lanes cross over and one becomes more important than the other and maybe you don't need to treat all the different lanes. That's where the conflict arises where we have other drugs that GLP1s and other weight loss drugs. We have other diet lifestyle changes that are more potent than the ones that have been studied in the past. The ones that have reached to you large national studies were not very powerful diet changes. the the studies uh now are using keto diets for example that really do have major change in have probably a reduction almost as good or better than the medications that are at a doctor's disposal that are at a doctor's comparable or maybe even better than the tools that we have in the doctor's tool chest currently.
And that leads me on to the question that most people are probably asking right now. Is high cholesterol or specifically high LDL actually dangerous? And before we talk about whether statins make sense, we need to talk about this elephant in the room? Because if you've been following the online debate, you've probably seen countless people claiming that high LDL isn't actually dangerous. That it's a myth created by pharmaceutical companies or doctors like me to sell statins. that the real problem is inflammation or oxidized LDL or insulin resistance and the LDL cholesterol itself is irrelevant. And look, I understand why people are confused about this. All of those things are super super important.
So, I recently made an entire video diving deep into this exact question. Is high LDL actually dangerous? I went through the evidence from both sides as fairly as I could, almost like an academic review. I looked at the strongest evidence suggesting that high LDL and Apo B do increase your risk of cardiovascular events and death. And then I turned to the papers and arguments that people refer to when they say there's no link. I covered the big farmer concerns. I looked at what LDL levels look like in the world's longevity hotspots. And at the end, I told you where I stand as a doctor who's been watching people die from heart attacks and strokes for a decade. I'm not going to just rehash all of that entire video here because it's long and it's detailed. And if you want the full breakdown, then you should watch it and I'll link it either here or at the end of the video. But let me give you the core conclusion because it directly impacts how you should think about statins in general. For me, the weight of the evidence supports LDL and especially APOB containing particle burden as causal for atherosclerotic cardiovascular disease. That's based on randomized control trials showing that lowering LDL with different drug classes consistently reduces cardiovascular events.
>> Yeah. You know, I I heard that I was taught that and without direct evidence of it. This is a correlation and not really definite. I had read a course on cholesterol personally to a teacher of mine years ago said, "How do you know something, Dr. Westman?" I said, "Do you teach it?" And he said, "No, no, no." He said, "No, you write it." So to really understand something, you take in the information and then you bring it out and you write it. So in writing a course on cholesterol, if if we put LDL on trial, like a civic uh or a criminal trial, LDL would get off. LEO would not reach the bar causal in the court of law. I would love to have a mock trial, put that on and and have the world's experts come and and have the judge require the level that legal evidence, not what we're talking about here, which is we have a Bradford criteria, we have RCTs that show changes here, but it doesn't really prove it. there are these other players that could be the culprit. So, I'm not saying that I'm careful about language. I don't say LDL is the cause and I don't say that statins are dangerous. I don't say that LDL is dangerous if it's high. It's a risk factor and we can lower the risk by using drugs, lifestyle, even other drugs. So I'm a little disappointed that he's still using the dangerous language at this stage of the discussion, but I like his approach.
The cholesterol treatment trialist collaboration showed about a 22% reduction in major vascular events per 1 mill per liter reduction in LDL cholesterol across more than 170,000 participants. So, as a clinical trialist, when I hear about a huge study showing some effect, I think if you needed a huge study, the effect's not very big. Let me rephrase that. If you have a treatment that works every time, like an antibiotic, all you need is two people to show that the antibiotic works. And you could use a placebo and and you you do 10 people in a row, the antibiotic fixes the infection. You don't need many people in that study. So when someone like drug companies make big studies with hundreds of thousands of people and combine them all together to find an effect, it typically means the effect is very small. And I'm not impressed when people talk about huge studies about the effect size or the magnitude of effect of these drugs just not that big.
There's also genetic evidence from mandelian randomization studies looking at people born with gene varants that give them lifelong lower LDL. Those people have substantially lower lifetime cardiovascular risk. And then there's meta regression work showing that regardless of how you lower LDL, the benefit for cardiovascular events scales with how much you lower it. But what about the studies that seem to show no link? Well, the most common one is a systematic review that looked at older adults and found that higher LDL was sometimes linked to lower mortality. That sounds really damning until you understand that all cause mortality isn't the same as cardiovascular events and that there's a phenomenon called reverse causation. If you're frail or chronically ill, your LDL often drops. So, low LDL becomes a mark of illness, not a cause. People also say half of heart attacks happen in people with normal LDL, but risk is probabilistic, not deterministic. LDL is one of several risk factors, and plenty of heart attacks happen because of other risk factors or because plaque has been forming for decades. Others claim it's oxidized LDL, not LDL itself, that causes problems. They're partially right. Oxidized LDL does drive inflammation in the artery walls, but you can't oxidize LDL particles that aren't there in the first place. Lowering your Apo reduces the substrate available for oxidation.
So, here's where I land. As a doctor who spent a decade watching people die from heart attacks, the totality of the evidence supports LDL and Apo B as causal for atheroscerotic cardiovascular disease. That doesn't mean that everyone with high LDL will have a heart attack. But on a population level, higher LDL and higher APOB clearly increases your risk.
>> So I guess the same could be said that high triglycerides are causal for heart disease or you could say that low HDLs are causal for heart disease. So it doesn't in violate what he just said. It's just there other causes. And so the perception, which I I like that he brings in the idea that the perception of risk reduction is that statin and drug treatment will reduce the risk to zero when the reality it just lowers it a little bit. And I think the idea that there's only one cause. Maybe that maybe that's the the issue here. I'm reminded of figuring out who caused the death of somebody. Was it the gun? Was it the person that pulled the gun? The trigger? Was it the bullet? Was it the the heart stopping? You know, if you have a chain of events and we all focus on one thing, then we all think that's the cause when you you uh need really the whole chain of events and inflammation being the root cause of all this is kind of the the new kid on well it's actually 100 years old but new in the popular uh discussion. And then the insulin resistance metabolic syndrome is new in the popular discussion. It's also been around for decades. These other factors and I think it boils down to now we have other tools in the tool chest. So that the focus on just statin may change may fade away.
Well the clearest case is secondary prevention. If you've already had a heart attack or a stroke or a TIA or if you have angina, then the evidence is overwhelming. Statins reduce the risk of another cardiac event or death. They also make sense in people with very high baseline risk. Things like strong family history, familial hyper cholesterolmia, multiple converging risk factors, or established atheroscerosis on imaging. In those cases, statins are strategic. They're not replacing healthy behavior. Far from it. And that's an important point. They're just adding a layer of protection where the risk is already high.
What doesn't make sense is using statins as a substitute for addressing metabolic health. If someone is sedentary, if they're overweight, if they're poorly nourished, chronically stressed, and they're sleepd deprived, then a statin alone won't make them healthy. Statins also make sense when lifestyle optimization hasn't been enough. If you've improved your diet, if you've improved your exercise, if you've improved your sleep and your stress and your LDL remains high, adding a statin can be reasonable for the next step. That's very different from prescribing a statin and expecting it to do all the work.
So, here's the reframe. Statins are powerful, they are limited, and they are situational. They're powerful because they reliably reduce LDL exposure and lower cardiovascular event rates in the right populations. They're limited because they don't reverse disease. They don't address all the risk factors. And they come with big tradeoffs. And they're situational because whether they make sense depends on your baseline risk, on your broader health profile, and what you've already addressed. The mistake is thinking in absolutes. Statins don't make you healthy. They make high risk less dangerous. And if you understand that going in, you're far more likely to use them appropriately, to tolerate them better, and make decisions that genuinely serve your long-term health, not just your cholesterol numbers.
>> Yeah, I I like the discussion. A couple things I would have included is what happens if your calcium score is high? Should you go on a statin or not? don't have clinical trials there, but the higher your calcium score, coronary artery calcium score is, the more risk there is, and you might want to treat that with medication or or lifestyle. And then I guess my take-home point is the effects are not all that powerful even though people say it is. It's the power of it is being overstated in order to you to just take it to call it you know LDL elevation dangerous and to be on the drug will you have to have this know I think a measured discussion of what your risk is now and what it might be if you use one of these medicines but how about also looking at the risk if you actually lost weight and reversed the diabetes that you have with lifestyle alone or with the GLP P1 or other medications.
So, stepping back, obesity medicine, the field that I'm past president of, the obesity medicine association, the organization I'm past president of, understands that for a lot of these things, the root cause is obesity. And targeting obesity will be much more powerful than targeting just the LDL cholesterol with a statin. I like this. It's just a tool in the tool chest. or other tools. And you know, if you're being bullied to be on one, then you have evidence that you have no cardio, if you're bullied to be honest that then you have evidence that you don't have any heart disease even after years of LDL cholesterol elevation. Remind the doctor that we're not treating cholesterol as a disease. Cholesterol is a risk factor. The disease is atherosclerosis, coronary artery, corroded aorta, even cerebral artery atherosclerosis. That's the disease we're trying to prevent. Whether it be drug treatments or lifestyle change, even you could throw in surgery, beriatric surgery as a treatment to lower your cardiac risk. I like Dr. Alex's approach. And if you like this video, please like, subscribe, and ring the notification bell so you don't miss out on further content. If you enjoyed this video, consider joining our YouTube membership for early access and exclusive live Q&As's with me. Just click the join button below or support us with a PayPal in the description.