Cardiovascular disease: testing, prevention and reversal

I am not a doctor: I am a nutrition and fitness coach and a health researcher. The following information is based on dozens of hours of research predominantly using studies and lectures from the very top specialists in Metabolic disease, Cardiovascular health, Endocrinology and Health Science So while it is advice that I myself trust and use for my own screening and prevention, in no way do I write this as a personal recommendation for your health. This is just some information for you to add to your toolbox to help you advocate for your own health.

This is a deep dive article to help you understand terminology, testing protocols, prevention and reversal measures. I have tried my best to keep it simple but thorough. You can scroll to the bottom for the main takeaways but many of the important details are throughout the text.

Atherosclerotic Cardiovascular Disease (ASCVD), as understood by many, is a disease of the tissue, a calcification of arterial walls and includes conditions such as Coronary Heart Disease, Angina, Coronary Artery Sterosis, Acute Coronary Syndrome, and other related diseases.. While this is a large part of what creates lethal cardiac events, I am going to outline some evidence that suggests, this is an incomplete definition of what ASCVD is. To better prevent these diseases we need to better define what it is, how it is caused and how to test for it.

Cardiovascular disease begins decades before we have any inclination to check for its threat. It is the most prevalent disease of mankind, creeping into our arteries quietly and persistently, sometimes as early as in our 20s. Although ASCVD is highly preventable , approximately 40% of the time, the first sign of disease is death by heart attack and yet we do little to educate the public about prevention. Currently, the clinical measurement we use to determine 10-year risk is rarely applied until the age of 55 but most adults have their first heart attack before the age of 60. According to the INTER_HEART Study (1), a global study on acute myocardial infarction, 90% of myocardial events are due to preventable risk factors. Given that we have a very clear understanding that cardiovascular disease will eventually touch most of us, we know a good deal about what causes it and how to measure it, it seems suspect that we are not better at detecting it way ahead of time and preventing so much disease and death.

ASCVD is the leading cause of death for women over the age of 65 and is slowly overtaking cancer (predominantly breast cancer) as the leading cause of death for younger women as well. In fact, 30% of women who have their first major cardiac event will have it before the age of 60. This is not just a disease of men, which it is often thought of as. For both women and men, the risk increases if you have had even moderately high LDL levels for an extended period of time. While this is clearly not the only factor, this is the most widely studied correlate. These lipids are silent killers because unless you test for them early, there aren’t any symptoms. Focusing on immediate symptoms and short term risk is the current operating method of modern Western medicine and it is doing so at the peril of millions of people.

The current calculation for 10-year risk of disease uses a few confounding numbers including one for age and one for sex – both of which I have already suggested are more complex than we have assumed. If you sit below a certain age group then it automatically and dramatically lowers your risk for the next 10 years, removing any urgency to look closer. Same thing for sex; if you are a woman then your score in the risk calculation is going to be much lower than maybe it should be. We know that this disease begins as early as in our 20s. You may not be at risk of a heart attack in your 20s, but the build up of calcified lipoproteins or metabolic disease (which I will touch upon a bit later) may have begun and without a clearer screening process this will go undetected until it is a problem. Even when this vastly incomplete risk assessment formula is used, cholesterol and blood pressure don’t play enough of a role in the calculation in order to make it a priority in some doctors minds.

I myself have had to demand further tests to make sure my cholesterol and blood pressure levels are indeed safe. The general assessment didn’t even include the one test we could have used to get a clearer picture on lipids. If I didn’t know to ask for this test it would not have happened and I could have gone another 10 years before my doctor thought it wise to check again. I’m not proclaiming the need to self advocate because your doctor is purposefully holding back preventative measures, but more because they just don’t know how to do so. They have been instructed a certain way, they are busy and can’t keep up with every new study on one condition. Moreover, they are generalists not specialists. If you have the luxury of seeking out a private Internal Medicine doctor(s) then you will probably be taken care of with a more holistic, preventative approach – but you can also do the hard work of talking to your doctor about creating a constellation of doctors that look after your health in a similar fashion. This is what I have done. Its super fun and easy! Convinced?

Lets take a look at standard testing practices…

One aspect of preventative medicine that can and should be part of your toolbox concerning ASCVD is gene testing. You may have a genetic predisposition for cardiovascular disease and you can find out relatively easily at low cost from private DNA testing services online, like 23andMe. Often-times the testing service includes red flags for the markers so you don’t have to research which ones to look for.No matter how young you are, I think this is a good starting step to prevention. If you end up having some genetic markers of risk then you can begin to set up other assessment tools a bit earlier and more regularly.

The total cholesterol number is not entirely useful. Individually, each marker carries some information and how you interpret it can give you a much better idea as to how to approach things; but total cholesterol is not a worthwhile marker of risk. Or at least, it shouldn’t be the main marker. It is important to note that cholesterol is not inherently bad: in fact we need it to survive. We need it in the creation of cell membranes; it helps make certain hormones, it is fundamental to metabolism, and building vitamin D. BUT our cells make most of their own cholesterol and cholesterol synthesis in the brain is independent of the cholesterol in your blood. So, yes, we need to measure clood cholesterol levels to make sure they stay within certain parameters, but what levels are actually important in testing?

What are we measuring when we take blood to assess cholesterol levels? For the most part your test results show the density concentrations of the following lipid markers; TC (total cholesterol), HDL-C (high density lipoproteins) LDL-C (low density lipoproteins) and TG (triglycerides). it can be very confusing once you are in the weeds of it so for the sake of comprehension I am going to try and simplify the definition and function of these lipoproteins.

A lipoprotein is like a taxi. These taxis transport fat (lipids) in the form of cholesterol and TG through the blood. You can think of it like the lipids are the passengers of the taxi and the taxi itself is the protein (or the apolipoprotein). There are different classes of lipoproteins, divided mostly by their density. Chylomicrons (CM) – are produced in the intestine; the other 4 are made in the liver and include – High Density Lipoproteins (HDL), Intermediate-density Lipoproteins (IDL), Low Density Lipoproteins (LDL), Very Low Density Lipoproteins (VLDL) and Triglycerides (TG).

HDL levels, to some degree, have a protective effect. High levels of this kind of cholesterol are usually a good sign because it plays an anti-inflammatory and anti-oxidant role. HDL is a mode of lipid particle transport away from tissue stores towards the liver for further metabolism – a recycling of sorts. It carries the highest proportion of proteins to lipids, which gives it its density. Studies suggest that a higher level of HDL is correlated with a reduction of heart disease – High HDL seems to be mostly genetic so it is a bit difficult to change your levels and research suggests that trying to manipulate HDL levels does not reduce cardiovascular events. This may be because the ratio of HDL and other lipids may be more important; or that it is simply not the complete picture and other factors are at play. Interestingly enough, a number of population studies (2) show that people with high HDL have very few cardiac events even with correlating high LDL numbers. .

While HDL tend to carry lipids away from tissues, triglycerides tend to offload into tissues. Triglycerides provide calories for energy use, but they also store calories as fat. When this happens the lipids can become dangerous. So in very simplified terms we have two mechanisms that may, in a way, work against each other – Triglycerides bring problems and HDL take them away. While not perfect, knowing this gives us something to look for in our lab results: the triglyceride to HDL ratio. This is one of the stronger markers for cardiovascular risk that we can get from a simple blood panel, other than an ApoB test (more on this later).An ideal ratio is about 1.5 or less; this will give you a pretty clear idea of your general heart health in the moment. It is NOT the only thing you should look at for long term prevention but it is a very good start, If your ratio is about 2.5 or more then you need to act on it. It is important to note that ratios are race dependent – hopefully your doctor knows how to best judge for you

Many metabolic health specialists argue that a high ratio may be a sign of insulin resistance and so there is good reason to be checking your fasting glucose and fasting insulin levels if you have high triglycerides. To the best of my knowledge, a healthy TG number is at or below 100 mg/dl. Lower is always better. The standard “normal range” goes up to 150 mg/dl.

LDL or LDL-C is the measurement of the concentration of cholesterol contained in the LDL particles. You may have an LDL-P reading instead, which is the number of particles – but this is rarely measured. High LDL doesn’t really tell you much about any potentially harmful agents. There are a few different variants of LDL; some are larger and buoyant, but others such as IDL VLDL and Lipoprotein (a), are increasingly smaller and denser. The large, fluffy kind are seemingly more neutral to cardiovascular health. They don’t really gather under the endothelial cells of your arteries so they do not accumulate and cause damage. They also tend to make up 80% of your overall LDL number which playsinto why total LDL is a bit confusing.

The variants of small dense LDL particles are more like annoying tourists, making stops to see the arterial sites and sometimes they end up getting stuck and becoming plaque. These little troublemakers only make up about 20% of the total LDL value in your lab results so you can see that the total value is often too vague to give any real information. It doesn’t mean it is not important. There is clear evidence that long time exposure to high LDL levels comes with an increase of cardiovascular disease. I think that we can get a clearer image with better individual testing but these numbers don’t make it into longitudinal studies.

Your blood panel is really just giving you a look into what your lipid taxi service is doing at that very moment. It is a screenshot of a complex system, so multiple shots would be ideal. I would suggest that if you are at risk, do these tests 2-3x a year. You want to make sure that what you originally assessed is real, and you want to see the trajectory. Something to remember – one of the best ways you can get a good original snapshot is to fast before your test. 12 hours is good, 24 hours is better. If you fast overnight but eat a muffin in the morning and then have your blood taken in the afternoon, your triglycerides. will show up high on the report and now be useless. Because this happens a lot, doctors will overlook or downplay a high number due solely to the muffin effect. Another interesting confounder is thyroid hormone levels. If you are hyperthyroidic then your triglycerides may look much higher than they are at a functional level. You want to avoid as many false positives as you can, so you have to make sure you take care of your thyroid levels first.

So what can you do to accurately assess risk? As mentioned above, you can look at the triglyceride to HDL ratio and begin to figure out if there is a potential threat. Triglyceride count is kind of like your small dense LDL reading. It is not perfect, but it is a start. You can also ask to look at another measure that seems to correlate better with ASCVD risk – your Apolipoprotein (b) or ApoB.

Researchers have discovered that each and every LDL, IDL, VLDL and LP (a) carry one ApoB, so testing for ApoB gives us a particle concentration score. Thus, instead of density concentration of cholesterol levels ,you get the number of potentially atherogenic particles. This has been widely agreed upon as a more accurate testing method for risk of ASCVD (3). A study in the Lancet even suggests that “a higher APoB is detrimental to lifespan and increases the chances of coronary heart disease and type 2 diabetes.” (4). ApoB Tests are not part of the standard cholesterol measure or heart health risk assessment. Luckily, it is a very cheap and widely available test. It is covered in Canada and I believe it is something like 5$ in the U.S. There is no reason to not include it, but unfortunately you will have to ask for it yourself, as I did.

Why ApoB tests seem to be better at predicting ASCVD is a little complex and requires much a more jargon-laden research breakdown than I think is necessary; but in general, because this is a particle test rather than a density test, you get a clearer look at the risk from a probability standpoint. If we think of it like over enough time, the more darts you throw at the board the more will inevitably hit the bullseye,, then we need to know how many atherogenic particles there are rather than density concentrations. Time and number of particles aren’t the only factors though; variables such as blood pressure (among others) will increase the risk. But it stands to reason that if we want to reduce the risk of hitting the bullseye, we should lower our ApoB particle count, and that is what many specialists currently prioritize, including Allan Sniderman, one of the top lipoprotein researchers on the planet.

As insinuated, this is not the whole picture. Something fairly new has occurred in the (North American and Western European) population over the last decade that may suggest we need a broader approach to ASCVD prevention and treatment.

More and more people have shifted out of low fat diet trends and into high fat ones such as the ketogenic diet, and various other low carbohydrate diets. Many of these have become popular on the back of research suggesting that various metabolic diseases come from high sugar intake rather than a high fat diet.

Emerging from this trend reversal is a growing population who have been labeled by some as Lean Mass Hyper Responders- (LMHR) – people who are metabolically healthy but with strikingly high LDL scores. A few preliminary studies suggest that high LDL and/or high ApoB may be coincidental rather than causal. The theory posits that under conditions of low carbohydrate intake and relatively low total fat, we rely more on lipids for energy – specifically triglyceride rich lipoproteins (TGRL), including VLDL, made in the liver. In this scenario increased TGRL coincides with an increase in lipid breakdown throughout the body with the help of an enzyme on your arterial wall (LPL). This particular set of events leads to high HDL, low TG but also high LDL.

ApoB particles are indeed the ones getting stuck in the arterial walls and causing a build up of plaque and increase of cardiac events, but what is driving them in there? Is it really just a numbers game? The LMHR population seems to suggest something else is happening. Some early research, led by Dave Feldman and others show baseline data that encourages this theory. A cohort of about 100 people who followed a high fat/low carb diet for an average of 4 years show little to zero plaque build up in their arterial walls, while also having very high LDL/ApoB levels. This is not conclusive, and more studies are under way with a control group and a more randomized study cohort, but it does remain very intriguing. Perhaps this is more a metabolic issue and not just a lipid overload problem.

We know that the liver plays a crucial role in synthesizing and recycling cholesterol, and so we should assume that assessing liver health is pivotal in determining risk for heart disease – and yet this is rarely the case. You may get a basic liver enzyme profile done with an annual check up, but doing a deep dive into your liver’s heath is often done after an event…or post mortem. The truth is that the liver is so important in maintaining good health that we should constantly be keeping an eye on it. One of its most important roles outside of lipid management is regulating blood glucose levels.

When we get sugar spikes in our blood from the food we eat, normally, Insulin is released by the pancreas and this signals different cells in the body to pull the glucose in to use or store as energy – iInsulin is essentially an energy storage hormone. But if your blood sugar spikes, insulin is released and your cells do not respond to the insulin, things begin to run a-mock – and this is called insulin resistance. If this becomes chronic? Welcome to hyperinsulinemia, population, too many! This condition is often a precursor for type 2 diabetes, which we know is a risk factor for ASCVD,

Let’s take a tiny step back. When we have extra glucose in our blood, it is stored in the muscles as glycogen, and in adipose tissue and in liver cells as fat. Generally speaking, when glycogen is stored in muscles, there is nothing to worry about. When it is stored in subcutaneous fat (the fat under your skin), there is little to worry about unless other factors are involved. When it is stored in visceral fat (the fat around your organs), this becomes worrisome and when it is stored in the liver, we have a problem. Liver is supposed to store glucose, but when it is doing so dysfunctionally – we begin to see fatty liver.

The liver’s ability to function is severely hampered by its own fat storage, so once this fat buildup begins, so does the cycle of insulin production from the pancreas and more fat storage in the liver. Not goodah! This is bad for your liver, your heart and pretty much anywhere else insulin can go because another thing insulin does is cause cell proliferation (5). Cancer is a kind of cell proliferation.

How do we monitor for this and is it represented on our lipid profile? A fasting insulin and fasting glucose test is one way to see if you are insulin resistant, hyperinsulinemic or diabetic, and yes, as mentioned earlier insulin resistance is correlated to higher triglyceride and vldl count (your TG to HDL ratio). One of the ways this happens is Insulin stimulates certain receptors in the liver (x receptors) that upregulates lipid synthesis.

If you get your fasting insulin and fasting glucose and are able to read your HDL to TG ratio, you now have some very useful information. Fasting insulin levels should be under 7 mlU/L and can go as low as 2 and still be healthy. If you are above 7 then you need to be careful and a count of 15 suggests insulin resistance. Just for reference, the normal range is 2-20 or 24mlU/L – If you have an overly optimistic doctor, this could go on for some time without getting addressed.

A liver ultrasound is another way to see if you have fatty liver, but visual confirmation of fatty liver, especially if minor, does not mean you have or are in danger of having insulin resistance. Its a good start though, and maybe the cue you and your doctor need to order more tests.

In addition to an ultrasound you can also measure liver function/enzymes (AST, ALT, Biliruben) in a blood test. As mentioned above, these are usually included in any general blood exam but often overlooked as long as they exist in the “normal” range. This is a serious problem with current testing practices. The high normal for liver enzyme tests are still much too high and may suggest that you have fatty liver. Normal ranges are built on averages. In the last 40 years, what has been considered normal has shifted about 15 points, so a high normal now would have been considered off the charts 40 years ago. Nothing above 25 U/L on your ALT should be considered normal. The current normal range is between 7-50 U/L.

Bottom line, if you do have fatty liver, no matter what stage, this is not something to sleep on. If your liver is not functioning in glucose management, it most likely is not doing great at cholesterol synthesis and recycling.

Prevention & Reversal

Because of the lack of research, I am not sold on ignoring LDL levels and focusing solely on liver/metabolic health. So for the meantime, I personally take a multi pronged approach. The first thing to focus on is reducing LDL particle concentration, more specifically, ApoB. There are two direct ways to do so; pharmacology and nutrition. Exercise has a more direct effect with concern to metabolic health, so you should always be using it as a way to thwart further disease and increase health and life span. By beginning a regular and fairly intense routine earlier in life you may severely reduce your risk. A preliminary study (6) showed only 1% reduction in plaque from very high intensity interval training for 6months. It is very interesting but perhaps not the quick fix you may need in reversing an ongoing condition. Exercise for heart health is still a must.

There are three main approaches nutritionally; the first is to lower carbohydrate intake. By restricting carbs you end up lowering triglyceride levels and thus needing less cholesterol (ApoB) particles to move the triglycerides around. When I say carbohydrates I mean sugar, and specifically things like bread, pasta, rice, potatoes, processed foods and sugary drinks.

The second approach to lowering ApoB with food is to lower or eliminate saturated fats. Lowering saturated fats reduces the creation of cholesterol in the liver and up-regulates LDL receptors. As you reduce saturated fat intake, the liver signals that it needs to bring in more cholesterol and will pull more LDL out of circulation, thus lowering the ApoB in your blood. Whether or not saturated fats cause an increased risk in atherogenesis is another question, and there is very little convincing evidence that they do (7). But it does technically reduce serum LDL so it is still used by doctors and nutritionist alike.

I do not fully prescribe to this method. I do however focus on selective saturated fat intake. For example, I do not severely limit high fat yogurt, animal protein, eggs or coconut milk. I do limit cheese but only because I can’t find a very clean, local source yet. I do limit all processed foods, including processed meats. Though other than processed meat, the main reason I avoid processed foods is to reduce sugar, omega 6 fatty acids (in highly processed form) and other harmful ingredients. To be clear, I do regulate my saturated fat intake. I mix my protein sources between animal and plant, I lean heavier into fish, legumes and then lean meats and poultry. I also make sure to add a lot of fibre to my meals.

A meta-analysis of 87 different studies looking at nutritional management of ApoB (5) suggests that an increase of unsaturated fats will lower ApoB, the third way. These include both mono and poly-unsaturated fats. Mono-unsaturated fats include olive oil, avocados, pumpkin seeds, and almonds. Poly-unsaturated fats include, salmon, mackerel, sardines, Omega 3 & 6 fatty acids, flax seeds, etc. Both margarines and vegetable oils carry a heavy load of omega 6 fatty acids. While we do need these, we need much less of them than we get in a traditional “American” diet, filled with processed foods. Other than a high-quality olive oil, I would steer clear of all vegetable oils and margarine, If you can find cold pressed vegetable/seed oils I actually think they are fine as long as you are not reheating them. I’m not anti-omega 6, nor am I anti-seed oils. But I think there are some low quality ones on the market and thise ones have been degraded by the processing methods.

I guarantee you that your doctor will prescribe a low saturated fat diet, and I think it is flawed or at east incomplete. You can always try lowering saturated fats along with reducing glucose until you are in a safe zone with your blood panel and then reintroduce selected saturated fats. But If you are taking care of your metabolic health and exercising regularly, I really see no reason to eliminate these foods.

There are a select few supplements that appear to have a significant effect in reducing inflammation and ApoB levels, one of which is Omega3 fatty acids. Your best bet is to get a clean sourced high dose EPA/DHA blend. You ill want to take upwards of 2-6g/day to maximize anti-inflammatory effects. If you are vegan, try and find Algae based EPA & DHA. The ALA in flax seed oil does not convert very well into EPA and DHA. In fact it barely works at all.

For liver and metabolic health, the very best thing you can do is cut your sugar intake. First and foremost are processed foods, sugary drinks and alcohol; but reducing carbohydrates in the form of bread, pasta, potatoes and rice is also important. As mentioned above I am a nutrition coach and help design sustainable healthy eating plans for a living. It is a very individualized process and so I can not give specific recommendations here in any meaningful way. However, because most doctors do not study nutrition, It is in your best interest to contact a professional in finding a way to eat properly to reduce your risk (our nutrition services).

Before we talk about cholesterol lowering medication there are a couple more risk factors that you can control to lower the probability of ASCVD; smoking and blood pressure. I’m not sure I need to make a big case for not smoking. It will almost certainly kill you and in a wide variety of horrible ways, including through heart disease. The chemicals in cigarettes directly damage arterial walls which make them susceptible to plaque build up. If you smoke you have a 4X greater chance of dying due to ASCVD.

It doesn’t seem like we know the exact mechanism of how high blood pressure increases ASCVD risk. We know that it reduces arterial elasticity but we don’t know how. It is possible that part of the problem is that the added pressure increases the rate at which lipoproteins can “hit the wall” and get stuck. But regardless of the how, there are several measures you can take to regulate your blood pressure; regular exercise (both cardio and strength training), maintaining high sleep quality and quantity, lowering sugar intake, and practicing meditation or breath-work. Oh yeah, and quit smoking ya nut!

Pharmacology

While the above changes in nutrition can certainly do wonders for reversing type 2 diabetes they will only lower your ApoB by so much. If you need a drastic drop due to high numbers, co-morbidity factors, or post cardiac event, you may need to add some kind of medical assistance. If your levels are low or normal you can probably get away with simply lowering glucose in a healthy way and exercising . If you have done the genetic testing and you know that you have a predisposed risk for ASCVD, then I understand why you would consider drug therapy as soon as your levels reach high normal range. Even if you are eating perfectly, exercising and are under the age of 40 this might be wise. Prevention is key and it is hard to ignore the vast amount of evidence showing a reduction in events while on certain medications.

As far as the pharmacological route, obviously Statins are the most common and most potent drugs on the market right now. And while they do come with some potential side effects, the benefits outweigh the risks for many people. That said, if you do have severe muscle cramping or any other intense side effects you should definitely talk to your doctor about lowering the dose and/or taking another approach. You need to maintain physical ability in order to exercise and live a worthwhile life. If you get your metabolic health in check and have a reasonable LDL level, I see no use for cramming the body with medication.

Interestingly, most Statins reach near peak efficacy at quite low doses. Something like 5mg should give you about 85% of its benefit. So if you are mega-dosing on a statin, it’s worth questioning why. Your doctor may have good reason, but if you do have side effects I would still get more info on the strategy.

Other drugs commonly used to fight ASCVD are PCSK9 inhibitors and Bempedoic acid. Because of the high cost, I am not sure that Canada provides PCSK9 inhibitors for its patients, but you can ask about it. PCSK9 inhibitors work by inhibiting a protein (PCSK9) that binds with LDL receptors, allowing them to work freely in taking up LDL particles from the blood. They have been shown to lower blood lipids by up to 47% and have the potential to prevent a heart attack by 27%. Bempedoic acid inhibits cholesterol synthesis in the liver. It is activated in the liver rather than Statins – which also inhibit cholesterol synthesis – but they work throughout the body. A combination of Statins and PCSK9 inhibitors can drop LDL levels by half. These are powerful and relatively safe drugs, especially at low dose. I am not a drug pusher, not unless things are dire and we don’t have any other tools that will do the job that needs to be done promptly. This can often be the case when you have a medical system that is not built for preventative, holistic medicine.

The reality is that if you are at risk – the older you are the closer you are to a major event and the harder you have to put on the breaks. This means a huge lifestyle change but also, potentially, a big pharmacological shift (and all the side effects that tag along). You can avoid this. You just need to get the complete picture of your current risk level. See what areas need work and how you can change your lifestyle. A lot of it does come down to that. But even if you need medicine to regulate, better to know earlier before it becomes harder to reverse or even worse, before that first event that may kill you. Without warning. It happens much too often. There seems to be many different pieces at play when it comes to ASCVD; genetics, inflammation, degradation of endothelial cells on the arterial wall, blood pressure, metabolic health and lipid regulation all come together in different ways to make heart disease the most prevalent disease globally. I think if we define heart disease as multi-faceted, we have a better chance of preventing or reversing these conditions. Instead of practicing prevention based on averages, it is best for us to take an individual, holistic approach and do all the necessary testing to see which factors play a bigger role for each of us.

I have purposefully left out or glossed over a few things that may be addressed in a follow up article. If you do have any questions, feel free to comment or stay tuned for more details. If you are in need of and ready to make some lifestyle changes, but need some guidance, please contact us for more information on our services.

Until then. Peas out

SUMMARY POINTS

• ASCVD is highly preventable and still it is the leading cause of death globally.
• 90% of myocardial events are due to preventable factors.
• Heart disease affects women almost as much as men.
• The standard 10-year risk assessment is used too late and is faulty at best.
• Genetic testing for predisposition is a good place to start.
• Total Cholesterol is not important in assessing risk.
• High HDL is good & your Triglyceride to HDL ratio is an important marker.
• Triglyceride levels are like your small dense LDL reading.
• An elevated Triglyceride to HDL ratio may suggest insulin resistance.
• Current standard normal ranges for blood tests are often too high.
• Total LDL is also not a good risk assessment marker.
• ApoB correlates higher with ASCVD risk and the test for it is widely available.
• Metabolic processes and liver health may be a good place to look for early risk.
• Fasting Insulin tests and fasting glucose test show risk of insulin resistance and potential ASCVD.
• Liver ultrasounds show fatty liver and hint at metabolic dysfunction.
• Blood tests for liver enzyme counts can be used to assess liver function and ASCVD risk.
• Exercise plays a role in both prevention and reversal but is slow acting.
• To reduce ApoB you can lower sugar/carbohydrate intake, increase unsaturated fats or reduce saturated fats.
• Though lowering saturated fats do reduce LDL levels there has been no solid research demonstrating that it also reduces cardiac events or risk.
• Certain saturated fats like processed meats and other processed foods are likely contributing to risk factors.
• Unsaturated fats heavy in Omega 6 fatty acids (vegetable oils and margarine) may be harmful to your heart health.
• Supplementing with 2-6g of marine sourced Omega 3 fatty acids helps reduce inflammation. Seed based ALA is not very helpful.
• Lowering carbohydrates and alcohol are also very helpful in preventing and reversing metabolic disease.
• Adding soluble and non-soluble fibre through whole foods helps prevent and reverse metabolic disease.
• Statins, PCSk9 inhibitors and Bempedoic acid are all common medications for combatting heart disease.
• Statins are relatively safe and definitely surpass a cost-benefit analysis. They also reach near maximum efficacy at low dose.
• Heart disease is complex and everyone has a different set of risk factors. Taking a preventative and holistic approach will add years to your lifespan and healthspan.