Episode 56

Cholesterol and Heart Disease

Published on: 19th September, 2024

Apolipoprotein B (apoB) is the causative agent in atherosclerosis. If your apoB is low, you will not develop atherosclerosis. However, if your apoB is high, you could die young.

We know this because of genetic studies of people with different levels of apoB and their health outcomes.

What is Atherosclerosis of the heart?

Atherosclerosis is a progressive laying down of "plaque" in the wall of the coronary arteries.  Since the coronary arteries feed the heart, this can lead to three outcomes:

  1. The plaque impinges on the artery. Thus, the plaque will decrease blood flow to the heart. This can lead to angina or a poorly working cardiac muscle.
  2. The plaque can rupture (burst) into the artery. Next the body repairs this by clotting the blood. Thus,  the blood flows to that portion of the heart is stopped. Without blood flow, the heart muscle starves, and if the flow isn't restored, that part of the heart will die. This is a heart attack or myocardial infarction.
  3. The plaque can have no result.  Meaning, it isn't stopping blood flow to lead to angina, and it doesn't occlude the artery.

What is in the plaque?

In the above artery, you can see the yellow cholesterol in the wall. This is a "soft" plaque, like porridge.

The plaque is not inside the vessel. The artery is lined by a layer called the intima. So how does cholesterol get from the inside of the blood vessel to behind the layer?

The Process of Atherosclerotic Plaque Formation

Lipoprotein Entry into the Arterial Wall: The process begins when ApoB-containing lipoproteins pass through the endothelial layer of arteries. Normally, this layer acts as a barrier, but factors like high blood pressure or inflammation can make it more permeable, allowing these particles to accumulate beneath the endothelial cells.

Retention and Modification: Once inside the arterial wall, ApoB lipoproteins are trapped by proteoglycans (components of the extracellular matrix). These retained lipoproteins undergo modifications, such as oxidation, which makes them more likely to trigger inflammatory responses.

Inflammatory Response: The modified lipoproteins activate endothelial cells and attract immune cells like monocytes. These monocytes enter the arterial wall and transform into macrophages. Macrophages engulf the modified lipoproteins, turning into foam cells, which are a hallmark of early atherosclerotic plaque.

Plaque Development: Over time, foam cells accumulate, leading to the formation of fatty streaks in the arterial wall. Smooth muscle cells migrate into the intimal layer of the artery, contributing to the formation of a fibrous cap that covers the plaque. This cap consists of connective tissue, calcium, and cholesterol deposits.

Progression and Complications: As the plaque grows, it narrows the artery and restricts blood flow. If the fibrous cap ruptures, it can lead to the formation of a blood clot (thrombus), which may block the artery entirely, causing a heart attack or stroke.

Preventing Plaque Formation

Understanding how ApoB-containing lipoproteins contribute to atherosclerosis underscores the importance of managing blood cholesterol levels. Lifestyle changes such as diet, exercise, and medications like statins can reduce LDL levels, lowering the risk of plaque formation and subsequent cardiovascular events.

Atherosclerosis is a gradual process that starts with the seemingly harmless entry of ApoB lipoproteins into arterial walls. By addressing the risk factors that promote lipoprotein retention and inflammation, the progression of atherosclerosis can be slowed or prevented.

LDL particle size

LDL particles can vary in size, and it was previously believed smaller, denser LDL particles were more atherogenic than larger, buoyant ones. However, research has shown that the number of LDL particles, regardless of size, is a more significant determinant of cardiovascular risk. Studies indicate that the concentration of LDL particles is more closely associated with atherosclerosis than the size of the particles themselves.

The ApoB Factor: Why It's a Big Deal

ApoB is a protein found on the surface of atherogenic lipoproteins, including LDL, VLDL, and IDL. Each of these particles contains one ApoB molecule, making ApoB a direct measure of the number of atherogenic particles in the blood. This measurement is crucial because it provides a clearer picture of the atherogenic burden in the bloodstream than LDL-C alone.

Why ApoB is the Star Player

Direct Measure of Risk: ApoB directly measures the number of atherogenic particles, providing a more accurate assessment of cardiovascular risk.

Independent of Particle Size: Unlike LDL size, which can vary and complicate risk assessment, ApoB consistently reflects the number of risk-contributing particles.

Predictive Power: Numerous studies have shown that ApoB is a better predictor of cardiovascular events than LDL-C or other traditional lipid measures.

ApoB: Direct Measurement of Atherogenic Particles

Apolipoprotein B (ApoB) is the main protein component of several lipoproteins, including low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and lipoprotein(a). Each atherogenic particle contains one molecule of ApoB, making ApoB a direct measure of the number of atherogenic particles circulating in the bloodstream.

Key Points:

Direct Indicator of Particle Number: Since each atherogenic lipoprotein particle has one ApoB molecule, measuring ApoB provides an accurate count of these particles. This is crucial because the more atherogenic particles present, the higher the risk of these particles penetrating the arterial walls and contributing to plaque formation.

Independent of Cholesterol Content:

The cholesterol content does not influence ApoB measurement within these particles. Therefore, it provides a clearer picture of cardiovascular risk, especially in cases where LDL cholesterol (LDL-C) levels might be normal, but the number of LDL particles (and thus ApoB) is high.

HDL-TG Ratio: A Marker of Lipid Metabolism

The HDL-TG ratio, which is the ratio of high-density lipoprotein cholesterol (HDL-C) to triglycerides (TG), is used as a marker to assess lipid metabolism and insulin resistance. A high HDL-TG ratio generally indicates a favorable lipid profile and a lower risk of cardiovascular disease. However, this ratio has limitations:

Indirect vs direct measure:

Indirect Measurement: The HDL-TG ratio provides an indirect measure of cardiovascular risk. It does not directly quantify the number of atherogenic particles but rather gives a sense of lipid metabolism status. While a low HDL-C and high TG level can indicate higher cardiovascular risk, it doesn't directly account for the number of atherogenic particles present.

Variability and Confounding Factors:

Several factors can influence the ratio, including lifestyle, diet, and metabolic disorders, which can confound its predictive value for cardiovascular risk. Additionally, HDL-C levels alone have not consistently been shown to correlate with reduced cardiovascular risk, as HDL particles can vary in functionality.

Why ApoB is More Important

Predictive Power: Numerous studies have shown that ApoB is a stronger predictor of cardiovascular events than the HDL-TG ratio. For instance, the INTERHEART study highlighted that ApoB levels were more predictive of myocardial infarction than other lipid markers, including the HDL-TG ratio.

Comprehensive Risk Assessment: ApoB accounts for all atherogenic particles, providing a more comprehensive assessment of cardiovascular risk compared to measures that only consider cholesterol content or ratios of different lipid components.

 Focusing on the Right Metric

In summary, the focus has shifted from LDL particle size to the number of atherogenic particles, as measured by ApoB. This shift is grounded in the understanding that cardiovascular disease risk is more closely linked to the number of these particles rather than their size or cholesterol content alone. Therefore, ApoB provides a more accurate and reliable measure for assessing cardiovascular risk.

Conclusion

While both ApoB and the HDL-TG ratio can provide valuable information about lipid metabolism and cardiovascular risk, ApoB is considered more important due to its direct measurement of atherogenic particles. This makes it a more reliable and comprehensive marker for assessing the risk of atherosclerosis and related cardiovascular events.

 

Citations:

Sniderman, A. D., & Tsimikas, S. (2014). Apolipoprotein B. Circulation, 129(11), 1112-1120.

Packard, C. J., & Shepherd, J. (1999). Lipoprotein heterogeneity and apolipoprotein B metabolism. Atherosclerosis, 141(1), 27-42.

McQueen, M. J., Hawken, S., Wang, X., Ounpuu, S., Sniderman, A., Probstfield, J., ... & Yusuf, S. (2008). Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case-control study. The Lancet, 372(9634), 224-233.

Cromwell, W. C., & Otvos, J. D. (2004). Low-density lipoprotein particle number and risk for cardiovascular disease. Current Atherosclerosis Reports, 6(5), 381-387.

Mora, S., Otvos, J. D., Rifai, N., Rosenson, R. S., Buring, J. E., & Ridker, P. M. (2009). Lipoprotein particle profiles by nuclear magnetic resonance compared with standard lipids and apolipoproteins in predicting incident cardiovascular disease in women. Circulation, 119(17), 931-939.

Packard, C. J., & Shepherd, J. (1999). Lipoprotein heterogeneity and apolipoprotein B metabolism. Atherosclerosis, 141(1), 27-42.

Sniderman, A. D., & Furberg, C. D. (2008). Age as a modifiable risk factor for cardiovascular disease. The Lancet, 371(9623), 1547-1548.

Cromwell, W. C., & Otvos, J. D. (2004). Low-density lipoprotein particle number and risk for cardiovascular disease. Current Atherosclerosis Reports, 6(5), 381-387.

Sniderman, A. D., & Tsimikas, S. (2014). Apolipoprotein B. Circulation, 129(11), 1112-1120.

Harchaoui, K. E., Visser, M. E., Kastelein, J. J., Stroes, E. S., & Dallinga-Thie, G. M. (2009). Triglycerides and cardiovascular risk. Current Cardiology Reviews, 5(3), 216-222.

McQueen, M. J., Hawken, S., Wang, X., Ounpuu, S., Sniderman, A., Probstfield, J., ... & Yusuf, S. (2008). Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case-control study. The Lancet, 372(9634), 224-233.

Transcript
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>> Dr. Terry Simpson: In the topic about heart disease, you're going to

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hear a lot about cholesterol. And it

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gets confusing, because you're going to hear about good cholesterol,

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bad cholesterol, LDL, hidl,

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apob, small size, large

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size, what does it all mean?

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You're going to hear people state that LDL isn't important, but

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that the size of particle or the oxidation is important.

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And while all of this gets obscure,

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today we're going to make sense of the madness

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and show you how size isn't

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important.

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I am, your chief medical explanationist, doctor Terry Simpson,

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and this is fork U forked

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university, where we make sense of the madness. Busting

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a few myths and teach you a little bit about food

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is not always medicine.

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Maybe you heard about LDL being the bad

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cholesterol and HDl being the good cholesterol. And we

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have to check your HDl triglyceride level

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on and on and on. It really gets

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confusing. Stripping away the good and bad

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labels, we know that cholesterol, first of all, doesn't just

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float around in your blood. Cholesterol is oil based

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or waxy. And since your blood is water

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based, we have to carry the cholesterol in

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something. And so the cholesterol is placed in these

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little packages of protein, and

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those proteins are classified by their weight in a

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centrifuge. And over time, we found that these

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low density lipoproteins, that those

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packages are responsible for

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leaving deposits in the walls of your

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arteries. And those deposits are called

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atherosclerosis. And if you get a bunch of them together,

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it's called a plaque. And those

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plaques, when they rupture, lead to a heart attack

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or to a stroke, or if they impinge on the

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artery, meaning they start decreasing the flow of the

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artery to the heart, they lead to heart ischemia

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or angina. So

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LDL isn't a one size fits all villain.

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All the LDL particles vary in size, density,

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oxidation, et cetera. So we're going to sort

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of strip away one of the more common myths that I

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heard, that you have to worry about

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LDL, particle size. As if you couldn't hear

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enough. We're going to strip that away because you don't

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need to care about the size anymore. Size of the

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LDL particle isn't important. And you don't have to

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remember these old terms, like pattern a, large fluffy

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particles are good. Pattern B, small dense

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particles, are bad. Because the recent

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research has shifted focus from the LDL particle

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size to one of the lipoproteins

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that surrounds the cholesterol, called apolipoprotein B,

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which we will call ApoB.

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Think of it this way. If you want to

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not have messy tea, you

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put your loose tea in something

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like a teabag. Think about the

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teabag as being partially held

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together by one of these apob molecules,

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right? So every single teabag, or

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LDL particle carries one of

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these little proteins, that Apop protein. Think of the tea

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as the cholesterol. But that protein is a

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passport that allows that

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teabag to enter into the cell

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wall of the artery,

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not just passively, but it's actively

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transported in. If there's an LDL particle, it's actively

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transported into this cell wall.

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And if there are too many LDL, particles in

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that cell to be metabolized by that

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cell, it tosses the LDL particles

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out the backside of the cell into the wall of the

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artery between the first and second layer.

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That's where they build up, that's where they oxidize,

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and that's where they can ultimately get so large

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that they impinge on the artery wall, leading

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to less blood flow to, like, the heart

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artery, or less blood flow to the brain,

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which can cause ischemia, a heart attack, or stroke.

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The key is how many apob

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particles there are. Now, we used

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to think that that was the answer. The size

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of the particle. We used to think small particles.

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Wow. They're the bad ones, because when we looked at the research,

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we saw small particles had more atherosclerosis. Is this

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confusing you? But think about this. The more small

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particles you have, you're gonna have more

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apob, because if you bake a lot of little tea

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bags, you gotta sew it together with that apolipoprotein

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b, and that's a problem.

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The particle number gives us a count of

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how many of these atherogenic particles there are.

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We call them atherogenic because the ApOB

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particle is the thing, the particle that

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leads to atherosclerosis. Doesn't matter

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how large, how much tea is in the

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teabag, how much cholesterol

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is in the LDL particle. What matters

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is how many of them are circulating in your blood.

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Now, I've, heard people say, well,

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cholesterol's important. It is. Cholesterol's

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used in every cell. It is. Cholesterol's used to

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make steroid hormones, like testosterone, estrogen.

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It is. Cholesterol's important to your brain. It

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is. But too much cholesterol, like too much

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water or too much salt, or too much blood

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sugar, is bad. Too much

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cholesterol leads to atherosclerosis.

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Some people say God doesn't make mistakes. Well, I don't know if God

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made a mistake or not. We're not going to live forever. But if

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you want to live longer, you want to have less

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atherosclerosis. There have been

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a number of articles that have shown this, that it is

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the number of apob particles,

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nothing, not the size of

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the molecule. And there's two ways of looking at this.

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If you have a bunch of little tiny molecules of ldl, which

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have small particles, and they get in and they're tossed out

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to the back, well, it's going to take a lot of those

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to build one large cholesterol particle which is

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equally actively transported in. So

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you have a lot of large, fluffy particles, you'll have a

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faster buildup. Now, what are things that increase

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apob in your body? One of them

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is sugar. That's why

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diabetics need to be under better control, because

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more glucose in your blood, the more spikes you have, the more

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insulin resistance you have, the more diabetes you have, you're making

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more APOB particles. The more apob particles, the more

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atherosclerosis, the higher your risk of heart disease.

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That's all. That's as simple as that.

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So here's the key. This month,

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when you go to your doctor, APOB is the

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test you want to ask for. They'll give you a standard

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cholesterol panel. It'll have your hdl, your

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ldl, your total cholesterol, your

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triglycerides. Ask to get an

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APOb test. And while you're at it, also ask to get a

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PSA test, because this month, this month,

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we want you to do cancer screening. So, American

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Cancer Society, what's my number? Screen me,

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etcetera. So there's been lots of

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meta analysis of participants showing how APOB is a stronger

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predictor of heart events than cart particle

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size. And I won't bore you with it, but if you want to find out more of

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the detail and more of those for the nerdy bunches of

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you, and most of you are nerds, go to the blog associated with

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this@yourdoctorsorders.com or four

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q.com.

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now, how can diet and lifestyle affect the

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apob number? We already talked about refined grains,

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but saturated fat like red

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meat increases apob

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particles. Lean meat,

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plant based fats like olive oil and

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avocado don't. They might actually

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decrease APOb number. So changing your diet from

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saturated fats to less saturated fats when you get

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below 9%, we see that change.

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I know the low carb people never like this because

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they want to wave off cholesterol, because every

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article out there shows that low carb and keto diets lead to

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higher ldl numbers,

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increasing the fiber in your diet. Soluble fiber, like

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foods found in oats, beans, and fruits,

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reduce the number of ldl and apob particles in your

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bloodstream. How do they do that? Because here's

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what happens when your liver

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makes ldl. Because this cholesterol is made and you're packaged

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in your liver, what happens is it doesn't

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just throw it into your bloodstream. It makes

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all these ldl particles and puts it into your bile.

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Your bile is secreted by your liver and goes into your

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intestine, and from your intestine, it goes into your

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bloodstream. Now, when you eat more

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fiber, the fiber binds

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to those LDL particles, and those fibers

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that bind to the LDL particles

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passively go out of your backside

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into the toilet. Right.

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Diets that are high in processed carbs and sugar raise apob

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levels. And so those diets also have less

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fiber. So increasing the fiber in your diet not only makes

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you feel full longer, it decreases your

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apob particles. I'll give you another

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example. Whole grains, brown

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rice, quinoa,

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oats, corn,

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all have fiber that

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decrease apob. Refined grains don't have

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fiber. Lead to sugar spikes lead to more

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manufacturing of apob. That's why refined

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grains aren't good. That's why whole grains are.

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Okay? Okay, so to wrap

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this up, while we used to think the size of the

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LDL particle was important, it really is apob.

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Ask your doctor for an apob. That's how we

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get a better picture of your heart. What should your levels be? In the

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United States, we want your apob levels to be under 100.

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In Europe, we want them under 70. We'll probably go to under

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70. Why do we keep changing this every

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year? Because we have discovered over time that the lower

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your total cholesterol number is, the healthier

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you are. Now, there are m those people who say, well, you know,

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long live people have higher ldls.

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Okay? If you get to be old, you can have a

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higher ldl. But remember, there are many other things that

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influence this. Meaning this. I'll

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give you one example. There's a genetic

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predisposition to people called the PCSK nine

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transport system. And if you have a genetic

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defect in that, you can have high ldl,

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but you also have high ldl

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receptors. Because you have high ldl receptors, you

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don't have that much ldl in your body. It's cleared very

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quickly. And those people live

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long. Remember, longer lived people,

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still die of heart disease, still die of cancer, still

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have diabetes, still have cognitive decline. They

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just put it off for a while.

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So get your ldl down. Is there a

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lower level? Well, we know below. I think it's 53. You're probably

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not going to have heart disease. What do kids

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need? What do you need to maintain the amount of

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testosterone and keep your brain well? Remember your lDl.

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Your brain makes its own cholesterol. It doesn't rely on your

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liver. Your gonads

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make your own testosterone and estrogen. They don't rely on your

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liver. So don't listen to people who say, that's

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all I terribly important because too much cholesterol, like

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too much salt, like too much blood sugar is

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deadly.

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All right, go to my blog, yourdoctorsorders.com, or

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fork u.com, to see all

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of the references and you can look them up for yourself. This

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episode was written and researched by me, doctor Terry Simpson.

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And while I am a doctor, I'm not your doctor. Please

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see your doctor, a western trained, non

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chiropractic, non eastern trained

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physician. And if you're curious about, what

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your LDl APOB number is, please see your regular doctor for

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that. Podcast is distributed by our friends

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at Simpler Media than the pod God, Mister Evo

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Terra. Our production is done by producer Girl Productions, who

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insist on my hair being perfect even though we're not

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doing video today.

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Until next time, stay curious. And

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remember, food can be a powerful influence on your

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health.

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This month is cancer screening month for

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prostate cancer. See, we want you to know your PSA

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number, just like I know my APOb number, which is 63.

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My PSA number is three. We want it under four.

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So I hope this month you go to the American

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Cancer Society, get screened, find out your

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psa number. Because after all, min 50

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and over, we need to know the number. And I hope

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yours is less than four. And be sure and check

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out your apopee number. Also.

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>> Speaker B: 2.97, I'm happy to report. And

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yes, that is checked on a regular and frequent basis with

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me. And thanks for the information on the

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APOB. I'm never going to drink tea in a

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teabag again.

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About the Podcast

Fork U with Dr. Terry Simpson
Learn more about what you put in your mouth.
Fork U(niversity)
Not everything you put in your mouth is good for you.

There’s a lot of medical information thrown around out there. How are you to know what information you can trust, and what’s just plain old quackery? You can’t rely on your own “google fu”. You can’t count on quality medical advice from Facebook. You need a doctor in your corner.

On each episode of Your Doctor’s Orders, Dr. Terry Simpson will cut through the clutter and noise that always seems to follow the latest medical news. He has the unique perspective of a surgeon who has spent years doing molecular virology research and as a skeptic with academic credentials. He’ll help you develop the critical thinking skills so you can recognize evidence-based medicine, busting myths along the way.

The most common medical myths are often disguised as seemingly harmless “food as medicine”. By offering their own brand of medicine via foods, These hucksters are trying to practice medicine without a license. And though they’ll claim “nutrition is not taught in medical schools”, it turns out that’s a myth too. In fact, there’s an entire medical subspecialty called Culinary Medicine, and Dr. Simpson is certified as a Culinary Medicine Specialist.

Where today's nutritional advice is the realm of hucksters, Dr. Simpson is taking it back to the realm of science.

About your host

Profile picture for Terry Simpson

Terry Simpson

Dr. Terry Simpson received his undergraduate, graduate, and medical degrees from the University of Chicago where he spent several years in the Kovler Viral Oncology laboratories doing genetic engineering. Until he found he liked people more than petri dishes. Dr. Simpson, a weight loss surgeon is an advocate of culinary medicine, he believes teaching people to improve their health through their food and in their kitchen. On the other side of the world, he has been a leading advocate of changing health care to make it more "relationship based," and his efforts awarded his team the Malcolm Baldrige award for healthcare in 2018 and 2011 for the NUKA system of care in Alaska and in 2013 Dr Simpson won the National Indian Health Board Area Impact Award. A frequent contributor to media outlets discussing health related topics and advances in medicine, he is also a proud dad, husband, author, cook, and surgeon “in that order.”