About 34 minutes of reading time.
Ask questions. Learn. Evolve.
As of April 2023, this is the latest update in my learnings. I have gone down a “few roads” in trying to understand cholesterol and its assumed role in cardiovascular disease, what caused my heart attack, and of course how to not have another. First, it is important to realize that cholesterol (actually lipoproteins) is only ONE component of cardiovascular disease.
There are many thoughts and views on this subject and it can be very confusing! In fact, once I think I really understand it, I get thrown a curveball, and my understanding changes. That is part of the process of learning and evolving, isn’t it? When we receive new information, we should expand upon that WITH LOGIC by applying it to what we currently know and have experienced. I want to stress the importance of that, however sometimes things don’t seem logical in one sense, but overall they can once you look at different things in context.
Once I cover some bases, I’ll do my best to communicate my thoughts and experiences in shorter bits than this article used to be. So if you’ve already read it in the past, check it out because this version contains different information and is laid out a bit differently.
This article got LONG! So I’m shortening it up by making supplemental posts. You’ll see the links, and I HIGHLY suggest that you read those too!
Is cholesterol bad and who knows best?
No, yes, maybe; it depends on with whom you discuss this topic. What is the information we’re being told based upon? A study or an analysis of studies, or someone’s theory? How good is the data? Are the subjects human? If they are human, how was the data collected? Was it a questionnaire like, “How much _____ did you eat and how often in the past week, month, or year?” WHO are the subjects? How is the data filtered? What are the goals of the study? What is the goal of who is telling us what they are telling us? Who was it funded by? I don’t even want to post links to studies anymore because holes can be found in most of them and for every study that exists, there can be another one published to contradict it! If I don’t then people will then say I’m making stuff up. I’ve posted links and even some videos from people who make a lot of sense, but I’ve seen other videos and links that really contradict them in various ways.
Perhaps the best approach is to remove the noise, experiment with the things that make logical sense, and see what works. I will show you that a high-fat/low-carb (including saturated fat) way of eating (not KETO) for a few months dramatically IMPROVED my lipid profile. This goes against many recommended guidelines and suggestions from authoritative sources. The thing is I’ve taken information from a variety of sources that all contradict each other in some way!
Who is telling what?
I’ve read a lot and watched a lot of videos. One thing I look at is the source. Does the source have a personal history like mine? Has the source actually HELPED people? Does the source just blurt out information and what is that based on?
There are many people who are not doctors or are doctors specializing in another field who have a lot of knowledge about cardiovascular disease but are often fact-checked and “debunked” because they misspoke or didn’t provide supportive data to back up a claim. Then other people will dismiss them because they’re “just a chiropractor” and then I’m here thinking, “I’m just a video/media production guy here telling you about this stuff.” I’m like a sponge soaking this stuff up, experimenting, and sharing my experiences because I have made SIGNIFICANT advances in my health.
I’ve had even healthcare professionals including my own medical doctor tell me that I “should share this with other people.” I’m going to say this, “We didn’t need anyone’s permission or scrutinize the unhealthy foods that made us unhealthy, so why should we highly scrutinize anyone for trying to help others get healthier?” That is illogical to me. The purpose of this page is for me to share MY understanding and experiences with you. Again, cholesterol is ONLY ONE component of cardiovascular disease, but it can be pretty important and can tell us a lot about our overall health.
My goal all along when I created (and maintain) this site is to share what I learn and the results that I’ve achieved in my health journey. So is cholesterol bad? I don’t believe so because:
- Cholesterol is NOT THE cause of heart attacks or cardiovascular disease!
- Cholesterol IS an important molecule for the body AND the body actually makes it!
For your information and more understanding.
Red links will open in a new tab. I suggest that you click them and read them AFTER reading this article. Remember, every study and article can have another to contract it, AND there may be a lot of great information but a small bit of incorrect information in them too, so if you see something that doesn’t align with my article, THINK and then let’s discuss if you have reasonable thoughts or even experiences that may help me learn something new. I’m always open to learning new things.
If available, I STRONGLY SUGGEST that you read the supplement articles for each section! Those were written to reduce the overall size of this page. Some people thought this article is too long, so I’m trying to make it easier to read, but ALL of the information is important for the overall context of my learnings.
Some definitions we need to first understand in the scope of this article.
- Association: the state of being associated–related, connected, or combined together.
- Correlation: a relation existing between phenomena or things or between mathematical or statistical variables which tend to vary, be associated, or occur together in a way not expected on the basis of chance alone.
- Causation: the act or process of causing–a reason for an action or condition.
- Atheroma: an abnormal fatty deposit in an artery.
- Atherogenic: relating to or causing atherogenesis, which is the formation of atheroma.
- Cholesterol: a steroid alcohol C27H45OH that is present in human and animal cells and body fluids, regulates membrane fluidity, and functions as a precursor molecule in various metabolic pathways.
- Lipoprotein: a protein “ball” that transports lipids and cholesterol throughout the bloodstream to be used in other parts of the body.
- Triglyceride: any of a group of lipids that are esters formed from one molecule of glycerol and three molecules of one or more fatty acids, are widespread in adipose tissue (connective tissue in which fats are stored), and commonly circulate in the blood in the form of lipoproteins. (Referenced as TG for short.)
- Apolipoprotein: a protein that combines with a lipid to form a lipoprotein. Two in particular for short is ApoA and ApoB.
- Density: the mass of a substance per unit of volume.
- Moderation: the avoidance of excess or extremes.
Classifications & Descriptions of Lipoproteins that contain cholesterol.
We often hear about LDL being the “bad” cholesterol and HDL being the “good” cholesterol. There are more types based on their sizes and densities. Let’s see where LDL and HDL line up with the others.
Here is an image I made that shows the lipoprotein classifications in regard to their size and density.
LDL (Low-Density Lipoproteins): Created from VLDL and IDL particles and they are even further enriched in cholesterol. LDL carries the majority of the cholesterol that is in circulation. It is worth knowing as referenced here that LDL moves cholesterol around in the body to where IT IS NEEDED. Yes, LDL plays an important role. More will be discussed about these particles later, but the smaller LDL is considered more pro-atherogenic.
– Size: 18-25 Density: 1.019-1.210
HDL (High-Density Lipoproteins): These particles are important for returning cholesterol back TO the liver which makes them be considered anti-atherogenic. It is important to note that HDL particles have anti-oxidant and anti-inflammatory properties.
– Size: 5-12 Density: 1.063-1.210
Let’s note that ALL of the lipoproteins above EXCEPT for HDL contain ApoB. HDL is the only lipoprotein that does NOT contain ApoB.
“They” led me to believe cholesterol is bad.
I was conditioned to think (by hearing and reading regurgitated similar narratives) that I must get my cholesterol numbers down as low as possible. They said to especially reduce that LDL or “bad and evil cholesterol,” and raise my HDL. It didn’t really make sense to me, but they’re the experts and I’m not, so whatever. I quit smoking, started exercising, ate better, and took my statin like a good patient. My standard/basic lipid test results showed my “bad” levels returned to “normal” within four months except for the HDL. The LDL is the only thing my old-school cardiologist was concerned about. 🤦♂️ In all fairness to him, we only know what we’re taught. Just as I opened this article up; we MUST ask questions, learn and evolve!
Much better! Woohoo! My cardiologist lowered my Atorvastatin from 80 mg to 40 mg, and I continued my new healthy journey. Of course, I was excited when I got this result, but later on, I learned that cholesterol can be too low and according to this article, April’s results were getting too low!
Depression and anxiety can spring from many causes, including possibly low cholesterol. Symptoms include:
- Difficulty making a decision
- Changes in your mood, sleep, or eating patterns
I thought many of those were from a drastic lifestyle change of cutting out sugar, smoking, heart attack effects, etc. Hmmmm… 🤔
Ratios tell more than any of the individual cholesterol numbers.
Early on in my research, I learned from several places that ratios can be important indicators of cardiovascular issues. I discovered an online calculator where you enter your numbers, and it will update with the ratios. I ended up coding my own calculator based on some of its functions and added a button where you can compare the current results to an older test. Check out by Cholesterol Ratio Calculator, it’s pretty cool!
First, let me list the ranges for the ratios.
- LDL:HDL Ideal: less than 2.0 Good: 2.0-5.0 Bad: 5.0+
- TG:HDL Ideal: Between .5-2.0 Good: 2.0-6.0 Bad: 6.0+
- Total:HDL Ideal: less than 3.5 Good: 3.5-5.0 Bad: 5.0+
Let’s look at my ratios from the two tests.
When we look at these ratios, you’ll see that everything is in relation to HDL. As referenced above, that IS the only lipoprotein that is considered anti-atherogenic. This makes logical sense in that regard. However, note that this doesn’t tell us if the HDL is of good quality or not.
Did LDL cholesterol cause my heart attack?
One month shy of two years before my heart attack, I had a physical that included a standard/basic lipid panel. I didn’t notice this until late 2020 when I went through one of my online health portals. Knowing what I know now, I was a prime candidate for a heart attack back then, and NO ONE told me I was at risk! I called that doctor’s office to ask because it said the total cholesterol was high. The lady replied, “If the doctor thinks it is bad, he’ll call you.” He never called. I couldn’t stand that “doctor” anyways, and I never saw him again; however, I would LOVE to have a discussion with him! Let’s take a look.
At the time of my heart attack, my LDL-C was LOWER, and my Triglycerides were HIGHER than in 2016! My HDL dropped even lower and HDL is the driving factor to all the ratios, which were out of whack both times. That was a check engine light that I ignored, but in my defense, I didn’t know any better, and even the old doctor’s office said that if the doctor thought it was bad, he would have called. 😡
This is one reason I put this site together, to help inform of what I have learned, so hopefully, it’ll help someone change what needs changing so they won’t go through what I did. Based on this and IF LDL-C is the sole thing we should watch out for (old-school cardiologists and mainstream health sites), why didn’t I have a heart attack in November 2016 when it was higher? Because LDL is NOT the root cause of cardiovascular disease!
So no, LDL-C did NOT cause my heart attack. We can clearly see that it was lower than two years prior. That old way of thinking needs to be gone! It’s got to be something else.
Did higher Triglycerides cause my heart attack?
This is what I ended up thinking was the cause for a long time. I mean, in relation to HDL that ratio of 9.13 was 3.1 OVER what is considered bad. High TG serum count is basically from unused carbohydrates (sugars) that are stored as fat in the bloodstream. This makes a lot of sense considering I was a sugarholic AND my daily exercise was to go up the stairs to go outside to smoke.
Part of my early lifestyle changes was to cut out added sugars. As a result, that was very apparent in the January vs April image of the TG numbers, BUT everything else was also reduced while my HDL went up 6 resulting in an ideal ratio. This was good progress, but what did it really mean?
Something that kept coming up in my learning was chronic inflammation being the root cause of many diseases and ailments. What is a major cause of chronic inflammation? High consumption of sugars and refined carbohydrates! I consumed a lot of them and my triglyceride levels reflected that. Looking back on it now, I believe my triglycerides had a stronger association with my heart attack, BUT was that enough to cause it? Not 100% but we’re on to something.
9 months after my heart attack with better overall cholesterol ratios.
Let’s take a look at September 2019 vs April 2019. Keep in mind this is 9 months after my heart attack. I’ve been exercising by walking and running; eating much healthier than ever; and quit smoking while not using any nicotine products. Let’s look at April vs September.
My HDL went up by 10, TG went up by only 1, yet my LDL-C went up. I saw a fill-in physician for my PCP as she was out of the office at the time, but he was very knowledgeable about this stuff. I told him I wanted him for a cardiologist! 😆 He loved my progress and reduced my statin down from 40 mg to 20 mg, EVEN THOUGH my LDL went up.
So there is proof in the pudding that ratios do matter more than a single number. At least it did in this doctor’s opinion.
Does HDL really need to be 40 or more?
I often hear “I need my HDL up to 40.” Why? Because on the test results, it is suggested that we need it greater than 39. I have a problem with this (and other references for many test items.) What good is an HDL-C of 40? In relation to what? For example, IF we had an HDL-C of 40 and LDL-C of 100, then that would be a 2.5 ratio. What if that LDL-C was 200? Then we’d have a ratio of 5! That is too high! We would need HDL-C to be 80 to have the same 2.5 ratio if LDL-C was 200. So old ways of thinking, 80 would be “incredible” but really, only if LDL-C was 160 or lower which would have an ideal ratio of at least 2.0. I feel that all three ratios mentioned above are more important when looked at together rather than just one by itself. For example, having an ideal LDL:HDL ratio is great, but the whole situation isn’t great if your TG:HDL ratio is very high.
Making strides and wanting to make sense of things.
I’ve been doing some pretty incredible things that I never thought were possible. I ran track in middle school but never ran in my adult life, yet here I am now banging out Half marathons (13.1 miles if you didn’t know) and even placing in my age group in some local races! You may be saying there are runners who have heart attacks, but ok… walking 5 minutes at a time was all I could do early in my recovery stages and I had to do that 6 times a day to get my 30 minutes in! I coughed a lot from smoking. I was very unfit. So I went from that to this by doing particular things that work. I like knowing how and why things work and with that comes going down some rabbit holes. 😆
The basic lipid profile is just scratching the surface. All it does is weighs the MASS of cholesterol in the LDL-C and HDL-C lipoproteins. Milligrams per deciliter. That’s it. Weight. Not actually counted. In fact, LDL-C’s mass isn’t even measured as LDL-C is often calculated (not entirely accurate either) 🙄 What? YES! I have a problem with this because IF we’re supposed to put so much weight and decision-making into this LDL-C number, then WHY is it being calculated and not measured? That doesn’t make sense to me and seems a lot like the bogus formula of 220 – AGE = Maximum Heart Rate. 🙄 Let’s get deeper because some calculated LDL number can’t be causing cardiovascular disease. It doesn’t make sense.
What is atherosclerosis?
The American Heart Association states it as: Plaque (fatty deposits) build up in your arteries is called atherosclerosis. These deposits are made up of cholesterol, fatty substances, cellular waste products, calcium and fibrin (a clotting material in the blood). Atherosclerosis is a type of arteriosclerosis. Arteriosclerosis means hardening (sclerosis) of the arteries.
Johns Hopkins Medicine states it as: Atherosclerosis thickening or hardening of the arteries. It is caused by a buildup of plaque in the inner lining of an artery. Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin. As it builds up in the arteries, the artery walls become thickened and stiff. Atherosclerosis is a slow, progressive disease that may start as early as childhood. However, it can progress rapidly.
See where we can get confused right off the bat with this? The American Heart Association is saying it is just a buildup in the arteries. Johns Hopkins says it is a buildup of plaque IN the inner lining of an artery. THIS IS A HUGE DIFFERENCE! The AHA makes it seem like it is a pipe clogged with gunk. Johns Hopkins clearly illustrates it as the pipe’s walls are getting thick and closing up! Technically the AHA is correct, and if you watch their animation that you have to go to another page to view, it shows what Johns Hopkins is saying. BUT there are MANY people (myself included early on) who believe that plaque just builds up like mud in a drainage pipe. That is not the case!
What are two of the commonly accepted hypotheses of atherosclerosis causation?
First things first, it is commonly thought that atherosclerosis is a modern disease. I did until I was updating this article until I stumbled across this. Atherosclerosis is present in 5,000-year-old Egyptian mummies! That is interesting for sure.
I provide a link to each, but for now you don’t have to read through them. Just be aware of these two.
In essence, the theory is that atherosclerosis begins with injury to the endothelial lining of arteries. Refinements over the years lead to the inclusion/awareness of plaques resulting in foam cells which are essentially macrophages gobbling up the bad stuff. Read all about it here.
In addition to this, it is believed that the smaller particles can penetrate the artery wall more easily than the larger particles.
Of course, it seems logical to think that if there is damage to the arterial walls, then those particles can easily enter.
Basically, this suggests the subendothelial retention of ApoB-containing lipoproteins. Retained lipoproteins are chemically and enzymatically modified, inducing a chronic inflammatory response.
This makes sense too and seems to be secondary to the Response-to-Injury, but it’s not always 100% of the time. I’ll explain later so be sure to read the rest!
Digging deeper into cholesterol by actually counting particles and measuring their sizes.
It isn’t a good idea to get your news by reading only the headlines; it is best to read the whole story. Let’s think of the basic lipid panel/cholesterol test as a news headline. Then we can think of the ratios as a very short description of the story. A Nuclear Magnetic Resonance (NMR) test counts the particle numbers and measures sizes can then be thought of as being most of the story.
Around September 2019 after that doctor visit, I was learning about particle size and the NUMBER of LDL and HDL particles. I order this test through RequestATest.com and you can too. This NMR test is basically going to tell us about the QUALITY of the lipoproteins.
YOU CAN’T KNOW IF YOUR CHOLESTEROL IS “GOOD” BASED ON A STANDARD TEST! (Read that until it sinks in.)
Insulin resistance vs Insulin Sensitivity and Cholesterol Particle Sizes
Here is part of the reason for editing this article again. I’m basically combining an additional section that could have been a whole new article into this. This is why we’re going to see entries with big gaps in time. I will show 12/2019 which was a year after my heart attack, 12/2020 which was a year after that showing a big change, then 6/2022 where my cardiologist was THRILLED and kept me on my low 10mg dose of Atorvastatin, and 12/2022 where I had obtained a lipid profile that I didn’t think was actually possible. There are some key things to discuss with each. It is worth noting that I usually get this done every 3 months ON MY OWN. My ratios and overall results are great. My doctor and new cardiologist are ALWAYS very happy with me.
This image will look very confusing look at each item one at a time and note each triangle. Each triangle represents a different test date. We want to be going into the green. Green = good 👍.
It’s understandable if this is confusing to look at, but let’s break some of this down.
LDL Particle Sizes and how do they matter?
I initially learned to think of LDL as the particles that get stuck in cracks within the arteries that CAUSE plaques. Some sites even say they stick to the artery walls, but that’s not entirely true.
As briefly discussed earlier the Response-to-Injury hypothesis, it is believed that larger LDL particle sizes won’t get stuck in the arteries’ cracks and crevices that end up causing blockages. Simply put, an inflated beach ball won’t fit into a golf cup. While this theory seems perfectly logical, and one that I 100% FULLY AND SOLELY believed in until recently, it isn’t the entire reason we would want larger particles. We’ll discuss this later, but sizes ARE important!
Notice the LDL particles’ size got bigger as time went on, and how the LP-IR score also got better which we’ll cover shortly. There are two entries for this on the main image. The top one is just grouped into two categories and we want them to be in the “Large Pattern A” group. (Notice how this test has a range of sizes from 19-23, and earlier in the classifications LDL was from 18-25. It doesn’t matter, but does show an example of a discrepancy that exists.)
Larger particle sizes are generally considered to be healthier particles. Remember, good = green so we want to be on the left side of this scale. As you can see, I progressively got those LDL particle sizes larger over time. It is worth noting that they varied from test to test with different experiments. You are seeing the worst and the best that I’ve tested. I wish I had this test back when I had my heart attack!
The same LDL-C number can be of different sizes!
I want to note something very interesting and this will illustrate my case of why we shouldn’t necessarily go by just a number. The red triangle is from 12/2019 and the green one is from 6/2022. LDL-C was 108 vs 103 respectively, but look at the size difference between the red and green triangles! THAT IS INCREDIBLE!
Now some folks may say, well the LDL was lower, of course, it got better. Ok then, let’s compare to 12/2022 where the LDL-C increased to 137 and LDL-P increased to 1297. This is more LDL-P than June’s, but less than 12/2019. The size increased considerably once again. In fact, ALL of the sizes increased to some of the best I’ve ever had, AND I obtained the best ratios ever in December 2022. How? Keep reading…
What is Small LDL-P and its role in plaque buildup?
Small LDL-P is the smaller “Pattern B” group of LDL particles which range in size from 19.0-20.5nm on this test. Remember earlier in the article where we talked about the classification of lipoproteins? I’m now going to add more to that LDL section and quote directly from the National Library of Medicine article that I linked to: “An abundance of small dense LDL particles are seen in association with hypertriglyceridemia, low HDL levels, obesity, type 2 diabetes (i.e. patients with the metabolic syndrome) and infectious and inflammatory states. These small dense LDL particles are considered to be more pro-atherogenic than large LDL particles for a number of reasons. Small dense LDL particles have a decreased affinity for the LDL receptor resulting in a prolonged retention time in the circulation. Additionally, they more easily enter the arterial wall and bind more avidly to intra-arterial proteoglycans, which trap them in the arterial wall.” What is a proteoglycan? They are proteins that are heavily glycosylated. Glycosylation is the process by which a carbohydrate is covalently attached to proteins and lipids in this case.
I consider THIS is very important, particularly for how they are associated with higher triglycerides, low HDL, inflammation, Type 2 diabetes, and they’re MORE EASILLY TO GET TRAPPED IN THE ARTERIAL WALL! For these reasons, Small LDL-P “Pattern B” should be considered as damaged and not good for the body to utilize.
It is very interesting that in this test, the desired target is <527 and LDL-P is <1000. Remember I have a problem with a lot of test targets. This is why. They are alluding to it being acceptable if 52.7% of one’s LDL-P is Small LDL-P. So 52% can be damaged and that be ok? That doesn’t make sense to me. My Small LDL-P result was “<90” which is nice that they can’t actually count that low of small damaged LDL particles! Let’s say it was 90. LDL-P was 1297, so that is only 7% are damaged IF it was in fact 90, but it was actually less.
How much would you find to be acceptable? Seriously! If Small LDL-P is damaged and those are the particles that get stuck in the artery walls, how many do you want floating around in you? It is something to think about.
What is up with the VLDL?
You’ll notice from right to left that all the items EXCEPT for the Large VLDL-P and VLDL Size progress to the green in order of red, blue, green, and black. That is the order of older dates to the more recent ones. Progressively getting better and becoming more insulin sensitive according to this test. The Large VLDL-P count seems to be randomized and the VLDL Size from December 2020 and June 2020 was almost identical.
Since VLDL particles are predominately triglycerides, it makes sense that their sizes get smaller as TG is reduced. But, what’s up with the particle count seeming random? I honestly don’t know and can’t figure that one out, nor can I find out this information!
What is Insulin Resistance and its association with cholesterol particles?
Insulin is a hormone that is produced by the pancreas that delivers glucose in the blood to the cells in the muscles, liver, and fat where it is used for energy. This is important as it stops sugar (glucose) from building up in the bloodstream. However, when the cells are “full”, they don’t want any more glucose and tell insulin “go away, we don’t need more fuel.” Thus, over time, this makes one’s cells resistant to insulin. Insulin is also a “fat storage hormone” and that makes sense as unburned glucose is converted to fat. In short, those donuts and soda will pretty much turn to fat in varying degrees. Keep this cycle going long enough and Type 2 diabetes will follow suit (which IS reversible by the way!) An entire article could be written about this, and there are MANY on the web, but this is generally what it is.
Plain and simple, the following largely and commonly contribute to insulin resistance:
- inactive lifestyle
- being overweight
- heavy consumption of carbohydrates, especially sugars and refined grains.
- smoking or anything with nicotine
(Please note that this is not an inclusive list, nor do all the items have to be present to cause insulin resistance.)
The interesting takeaway is the lipid sizes and their relation to insulin sensitivity or insulin resistance.
Smaller LDL & HDL are associated with insulin resistance, whereas larger LDL and HDL are associated with insulin sensitivity.
Conversely, larger VLDL particles are associated with insulin resistance, and smaller VLDL is associated with insulin sensitivity. That makes sense as we want fewer triglycerides and that would result from not partaking in the things just above that contribute to being insulin resistant.
Lipid Profile-Insulin Resistance Score
The “bonus” result. I was concerned with insulin resistance as Type 2 diabetes runs on both sides of my family. Taking a statin can technically (but not very likely) increase insulin resistance and/or higher blood sugar count as a side effect, and that had me worried. Let’s take a peek at those results.
As you can see, I did become fully insulin-sensitive on this scale, BUT it wasn’t progressive like the particle sizes. An interesting comparison is to the Large VLDL-P of the blue and green triangles that are out of order. Does that mean anything? I don’t know, but I’m liking this insulin-sensitivity thing, ESPECIALLY since T2 runs in my family.
Is it possible to become “too” insulin sensitive?
Yes, it may be possible to become too insulin sensitive. This is a good read. My December 2022 results had the lowest TG:HDL ratio I’ve ever had of .63, and as the author was getting at, dipping to less than .5 is getting into dangerous territory as there are too few fats circulating in the blood for adequate energy. I’ll be keeping an eye on this, but I feel fine with all of my training, even during the higher-intensity workouts. I did get a fasting Insulin test in April 2023 and it was 3.0 uIU/mL and the lowest on the reference scale is 2.6. On June’s test, it was 4.7 after adding in some carbs. After a discussion with my cardiologist and being athletic, I’m fine and shouldn’t really worry.
IS INFLAMMATION + OXIDATIVE STRESS = THE ROOT CAUSE?
Throughout all of my research on various topics, chronic inflammation, and oxidative stress always kept coming up. They appear to be at the root of so many many ailments and diseases! Search for whatever disease + inflammation, and whatever disease + oxidative stress. The results are interesting to read through.
Inflammation is the body’s response to cellular injury and is often accompanied by redness, swelling, heat, pain, soreness, etc. Acute inflammation is necessary for the body to heal; however, chronic (long-term) inflammation wreaks havoc on the body. There are many things that can cause it, but we as a population consume a LOT of it through various highly processed manufactured food products, especially the sweets!
This is a long document, but the first sentence of the abstract says it all, “Inflammation triggered by oxidative stress is the cause of much, perhaps even most, chronic human disease including human aging.”
Oxidative stress is a phenomenon caused by an imbalance between the production and accumulation of oxygen reactive species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products.
And another description…
Oxidative stress is the imbalance of antioxidants and free radicals in the body that cause cell and tissue damage. It is a natural part of aging. It can also be premature due to an unhealthy lifestyle which includes a bad diet. (Sound familiar?)
This is a very long article, but I encourage you to read it sometime. It discusses the critical issue linking lipids and inflammation. It goes hand in hand with oxidative stress. Here are the first couple of sentences which are key, and I have bolded the very important parts: “The formation of an atheroma begins when lipoproteins become trapped in the intima. Entrapped lipoproteins become oxidized and activate the innate immune system. This immunity represents the primary association between lipids and inflammation. When the trapping continues, the link between lipids and inflammation becomes chronic and detrimental, resulting in atherosclerosis.“
Another few key sentences: “The entrapment is due to electrostatic forces uniting apolipoprotein B to polysaccharide chains on intimal proteoglycans. The genetic transformation of contractile smooth muscle cells in the media into migratory secretory smooth muscle cells produces the intimal proteoglycans. The protein, platelet-derived growth factor produced by activated platelets, is the primary stimulus for this genetic change. Oxidative stress is the main stimulus to activate platelets. Therefore, minimizing oxidative stress would significantly reduce the retention of lipoproteins. Less entrapment decreases the association between lipids and inflammation.“
Combo of Inflammation and Oxidative Stress
The two seem to be a pretty lethal combination, doesn’t it? Here is a good article that talks about the two and the role antioxidants can play within the body. Take note of the ROS (Reactive Oxygen Species) in the mitochondria. I discuss this in my Zone 2 Heart Rate Training article, but it is super important.
What about oxidized LDL?
I previously wrote about that but I now believe the context was incorrect. I’ve since learned that the LDL can only oxidize once it’s been retained in the arterial wall. Current evidence indicates, however, that pathophysiologically important oxidation can occur only after the retention of lipoproteins within the sequestered microenvironment of the arterial wall. Ok, that makes sense after reading that last section above.
What could be the root cause of cardiovascular disease?
This sounds like a very convincing case to me no matter if we are going by either the Response-to-Injury or Response-to-Detention theories. There are still many people who believe that LDL alone is the root cause. There is plenty of evidence to support yes or no, but I don’t believe LDL nor ApoB is the root cause. I FIRMLY believe Oxidative Stress and Chronic Inflammation are the root cause of cardiovascular disease and my heart attack.
What are some key takeaways so far?
- Neither Total Cholesterol, LDL-C, HDL-C, or Triglycerides are THE #1 cause for concern by themselves.
- Ratios to HDL-C can indicate more than any single number but still aren’t enough to go by fully.
- Larger LDL & HDL particles and smaller VLDL particles generally indicate a healthier lipoprotein.
- Lipoprotein sizes are related to insulin resistance/sensitivity.
- What we consume and our activity levels are two major things that can directly affect insulin resistance.
- Insulin resistance contributes to damaging lipoprotein particles.
- Damaged & trapped lipoprotein particles in the intima layer of arterial walls can cause chronic inflammation.
Do you see how it all is coming together?
Do large fluffy LDL and HDL particles guarantee safety?
Well, that is what I thought for a few years because I was ONLY believing in the “Response-to-Injury” hypothesis. There is plenty of evidence to support that idea, and there are naysayers too. There is one important thing to notice in the NMR test results right under the LDL Size. It clearly says, “Small LDL-P and LDL Size are associated with CVD risk, but not after LDL-P is taken into account.” What does that really mean? Basically, it could mean, “The sizes don’t associate with lower risk if the LDL-P is elevated.” This goes along with what some of the “naysayers” say. But why? Essentially it boils down to three things:
- Particles less than 70nm
- Apolipoprotein B
- Trapped lipoproteins
Particles less than 70nm?
Apparently, pretty much ALL lipoprotein classes except for Chylomicrons–all lipoprotein particles less than 70 nm in size can POTENTIALLY pass through the arterial wall through a process called transcytosis (through cells), which is known as the transendothelial transport of lipoproteins. This is where “Response-to-Retention” pretty much can “debunk” the “Response-to-Injury” scenario. I think it is important to realize that because they can doesn’t mean that they will.
Is Apolipoprotein B or ApoB the new “LDL scare” tactic about cholesterol?
Remember our classification of lipoproteins early on in this article? ALL except for HDL have ApoB, and ALL of those are considered pro-atherogenic. Chylomicrons are not considered pro-atherogenic due to their size being greater than 70nm. Why does this matter? There is ONE ApoB protein per pro-atherogenic lipoprotein and even the large fluffy LDL can still pass through the atrial walls because the largest is only about 25 nm (or 23 if we go by the NMR test.) Basically, more ApoB particles create more opportunities for trapped lipoproteins.
There is now a growing consensus to test for ApoB and THAT should be the main risk factor. Well, that doesn’t add up to me either as that is basically very similar to the “LDL is bad” mentality. When you think about it, you could get an idea for this based on VLDL-P & LDL-P from the NMR test. Again, why should we put so much weight into ONE component of ONE risk factor?
Trapped lipoproteins are the ones to watch out for instead of just cholesterol.
Not all lipoproteins that pass through the arterial wall will become trapped. Go back and read the Oxidative Stress section if you need. It is important in how lipoproteins become trapped.
If we go read the section snippets of this article, it is a pretty clear understanding of how entrapment occurs:
- Arterial wall proteoglycans are made up of a protein core and linear long-chain carbohydrates, called GAGs.
- GAGs assist in molecular interactions leading to LDL retention.
- Lipoprotein entry within the intima layer depend on plasma levels, lipoproteins size, charge and composition. The small, dense LDL subclass is associated with increased lipoprotein binding to arterial PG in vitro (test tube) and the conversion of apoB lipoproteins into a small, dense form by in vitro phospholipase A2 treatment increases their affinity to PGs.
- Retention of LDL in the intimal layer favors chemical modifications, such as reactive oxygen species-mediated oxidation, lipase modification, or glycation, leading to aggregation and posterior cellular uptake leading to foam cell formation. Modified LDL, including oxLDL, triggers inflammatory reactions.
- In later stages of atherosclerosis, endothelial cells, and macrophages secrete “accessory molecules”, such as sphingomyelinase (SMase) and lipoprotein lipase (LpL), which contribute to lipoprotein fusion and aggregation. This article explains this in more detail.
Are you getting this? Basically small, dense, damaged, ApoB/LDL is what is getting trapped! NOT ALL LDL! IF we were to go by “one” then wouldn’t it make more LOGICAL sense to go by the Small LDL-P? I think so, but we really shouldn’t go by just one number.
What did I do with all of this information?
Cardiovascular disease is complicated, but I sincerely believe without a doubt that chronic inflammation and oxidative stress ARE the root causes! I think addressing those two things should be our primary objective. THAT is what I’ve done in varying degrees since the day of my heart attack. How?
- Stopped smoking.
- Cut out added sugars and refined grains.
- Drank water.
- Started walking and being more active. (Being sedentary or inactive is the “new” smoking.)
- Ate more REAL food and not so much heavily processed food products.
- Slept more when I could.
Those are the things I started out doing from the beginning and you can see in the first cholesterol comparison image how much better things improved within that time in that regard. Oh yeah, I also lost 22 pounds in those first 4 months as well, 12 the first month! I was scared to eat because “they” said I couldn’t have fat, carbs, etc. 🙄 What’s left? Water? 😆
HOWEVER, if we look at the NMR results from 12/2019 which was a year after my heart attack, those results are NOT very impressive. Seeing the difference from 2019 to 2020, I can only imagine how terrible it was at the time of the heart attack! My ratios were good, but the particle sizes were not.
GET AN NMR TEST EVEN IF YOU THINK YOUR CHOLESTEROL NUMBERS ARE GOOD! I can’t stress this enough!
Experimentation with different foods.
As time went along, I tried different macro splits of Carbs/Protein/Fat, different types of foods, and different aspects of different diets. BTW, diet is a noun and not a verb! Also, all those named diets have varying degrees of success and all have good things about them and some of those things contradict each other, BUT none really promote added sugars or refined grains. I’m talking about the core concept of those diets and not products marketed as those diets’ names. There are plenty of “vegan” products loaded with sugar and plenty of “keto” products loaded with some funky things too! Don’t fall for marketed BS!
Progress and Results
Looking at the span of three years of my NMR results, you can see how I progressed very well as a result of those experiments. I tried many different things, but the best mix was in November & December of 2022. November was pretty much the same as December’s results, but December had the best ratios ever when all three were considered! My doctor was blown away by those results! Astonished! I first showed her the November results and she thought there was an error with the test! 😆 Then I showed her December’s results. We talked for a good hour or so during my 15-minute appointment.
Here is the kicker and I’m sure my old cardiologist would be kicking and screaming. Let’s look at the standard/basic numbers and ratios. I’m going to compare November’s results to the time of my heart attack because the total and LDL are very close to at the time of my heart attack.
Notice the two HUGE differences being much higher HDL and much lower Triglycerides. Not only that, but the QUALITY of the particles is pretty incredible!
The ongoing discussion about statins and cholesterol with my doctor.
As always, we discussed statins. There are basically three functions of statins:
- Reduce cholesterol
- Control inflammation
- Stabilize plaques (via calcification, I questioned if this is really a good thing?)
I’ve established the fact that the QUALITY is better than the quantity of cholesterol and my doctor and cardiologist are on board with that. I did a C-RP test last year for inflammation and it was very low being on the scale of Insulin Sensitive now, it’s pretty safe to say that chronic inflammation is non-existent. So that leaves stabilizing plaques…
Getting a CT Angiogram to see the calcified plaques.
I asked my doctor about getting a calcium score. She said I can’t because of my stent and that it would throw off the results, SO she ordered a CT Angiogram. Oh my, this is so cool and much better than a calcium score would have been! They gave me the disc before I left. It came with a BASIC viewer program and I was underwhelmed. It showed the images as black and white and you cycle through them layer by layer as if looking down from the top of the heart. I saw only a little bit of calcium deposits, but the stent lit up like a lightning rod! Being the techie person that I am, I found a trial version of a DICOM image viewer that can do 3D modeling and oh my did I go to town on that! Here you go. Here is a video of my coronary arteries! You’ll see my stent and very small calcium deposits in the RCA. They’re insignificant according to the result letter.
This is an expensive scan, but I now have a baseline and will do this in about 4 years to see what happens. I compared the notes to the stent procedure and it appears to be similar. After discussing this with my cardiologist and with everything that I’ve researched on this, there isn’t any cause for concern!
It is important to note that a 0 on a calcium score and even the little evidence of calcified plaques on this CT Angiogram is not a free pass. There very well can be soft plaques that exist that haven’t calcified yet. After a more in-depth conversation with my cardiologist, yes, statins do calcify soft plaques which ARE fine UNLESS there are many and if that calcium ends up big and blocks a lof of flow. So we can reduce that calcification by using Vitamin K2. Vitamin K2 (along with D) helps direct calcium out of the arteries and into the bones and other places where it should go. BTW, I take this Vitamin D3 + K2 supplement daily.
How I finally achieved incredible NMR lipo-profile results.
It happened by accident as a side effect of contracting THE virus. I instantly realized that my training was going to take a hit, so I immediately started consuming fewer carbohydrates. I didn’t want to get my triglycerides elevated as a result of training less. Since I wasn’t doing much of anything those first few days, I watched a lot of videos and did a lot of reading. I dug deeper into the whole “low carb” side of things. I wanted to make sure I was still getting the necessary antioxidants, flavanols, and many other nutrients that I had been getting.
Going low-carb was eye-opening!
I decided to keep this low-carb thing going after I recovered from that pesky virus. I was feeling GREAT! I haven’t measured my testosterone, but signs were pointing to something going on with that in a positive manner! Through all this reading and such, one of many things I stumbled on and learned was that healthy LDL is a component of Testosterone and other hormones and functions! There isn’t a lot of information out there to show this and I don’t know why, but here you go and here is a good read on how LDL and HDL can be used to make steroid hormones including testosterone, estrogen, and more! Remember reading above about small LDL lacking affinity for LDL receptors? Well, that means we can’t be making testosterone out of damaged LDL!
Then my logical side kicked in and I asked myself, “Why on earth am I taking medication (statin) and all these experts so adamant on reducing something that is so crucial as to making Testosterone?!” So what if I was still on a high dose and my T levels were low? Would they then give me Testosterone injections? Probably and that’s almost as illogical as giving T2 diabetics more insulin to fix their insulin resistance. It wouldn’t be fixing the root cause of the problem!
Ok so that was my eye-opener, but what did I actually do and what was the result? I went further with this and broke many “rules” and literally went “against the grain” if you will.
HELLOOOOOO EGGS & BACON! 🤣
Simply put, I increased my fat intake including saturated fat. The key to this was using QUALITY nutrient-dense foods. NO, I did NOT do KETO!
By the way, did you know that SATURATED FAT POSITIVELY AFFECTS LDL PARTICLES?
Specific ways I made my LDL, HDL, and Triglycerides healthier.
The keyword is “healthier” and not merely reducing like “they” want us to. This is how I got my cholesterol healthier. The interesting thing is some of what I mention in each category helps with others as well!
- LDL – Low-Density Lipoprotein aka “bad cholesterol”
- Don’t regularly consume fried foods! In fact, try to avoid them at all costs.
- Consumed wholesome fats including saturated fats from grass-fed/pasture-raised/wild-caught animals.
- Grass-fed butter and/or ghee, full-fat Greek yogurt from grass-fed milk, pasture-raised eggs, etc.
- Here is an excellent review that discusses the benefit of saturated fat and lipoprotein sizes.
- Consume good sources of some plant fats too such as dark chocolate , coconut BUTTER (not oil) and avocados, BUT NOT VEG/SEED OILS!!! I’ll even go on to say no olive oil! There is some evidence that some veg oils are “ok” but I cut these out and things went great. Heat, air, and sometimes light will damage and oxidize oils as well. IF you are going to use oils, I wouldn’t heat them very much no matter their smoke point.
- Consume soluble fiber and probiotics. Beta-glucan fiber from oats or barley is excellent! Yogurt as mentioned above and other fermented foods such as kimchi and sauerkraut are also good!
- Consume a variety of antioxidants such as berries, dark chocolate, kale, cabbage/Brussels sprouts, spinach, red grapes, watermelon, and many more! We want to control oxidation and antioxidants is what they do!
- Take magnesium It reduces LDL, TG and raises HDL.
- Eat macadamia nuts. They’re special with their Omega-7 & Omega-9 content and lower LDL and raise HDL. Remember that’s not THE goals that we’re after, but it will help the ratios AND they have some other amazing benefits. I LOVE these macadamia nut bars!
- Loose excess weight. I’m not “fat shaming,” but losing excess weight really will help your overall health and feeling!
- HDL – High-Density Lipoprotein aka “good cholesterol”
- Same as LDL because most also assist in HDL.
- Beets/beetroot supplements
- Magnesium raises HDL.
- Omega-3 in the forms of DHA, EPA, & DPA from food such as wild-caught fatty fish or a GOOD Omega-3 supplement , and some ALA forms from freshly ground flaxseed and soaked chia seeds. ALA is inefficiently converted by the body, but some is still good plus there are other benefits to those foods.
- Macadamia nuts (see above.)
- EXERCISE! DO NOT DISMISS AND OVERLOOK THIS ONE! Physical activity is GREAT for HDL!
- All the above because many end up assisting TG levels.
- Limit carbohydrates and sugar! I dropped my daily carb consumption to approximately 20-25% and I did great, even with my training load. Reevaluate every couple of months.
- Limit or cut out the bread, pasta, rice, cakes, pastries, cookies, pies, sweet beverages, biscuits & gravy, etc.
- Limit potatoes the like, AND there is no need to eat corn!
- Using 100% Monkfruit Extract helped me wean myself off of sugar!
- Again, EXERCISE!!! If you can, do high-intensity exercises such as sprint intervals, battle ropes, burpees, etc. If you can’t do high intensity, then do moderate/high for as long as you comfortably can. (High intensity = you can only say a couple of words at a time; moderate/high = you can say a full sentence but it is labored.)
How much of what?
Some. Seriously, some. Experiment and see what amounts work best for you and your results. I listed “moderation” in the definitions early in the article with the others, but here it is again because I hear it tossed around very frequently. Moderation is the avoidance of excess or extremes. How much is that and WHO determines what is excessive or extreme? Some people may think one soda a day is “moderate” yet I strongly feel that it is extreme ESPECIALLY if that person is inactive. I don’t eat fried chicken in “moderation”, I eat it about once a month.
It’s also important to note that if you have something “bad” or what I mentioned to NOT have, that doesn’t mean you’re going to lose any and all progress. One random soda won’t make you unhealthy, just like walking for 30 minutes one random day will make you healthy. However, if you did it with regular frequency, then of course that will add up and contribute to your overall health–good or bad!
Do genetics play a role in or determine if I get cardiovascular disease?
Some genetic factors can come into play for abnormally high cholesterol values and fat/carb metabolism. However, I cringe when I hear someone say “It is a genetic issue” (especially knowing or finding out what they eat and lack of exercise) because, more often than not, it is unhealthy habits that people tend to inherit rather than a true genetic issue. So before you say, “it’s genetic because this person and that person in my family has it.” I urge you to look closely at your lifestyle and compare to theirs. As I mentioned earlier, Type 2 diabetes runs on both sides of my family, and my first LP-IR score (a year after already making significant changes) was in the middle and could see that diabetes could be in my future too, but look what happened. I’ve trended all the way to being far from insulin-resistant. That is habitual changes, not genetics. 😉 Also, we all have a genetic makeup that we can’t control, BUT we do have some control over our genetic/gene expression–especially through what we eat.
Good information, but “they” push certain diets.
I didn’t post some videos and articles that explained really well some of what I’ve learned because they end up promoting the KETO and VEGAN diets, and I’m not a proponent of it or ANY named diet!
One reason I believe that KETO can work is mainly due to the highly reduced carbohydrate intake. Even too many of the good complex carbs can be bad and cause inflammation. Another reason I believe KETO can work is that it gets the body burning fat as fuel, but so does exercising primarily in Zone 2 heart rate and KETO can’t provide those benefits (especially with the ROS in the mitochondria) of low heart rate exercise! I could go on about this, but I’m not because this article is long enough. I only brought it up because if you research this further on your own, you will see it quite often, but understand that KETO is NOT necessary in most cases. If you’re T2 diabetic and need to quickly get on track, then it may very well be worth checking out for a few months! IF you do KETO, then at least eat clean while following it such as eating grass-fed vs grain-fed beef! 😉
There are many out there who have success with and swear by a 100% plant-based / vegan diet. PLANTS ARE EXCELLENT AND DO WONDERFUL THINGS FOR THE BODY AND I DO EAT PLANTS, however, there are other things we NEED from animals. I’ll say this, I’ve seen Vegans have heart attacks, get dementia, and have many of the diseases that “they” tend to say their diet cures. There is a lot of junk out there marketed as “plant-based” and “vegan.” Sugar is plant-based so there’s that! However, there are some great takeaways from Veganism.
What about statins and cholesterol?
I’ll say this. I believe medications can be good and have a purpose until one can correct the root cause of the symptom that the medications are treating and the condition(s) no longer exist, BUT you absolutely need to focus on addressing the REAL ROOT cause! The big questions that remain are, “How long does it take to reverse the effects of decades of unhealthy choices and what is my TRUE risk of another cardiovascular event?”
Statins do NOT reduce the Small LDL, and in fact, may increase the proportion to total LDL. Well… isn’t that interesting considering the Small LDL is what is the most pro-atherogenic!
Statins also do two other things. They control inflammation and stabilize soft plaques. Stabilizing the plaques is done so by calcification. I think that is another great reason to supplement with Vitamin D3+K2.
I believe there is a risk-to-reward ratio that the patient and doctor need to consider. Being on such a very low dose and not having any side effects, I’ll continue taking it.
It is important to question everything! This is a very long article about cholesterol yet it is only ONE component of one’s health in regard to cardiovascular disease. As you learned, we’re not managing cholesterol at all; it’s lipoproteins, chronic inflammation, and oxidative stress.
Just because there is an association or correlation with cardiovascular events, it doesn’t mean that thing is 100% causation such as:
- LDL isn’t THE cause.
- Triglycerides aren’t THE cause.
- Eating butter isn’t THE cause.
- Cholesterol definitely isn’t THE cause.
What actually caused my heart attack?
From everything I’ve learned, I sincerely believe that years and decades of chronic inflammation and oxidative stress were the root causes of my atherosclerosis–the buildup of arterial plaques. One of those plaques burst through the artery wall and formed a clot. It is called “hot plaque” when the plaque inside of those arterial walls is exposed to blood. A clot forms and stops the blood flow. All the years of sugar, pastries, pasta, fried food, smoking, and no exercise caught up with me and caused my heart attack. It was NOT LDL-C or even my triglycerides that CAUSED my heart attack. Chronic inflammation and oxidative stress is caused by many things and not limited to what I listed to be what I believe to be the main causes of mine.
Final words on managing cholesterol.
Really we are managing cardiovascular risk factors that associate with cholesterol’s protective carriers, the lipoproteins. My own focus is clear and I measure by shooting for IDEAL ratios (all green boxes on my cholesterol calculator), AND (very importantly) keeping the LDL & HDL sizes large, and the VLDL size low. I firmly believe we need to look at both and not just one or the other. The easiest way of doing this is to simply eat WHOLESOME food the way nature intended. Cows and chickens weren’t meant to be force-fed corn and grains. We eat what our food eats and that goes for the plants we eat as well. How do they fatten cows? Feeding them a lot of grains. How do you fatten humans? Feed them a lot of grains. 😉
While we address the causes of chronic inflammation and oxidative stress within our bodies, we’re not only making our lipoproteins healthier, we’re also addressing the root cause of MANY other diseases, cancers, etc. Our body is a system and what affects one thing, can greatly affect the rest of the system.
Evolve and progress.
I rewrote this article because I learned more and am evolving. I used to 100% believe in the “Response-to-Injury” theory, but now believe that it AND “Response-to-Retention” are equally important. I think of them as an “and/or” condition.
Doctors are learning and evolving too, and that makes me happy to see! If nothing changes, nothing changes. We as a population need to change because cardiovascular disease IS the #1 killer in the world AND it is becoming more and more prevalent in younger ages–so is childhood type 2 diabetes. Is there any relation? Of course, there is and it all is tied to insulin resistance. I think I illustrated how insulin resistance ties in with all of this. I 100% believe without a doubt from “our” love for sweet addictions which may very well start with something as simple as juice boxes given to toddlers. Don’t drink juice and don’t give it to your kids. There’s one way we can start to turn this health disaster around.
It’s never too late.
It’s never too late to make positive health changes. You can make the rest of your life feel better than it would if you continued with unhealthy habits–no matter how “small” they seem. A little adds up each day, good and bad. 😉 Plus, maybe our friends, family, and children near us will notice our positive changes and change too.
Check out this article I wrote about what I would do IF I had to start all over again.
Products mentioned in this article:
- RequestATest.com – NMR Lipoprofile Cholesterol Test
- Sports Research Vitamin D3+K2
- Stoneyfield Grass-fed Whole Milk Greek Yogurt
- Endangered Species 88% Dark Chocolate
- 100% Monkfruit Liquid Sweetener
- House of Macadamias Bars
- Bountiful Beets Capsules
- Tahiro Algae-based DPA, DHA, EPA Omega-3 Capsules
- Magnesium Complex – Intelligent Labs MagEnhance
- 100% Monkfruit Liquid Sweetener