What, we have been told, eating fats, especially saturated, results in them clogging our arteries, it’s a gross over-simplification, saying this is like shaming science. An article published in 2011, in the British Journal of Nutrition (1), states that `Epidemiological data does not support a link between dietary cholesterol and CVD’. Just a reminder, all the studies & articles that I’ll be mentioning in this episode, their links can be found in the show notes & I’ll be referencing each article with a number, so it’s easier for you to look it up. So, this one that I just mentioned is number one or first.

So, what I was trying to say is, Our ancestors have survived deep winters with nothing but fats & meats, no vegetation being around & here we are! In fact, there was a spike in cases of heart disease after the introduction of vegetable oils & high fructose syrup. And despite a major chuck of people following the mainstream guidelines of high carb, low fat, there has been an epidemic of heart disease like never before.

First, let’s clear a small confusion, LDL & HDL are not cholesterol, they are Lipoproteins, basically proteins that help in the transportation of fat because fat does not mix well with liquids like water & blood. We’ll get to them in a min. Cholesterol on the other hand is a very important molecule, made by our body, you heard that right! And the body adjusts the cholesterol it produces based on how much cholesterol we consume from our diets. Basically, the presence of cholesterol in our body is a must! Why, simply because it’s a precursor or raw material for all the steroid hormones in our body like, testosterone, cortisol, estrogen, progesterone, and aldosterone & not just that, it’s also needed for the formation of vitamin D (Vit D is actually more a hormone that being a vit), it’s also needed to manufacture bile without which we would not be able to digest fats, let alone getting Vit A, E & K2. In fact, referring to the second article, as per the study, published in the Journal of the American College of Cardiology, vol. 40, no. 24(2), concludes that half of heart disease patients have normal cholesterol levels, yet they have an underlying risk of plaque building up in the arteries. I’ve also referenced 2 more clinical studies, no 3 & 4, which concluded that Low Cholesterol is Associated with Mortality from cardiovascular diseases. One is a study that was published in the Journal of Korean Medical Science (3) and the other in PubMed (4) which again clearly concludes that ‘Low cholesterol was related to high mortality even after excluding deaths due to liver disease from the analysis. High cholesterol was not a risk factor for mortality

Now, getting back to the Lipoproteins. Without getting into too much depth, since I had prepared a webinar, link in the show notes. LDL that is low-density lipoprotein, contains fat-soluble nutrients, phospholipids, cholesterol & triglycerides & in short & simple words, one of its roles is to deliver its contents to the cells needing them & returning to the liver where its reabsorbed, whereas the other hand, the role of HDL is to collect unused cholesterol from the blood & deliver it back to the liver for recycling. Another thing that just struck me, LDL has been a part of the biology of our bodies, it always existed & played its role as determined by nature. Then how stupid is the fact that today it’s mislabeled as the villain? Esp. When you’ll hear about the role of LDL with regard to immunity, it’ll leave you astonished as to why it was ever misrepresented. Lipoproteins including LDL bind to the highly inflammatory endotoxins released by gram-negative bacteria that seek to invade our body. And not just that, it also binds to alpha toxins produced by the gram-positive organism Staph aureus which has antibiotic-resistant strains, as per articles published in The Journal of Immunology (5) & the Cell Journal (6), referenced as 5 & 6. Apart from this, there have been many studies conclusive of the role of elevated levels of Cholesterol & LDL, esp LDL with regard to immune function serving a protective role, as we age. And for this, I’ve given you references to 4 studies which you can refer to from numbers 7 to 10.

There’s an interesting point to note, in the mainstream theory, they state that LDL in the bloodstream can get stuck in the intima, which is located below the endothelium that’s the wall of the arteries & veins. And after getting stuck, it may become oxidized eventually leading to an immune response in which macrophages ingest the LDL & become foam cells & that’s how they say, the formation of plaque begins. And so, when a physician looks at a higher number of LDL in circulation, they hit the panic button & jump onto prescribing statins & other cholesterol-lowering medications. However, I’d like to emphasize here, the interesting part is, that there’s zero, and there’s absolutely no research that proves, that can correlate & link, the amount of those LDL particles that get stuck with the amount of LDL particles in circulation. So, how can they start lowering LDL? In fact, a study published in the Annals of Clinical & Laboratory Sciences found a 15 times higher risk of developing cancer in those individuals with LDL cholesterol below 70. This study, I’ve referenced as no. 11.

So, what is actually going wrong? There’s a good amount of evidence that the LDL particle & intima become sticky in the presence of insulin resistance & inflammation. I believe glycation is playing a role here. You can refer to studies 12 & 13, which have been published in the journal of the American Diabetes Association & American Heart Association, respectively. And yet another interesting thing to note is that, if LDL was the culprit causing atherosclerosis, why is it that the plaque formation is observed only in the arteries & not veins? After all, the amount of LDL circulating in the bloodstream throughout the body is the same. That’s because atherosclerotic plaques occur in locations where the endothelium has become damaged as a result of either turbulent blood flow or as a result of inflammation, insulin resistance, or other causes. For these, you can refer to article no 14 which is a study published in the journal of Physiology in the American physiological society. I’ve also referenced other articles from the same journal, no. 15.

So, pulling it all together, because of all the damage & inflammation to the arteries, LDL is attracted to the site, as a defensive & healing response, operating similarly, just as our immune system would, if we would have a cut on our finger. It’s like the firemen arriving at the site which is up in flames, to put off the fire & we blame it on them.

Lastly, the size of the LDL particle is also what matters. Since small-dense LDL particles can stick to the intima more easily, basically the wall of the arteries, you can refer to article 16 for this. The reason for this is its content when it’s oxidized linoleic acid. And even if linoleic acid is not oxidized, the chances for it to oxidize are much higher. In case you’re wondering what linoleic acid is, it’s a polyunsaturated omega-6 fatty acid & in this case, I’m referring specifically to vegetable oils & as I mentioned earlier, if you’d like to have a better understanding of fats, you can refer to the webinar on fats, cholesterol & heart disease. Anyway, moving on, the more omega 6 in the lipoproteins, the more likely it is for them to be oxidized within LDL, causing the LDL to no longer be recognized by the LDL receptor in the liver, instead it’s taken up by the macrophages, leading to foam cell formation, and atherosclerosis. A side note, linoleic acid-rich VLDL & HDL can also oxidize, increasing the risk of cardiovascular disease. The moral of the story is, what you eat matters, the fats you choose matter a lot, and the oils you cook every single day can make or break your health! So choose wisely!

All this while we’ve been told that saturated fat is the crook whereas the fact is, cholesterol that is bound to saturated fat will not get oxidized, at least not that easily because of it being tightly packed, it’s not only heat stable, it’s also resistant to oxidation, there’s no space for the molecules to get in. And studies have found that a higher intake of saturated fats is related to an increase in large LDL particles & a decrease in small dense LDL particles, which is what is ideal. To sum it up, replacing sugars & refined carbs with saturated fats & reducing the consumption of polyunsaturated omega-6 fatty acids, specifically eliminating vegetable oils & limiting your PUFA intake to nuts, seeds & wholesome foods, including olive oil for salads or very light sautéing, is all a good place to start for heart disease risk management. All that I just mentioned, especially in relation to LDL particle size & saturated fats, is backed by scientific studies & evidence which you can refer to. I’ve referenced them from articles 17 to 24.

(1) https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0007114511000237

(2) https://www.jacc.org/doi/10.1016/j.jacc.2017.10.024

(3) https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3247776/

(4) https://pubmed.ncbi.nlm.nih.gov/21160131/

(5) https://www.jimmunol.org/content/196/1/328

(6) https://doi.org/10.1016/j.chom.2008.10.001

(7) https://www.ahajournals.org/doi/10.1161/01.ATV.17.7.1224

(8) https://www.tandfonline.com/doi/abs/10.3109/10641968209060782

(9) https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(89)92865-1/fulltext

(10) https://academic.oup.com/aje/article/143/2/151/77587

(11) http://www.annclinlabsci.org/content/37/4/343.full

(12) https://diabetesjournals.org/diabetes/article/58/9/2018/23892/ApoCIII-Enriched-LDL-in-Type-2-Diabetes-Displays

(13) https://www.ahajournals.org/doi/10.1161/01.ATV.20.9.2140

(14) https://journals.physiology.org/doi/full/10.1152/physrev.00047.2009

(15) https://journals.physiology.org/doi/abs/10.1152/physrev.1995.75.3.519

(16) https://pubmed.ncbi.nlm.nih.gov/16371404/

(17) https://www.sciencedirect.com/science/article/abs/pii/S0009308497000959?via%3Dihub

(18) https://www.pnas.org/content/79/6/1712

(19) https://www.jbc.org/article/S0021-9258(18)90863-X/fulltext?keytype2=tf_ipsecsha&ijkey=8f5155dbadc0265032f52d28abbeff5ddb724368

(20) https://pubmed.ncbi.nlm.nih.gov/10634938/

(21) https://pubmed.ncbi.nlm.nih.gov/8432867/

(22) https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2891%2980263-3

(23) https://academic.oup.com/ajcn/article/67/5/828/4666151

(24) https://www.sciencedirect.com/science/article/abs/pii/S0958694609000041

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