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In looking for information regarding cholesterol and heart disease I found a bmj study that I need to better cite and make atomic notes on. This is a big wall of text I’ll divide up later.
Not sure of the relation, but they embed a (perma?) link that looks like this: https://doi.org/10.1136/openhrt-2018-000898
The intake of omega-6 vegetable oils, particularly soybean oil, began to increase in the USA starting in the early 1900s at a time when the consumption of butter and lard was on the decline.
This caused a more than two-fold increase in the intake of linoleic acid, the main omega-6 polyunsaturated fat found in vegetable oils which now makes up around 8% to 10% of total energy intake in the Western world.
The omega-6 fat linoleic acid should not be confused with conjugated linoleic acid found in pastured animal foods.
A systematic review of studies measuring the changes in linoleic acid concentration in subcutaneous adipose tissue in the USA revealed an approximate 2.5-fold increase in linoleic acid increasing from 9.1% to 21.5% from 1959 to 2008.2 Importantly, the concentration of linoleic acid in adipose tissue is a reliable marker of intake as the half-life of linoleic acid is approximately 2 years in adipose tissue. The authors of the study also noted that the increase in adipose tissue linoleic paralleled the increase in the prevalence of diabetes, obesity and asthma.2
The amount of linoleic acid in adipose tissue, but also in platelets, is additionally positively associated with coronary artery disease (CAD), whereas long-chain omega-3 (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) levels in platelets are inversely related to CAD.3 This provides rather compelling evidence that omega-3s protect whereas omega-6 linoleic acid promotes heart disease.
Importantly, the increased consumption of omega-6 polyunsaturated fat linoleic acid can reduce omega-3 in the body as it competes with the alpha-linolenic acid for metabolism to longer chain polyunsaturated fats.
The low-density lipoprotein (LDL) oxidation hypothesis gained traction during the 1980s because it was noted that in general, native unoxidised LDL does not cause foam cell formation. In other words, LDL had to become oxidised first in order for atherosclerosis to develop. Indeed, it was later discovered that oxidised LDL (oxLDL) caused direct toxic effects to the cell, recruitment and entry of monocytes into the subendothelial layer and increased foam cell formation5 leading to increased atherosclerosis and inflammation.6
Once linoleic acid becomes oxidised in LDL, aldehydes and ketones covalently bind apoB, creating LDL that is no longer recognised by the LDL receptors in the liver but is now recognised by scavenger receptors on macrophages leading to the classic foam cell formation and atherosclerosis.
dietary linoleic acid, especially when consumed from refined omega-6 vegetable oils, gets incorporated into all blood lipoproteins (such as LDL, VLDL and HDL) increasing the susceptibility of all lipoproteins to oxidise and hence increases cardiovascular risk.
In other words, cholesterol was protected from oxidation if bound to saturated fat but susceptible to oxidation when bound to linoleic acid. Again, this suggests is that eating more linoleic acid increases the oxidation of cholesterol within LDL particles further increasing atherosclerosis formation and the risk of coronary heart disease.
Endothelial cells oxidise LDL forming linoleic acid hydroperoxides.
Oxidised linoleic acid but not oxidised oleic acid is found in atherosclerotic plaques.
There is more thin fibrous cap atheroma, less thick fibrous cap atheroma, less stable plaque and a greater percentage of plaque rupture in patients given sunflower oil (high in omega-6) versus control
Furthermore, omega 6s:
I find this to be contradictory to fluffier online articles that discuss omega-6 as being helpful for heart health, but I think the problem is that these fluffier articles are lumping LA and CLA into the same group. There was another BMJ or elsewhere study on the efficacy of using CLAs to protect, but they were too indiscriminate about the presence of LAs in their CLAs. The process they used to manufacture CLAs from LAs was leaving high amounts of LAs in the solution. This study appears to focus only on LA and omega-3 (they literally only mentioned conjugated linoleic acid once, I had to go do a lot of reading to find descriptions of it, but I didn’t capture any of them in notes because they were low quality sources).
2024-01-14 - oleic acid is not found in atherosclerotic plaque
2024-01-14 - endothelial cells oxidize LDL bound to lineoleic acid
2024-01-14 - linoleic oxidation
2024-01-14 - linoleic acid oxidizes all forms of cholesterol
2024-01-13 - oxidized LDL and linoleic acid develop into foam cells
2024-01-13 - oxidized LDL is toxic
2024-01-13 - linoleic acide competes with omega-3
2024-01-12 - linoleic acid in adipose and platelets
2024-01-12 - increasing linoleic acid levels in fat paralleled obseity growth
2024-01-12 - half-life of linoleic acid in adipose tissue
2024-01-12 - 1959 to 2008 linoleic acid levels in human subjects
2024-01-12 - linoleic acid and conjugated linoleic acid
2024-01-12 - vege oils in 1900s
updated: 2024-01-19 09:51:03
generated: 2024-05-25