Does linoleic acid protect our blood vessels? Yes—but only CLA, which is found in butter!

If you think that vegetable (seed) oils protect your blood vessels, that is probably not true. This is suggested by studies examining their effects in older age or looking at lifespan. Vegetable oils may lower cholesterol, but low cholesterol levels are associated with shorter lifespan.

But what would you say to the information that simply adding 1% of a special mixture of polyunsaturated oils—specifically processed linoleic acid—to the diet causes vascular plaque to disappear in an animal model within a few weeks!

However, the processing of these vegetable oils was not carried out by any industrial food company. No—the processing was performed by bacteria in the cow’s stomach! The resulting product is called CLA, conjugated linoleic acid. There are several types, but the most interesting is rumenic acid, cis-9, trans-11 CLA. Another is trans-10, cis-12 CLA, but the first one is found in butter at ten to twenty times higher levels than the second. Could it be, then, that full-fat dairy products—especially butter and cream—are the key means of suppressing the clogging of blood vessels? Means of preventing cardiovascular disease? In other words, well-known plant polyunsaturated oils—but only after being processed in the stomach of ruminants by bacteria?

Let’s take a look at the results of an older study from 2005.

We can see that CLA at an amount of 1% of total calories repairs (% Area) damage to the mouse aorta caused during increased cholesterol consumption in a higher-fat diet over eight weeks.

After adding CLA, over the next eight weeks there is repair and dissolution of already formed plaque! Every two weeks there is continuous improvement. Isn’t that remarkable?

What mechanism do the study authors propose? It is the correction of fat metabolism, activation of the factors PPARα and PPARγ, activation of apoptosis, and the breakdown of dysfunctional cells.

Conjugated linoleic acid (+CLA) activates PPAR transcription factors much more than saturated fats (SF).

If we recall earlier posts regarding the vascular wall, it was always the case that endothelial cells lost the ability to obtain energy from fats. Fat metabolism is essential for maintaining strong antioxidant protection. This is important for preserving structural stability under mechanical stress. Once cells had to use another protective mechanism—such as cellular senescence or pseudohypoxia and glucose fermentation—antioxidant protection was always reduced, leading to damage of the vascular lining. This was prevented, for example, by vinegar—acetate.

Is insufficient activation of PPAR factors therefore the cause of vascular plaque formation?

If so, it would mean that the downstream effect is a deficiency of acetyl-CoA molecules and insufficient activation of pyruvate carboxylase (PC) and gluconeogenesis (GNG). This also explains sensitivity to acetate. Perhaps proper activation of PC and GNG is necessary for proper antioxidant function, for recycling NADPH and glutathione.

CLA helps preserve fat metabolism, maintain sufficiently high production of acetyl-CoA molecules, and sustain an overall metabolic rate based on fat oxidation. And that is exactly what our blood vessels need.


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References:

Profound resolution of early atherosclerosis with conjugated linoleic acid



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