22 March 2009

Blaming Burger King: The Genesis of Atherogenesis

In a previous post I wrote of my grandpa who eventually died of a myocardial infarction resulting from atherosclerosis, of which I attribute to a diet of $1 Whoppers. So cheap, so tempting was this Burger King specialty that it is perhaps what also took my grandmother via cardiovascular disease.

Apart from a “whopping” amount of calories each received on the diet, the biochemical backup to my conclusions has to do chiefly with the kind of macronutrients they got. Specifically the type of fat received is of focus because in the Whopper is particularly saturated (and likely some trans fat) as well as cholesterol.

Well and good is knowledge that a diet high in fat overall have a positive correlation with cardiovascular disease, but consumption of a diet high in saturated and trans fat is hypercholesterolemic, causing a shift to a poor ratio of higher “bad” LDL to “good” HDL cholesterol, according to latest research (1p155).

The circulation of extra LDL, which is the major transporter of cholesterol in the serum, is linked with atherogenesis mainly as LDL becomes oxidized (1p176). The oxidized LDL produces a toxic effect on endothelial cells possibly by attracting blood-borne monycytes, transforming them into macrophages and trapping them in endothelial spaces (1p176).

The resulting “foam cells” (macrophages engorged with lipids, mainly cholesterol) release cytokines that attract yet more macrophages that end up similarly (1p155). Together the foam cells, along with damaged smooth muscle cells, form a plaque much appearing in the form of a fatty streak that, if large enough, narrows the lumen to the point where blood flow is restricted (1p155).

Had my grandparents simply opted to focus their lipid-loving taste buds on monounsaturated and polyunsaturated fats, then their story would have been different. These fats present reverse results to the others causing hypocholesterolemic effects (1p155). Adoption of n-3 polyunsaturated fatty acids, specifically, may have even interfered with the platelet aggregation caused by fatty acid displacement and inflammatory cytokines that are involved in producing plaque formation as well as reduced tryacylglycerol concentration in the serum (especially from EPA/DHA-rich fish oil) (1p155).

Unfortunately this knowledge was not available to my grandparents. But may they rest in peace knowing their end was a wake-up call to their grandson.

Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

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