Cholesterol is a waxy fatty steroid constituent of mammalian cell membranes. When a cell requires cholesterol, it synthesizes the necessary LDL (low-density lipoprotein) receptors, and inserts them into the plasma membrane. These respond to circulating LDL molecules in the bloodstream and facilitate their transfer from outside of the cell to the inside (endocytosis).
As in many cellular receptor proteins, cysteine disulfide bonds are an important part of the LDL receptor. If acetaldehyde has disrupted these disulfide bonds,
See Acetaldehdye+disulfide bonds //www.curezone.org/forums/fm.asp?i=1958887
then, as with the thyroid not responding to its activating hormone TSH because of possible acetaldehyde damage to GPCR receptors,
See Acetaldehyde+thyroid //www.curezone.org/forums/fm.asp?i=1955669
it may be that the molecules of LDL containing the needed cholesterol for the cells will not transfer properly from the outside in. The cells will be starved for cholesterol and blood stream levels of circulating LDL will increase.
High blood levels of LDL cholesterol may actually be a sign of cholesterol deficiency "inside" the cells where it is needed, mediated by yeast-released acetaldehyde damage to the LDL receptors.
Circulating LDL that is not taken up by the cells may eventually oxidize from contact with elevated levels of free radicals, something that is also related to acetaldehyde toxicity,
See Acetaldehyde+reactive oxygen species //www.curezone.org/forums/fm.asp?i=1959622
and end up in macrophage foam cells, accumulating in atheromatous plaques.
In this model, artificially lowering the blood cholesterol levels by interfering with its synthesis in the liver (inhibition of HMG-CoA reductase by statins) may normalize cholesterol test results but does not address the intracellular deficiency state.