The optimum cholesterol for the manufacture of sexual hormones is LDL cholesterol, not HDL cholesterol.

High density lipoprotein is more protein than lipo, whereas low density lipoprotein is more lipo than protein.

OXIDIZED cholesterol is where the danger lies, and, obviously, cholesterol that’s more lipo than protein (LDL) needs more antioxidant protection than cholesterol that’s more protein than lipo (HDL).

Leland J. Smith (Cholesterol Autoxidation, 1981) wrote …

“Aqueous dispersions of cholesterol in protein solutions (albumins, gelatin, etc.), in dextrin or mannan solutions and in bile salt solutions have […] been prepared for various biochemical applications. However, cholesterol autoxidation in these media is generally not observed. Indeed, these aqueous cholesterol sols appear to be protected against autoxidation. Nonetheless, cholesterol autoxidation can be provoked in such dispersions, for Fe(III) salts catalyze cholesterol autoxidation in phospholipid dispersions. Moreover, phospholipids or glycolipids form good dispersions of cholesterol autoxidation products, and synthetic liposomes formed with phospholipids have been used for administration of cholesterol autoxidation products to experimental animals.”

Artificially lowering LDL cholesterol is dangerous.

The healthy way to “deactivate” LDL cholesterol is to USE IT for what it’s meant to do, namely, promote …

(1) hormone and protohormone synthesis (including estrogen, progesterone, testosterone, cortisol, etc.),

(2) vitamin D synthesis,

(3) wound healing and healthy scar promotion,

(4) cell wall integrity,

(5) nerve cell integrity, and

(6) blood vessel integrity.

Cholesterol itself opposes fatty acids, such as the ones that accumulate in classic shock reactions – overalkaline due to sodium chloride’s chloride ions combining with abnormal fatty acids and sodium ions joining with carbonate ions.

Emanuel Revici, MD. (Research in Physiopathology As Basis of Guided Chemotherapy: With Special Application to Cancer, 1961) wrote …

“In animals injected with cholesterol and then submitted to trauma in the Noble-Collip drum, shock was prevented. Injection of cholesterol prior to the experiment reduced mortality to zero while in untreated controls mortality was high. A similar but less constant effect was obtained when cholesterol was administered immediately after trauma. It is noteworthy that in animals injected with cholesterol before being placed in the drum, the blood not only did not become abnormally black but the usual bleeding from the nose, mouth and paws (if not taped during the trauma) was abnormally bright red.”

On the other side of the metabolic coin, Dr. Revici wrote in the same textbook …

“Cholesterol’s effect upon the central nervous system was interesting. Often, immediately after administration, both in animals and humans, transitory somnolence was observed. However, repeated administration induced convulsions. Exophthalmia [protruding eyeballs] was seen in mice after injection of cholesterol and was most manifest 24 hours thereafter. It contrasted with normals and especially with animals injected with fatty acids or similar lipoids, who showed enophthalmia [reduced orbital eyeball size].”

If the “cholesterol-as-sludge” theory of atherosclerosis is all there is to heart attacks, why does plaque accumulate faster in the bigger hoses (carotid and coronary arteries) under higher pressure, and slower in the smaller hoses (capillaries, arterioles, and arteriovenous anastomoses) under lower pressure?

Dr. Revici consistently lowered high cholesterol by administering a combination of glycerol, butanol, heptanol, and polyunsaturated fatty alcohols.

Interestingly, olives contain NATURAL butanol and heptanol.

Butanol has an octane rating of 100.

Dr. Revici assigned cholesterol to the cellular hierarchic level, whereas Mainstream Monocultural Medicine usually studies it only at the plasmatic (serum) level – the same level where today’s MMM scientists investigate the C-reactive protein that Revici wrote about decades before.