Year	Discovery/Scientist	Event/Occurrence	Comment
1940	JC Paterson	Studied atherosclerosis and intimal capillary rupture leading to stroke.	Postulated that rupture of intimal capillaries were due to pressure from hypertension, degeneration of tissues, and vitamin deficiency.
1941	JC Paterson	Follow up study on coronary occlusion using microscopic examination of plaques.	Postulated that hypertension was a main factor for intimal capillary bleeding and plaque formation; and capillary fragility may be due to vitamin C deficiency.
1953	GC Willis	Conducted experimental study on guinea pigs. Confirmed that atherosclerosis is linked to vitamin C deficiency.	The mechanical stress exerted onto the walls of arteries is link to the location of the atherosclerosis.
1954	GC Willis	Serial angiography studies showed vitamin C could reduce atherosclerotic plaques in humans.	Contrary to common assumption, plaques could build up or be reversed fairly quickly. Plaques build up at points of mechanical stress in blood vessels.
1957	GC Willis	Further studies showed that vitamin C could reverse atherosclerosis in guinea pigs.
1971	Constance Spittle	Studied the effect of vitamin C on healthy individuals and patients with atherosclerosis.	The transitory rise in serum cholesterol could be due to uprooting of cholesterol from the blood vessels.
1981	Holloway et al.	Observed that guinea pigs fed with a diet high in vitamin C could reduce cholesterol synthesis in the liver.	Simultaneously HMG CoA reductase was reduced.
1985	Green et al.	Studied the mechanism of vitamin C inhibition of HMG CoA reductase activity in guinea pig liver.	Study showed that vitamin C has an effect on reductase activity and cholesterol genesis.
1986	Harwood et al.	Advanced from animal model study to the study of human liver cells culture.	Low-level vitamin C triggered the HMG CoA reductase to catabolize cholesterol. High-level vitamin C reversed the effect.