The effect of feeding fish oil (Menhaden) on the progression of rhesus monkey atherosclerosis was determined by feeding diets containing 2% cholesterol and either 25% coconut oil (Group I), 25% fish oil/coconut oil (1:1) (Group II), or 25% fish oil/coconut oil (3:1) (Group III) for 12 months (n = 8/group). The average serum cholesterol levels were 875 mg/dl for Group I, 463 mg/dl for Group II, and 405 mg/dl for Group III. HDL cholesterol levels were 49 mg/dl for Group I, 29 mg/dl for Group II, and 20 mg/dl for Group III. An average of 79% of the aortic intima was involved with atherosclerosis in Group I, 48% in Group II, and 36% in Group III. The aortas of both fish-oil groups (II or III) contained significantly less cholesterol (total, free, and esterified), as well as less acid lipase, cholesteryl esterase, and ACAT activities when compared to the coconut-oil group (I) (p less than 0.05). Microscopically, the aortic and carotid artery lesions were smaller in cross-sectional area and in thickness, and contained less macrophages in the fish-oil groups (II and III) when compared to the coconut-oil group (I) (p less than 0.05). This protective effect was not consistently enhanced by increasing the proportion of fish oil to 3:1 (Group III) over 1:1 (Group II). The results indicate that fish oil-containing diets reduce serum cholesterol levels and inhibit atherosclerosis even in the face of lowered HDL cholesterol levels when compared to a pure coconut oil/cholesterol diet in rhesus monkeys. Therefore, fish-oil diets exert effective protective control of progression of atherosclerosis during severe atherogenic stimuli.

In general, the results to date in humans and experimental animals seem to indicate that substantial regression of advanced atherosclerosis is possible. The results also indicate that the advanced atherosclerotic lesions are much more likely to respond favorably if the serum cholesterol concentrations are reduced to the minimum that prevails in animals or people who consume a low-fat low-cholesterol diet. In human subjects and in rhesus monkeys, this value appears to be about 150 mg%. Under these circumstances, much of the lipid disappears from the plaques, and the remaining fibrous tissue and cells appear to condense and undergo remodeling, as they do in fracture or wound healing. Additional effort will be required to ascertain how rapidly and how much of the fiber proteins and calcium can be removed from the advanced plaques and to work out methods that will consistently produce regression of advanced atherosclerotic lesions in human subjects. This goal would appear to be worth working toward. Interruption of progression of atherosclerosis appears to be more easily achieved, and it also would appear to be a worthwhile goal. The diagram that is reproduced as FIGURE 2 presents the multiple methods of intervention in atherosclerosis that are now available to the physician and to the patient. To those of us who look on atherosclerosis as an almost completely preventable disease and one that is largely reversible, the following quotation from the perceptive essay by Lewis Thomas seems to be prophetic and most appropriate. An extremely complex and costly technology for the management of coronary heart disease has evolved, involving specialized ambulances and hospital units, all kinds of electronic gadgetry and whole platoons of new professional personnel to deal with the end results of coronary thrombosis. Almost everything offered today for the treatment of heat disease is at this level of technology, with the transplatned and artificial hearts as ultimate examples. When enough has been learned for us to know what really goes wrong in heart disease, we ought to be in a position to figure out ways to prevent or reverse the process; and when this happens, the current elaborate technology will be set to one side.

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