When ingested, pectin can lower serum cholesterol levels in humans. Pectin is degraded by fecal bacteria in the colon. We examined the release of methanol (MeOH) by this degradation. A 0.2% glucose (2 g/L) mixture was used as the control medium. A pure culture of pectinolytic Erwinia carotovora was the control bacterium. The chief substrates were, in set 1, 0.2% pectin (2 g/L) and, in set 2, 0.1% glucose (1 g/L) and 0.1% pectin (1 g/L). Cultures of fecal bacteria and E carotovora grew for 72 h in each of the solutions. By 72 h the fecal flora culture in set 1 cleaved 30% of the possible methoxyl groups on pectin. The fecal flora in set 2 cleaved 90.7% of all possible methoxyl groups. Balance studies suggest that all of the free MeOH comes from methoxyl groups on pectin. This study demonstrates that fecal bacteria are capable of degrading pectin to release MeOH.

Summary: Dietary intake of cholesterol has been linked to coronary heart disease. The effect of grapefruit pectin (Cirrus puradisi) on plasma cholesterol, triglycerides, very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol, highdensity lipoprotein cholesterol, and the low-density lipoprotein: high-density lipoprotein cholesterol ratio was studied. The study design was a 16-week double-blind, crossover (placebo or pectin) using 27 human volunteers screened to be at medium to high risk for coronary heart disease due to hypercholesterolemia. The study did not interfere with the subjects' current diet or lifestyle. Grapefruit pectin supplementation decreased plasma cholesterol 7.6%, low-density lipoprotein cholesterol 10.8%, and the low-density lipoprotein: high-density lipoprotein cholesterol ratio 9.8%. The other plasma lipid fractions studied showed no significant differences. We conclude that a grapefruit pectin-supplemented diet, without change in lifestyle, can significantly reduce plasma cholesterol.

Sustained hypercholesterolemia is a known risk factor for development of atherosclerosis. In animal studies, grapefruit pectin fed concurrently with a high-lipid diet inhibits hypercholesterolemia and atherogenesis. The purpose of the present study was to determine if grapefruit pectin affects cholesterol levels and atherogenesis of animals with established hypercholesterolemia. Microswine were fed an atherogenic diet to establish hypercholesterolemia. Plasma cholesterol levels rose rapidly and for 360 days were sustained at levels 6- to 12-fold the normal level. Then, half the microswine, selected at random, were fed a diet in which 3% grapefruit pectin was substituted for cellulose, and the remaining animals received the original diet. Animals were killed 270 days later, and the extent of atherosclerosis was determined. In animals with established hypercholesterolemia, pectin did not lower their cholesterol levels. However, pectin reduced the extent of atherosclerosis in both the aorta and coronary arteries. The mean surface area covered by atherosclerosis in the aorta was 13.6% in the group that did not receive pectin compared with 5.3% in the group that did receive pectin. The mean coronary artery narrowing was 45% without pectin and 24% with pectin. We conclude that pectin may have a direct beneficial effect on atherosclerosis by a mechanism independent of cholesterol levels.

Summary:We studied the effect of dietary grapefruit pectin on plasma cholesterol and the development of atherosclerosis in 18 miniature swine. Pigs were randomized to one of three diets: no added fat (I), added fat/cellulose (11), and added fat/pectin (III). Plasma cholesterol was measured monthly. Arteries were examined for atherosclerosis at the termination of the experiment. Pectin supplementation of an added fat diet resulted in a significantly lower average plasma cholesterol than did cellulose supplementation (168 mg/dl vs. 249 mg/dl, p