References: Lecithin
J Lab Clin Med. 1989 Feb;113(2):235-40.
Abnormal high-density lipoprotein composition in women with insulin-dependent diabetes.
Bagdade JD, Subbaiah PV.
Department of Internal Medicine, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612.
To determine whether alterations in lipoprotein phospholipid composition might be an unrecognized factor that contributes to the unexplained acceleration of atherogenesis and the loss of sex-related protection from the development of coronary heart disease in women with insulin-dependent diabetes mellitus, we have estimated levels of neutral lipids, apolipoproteins (A-I, A-II, B), and free cholesterol (FC) in plasma and the four major phospholipid constituents of the very low-density lipoprotein + low-density lipoprotein and high-density lipoprotein (HDL) fractions in 12 ambulatory female patients with varying degrees of diabetic control. Although levels of triglyceride, cholesterol, HDL-cholesterol, and lipoprotein phospholipids in whole plasma of the patients with diabetes were similar to those in controls, their FC levels and FC/lecithin ratio, a recently described index of cardiovascular risk, both were abnormally increased (p less than 0.01). In the HDL-containing plasma fraction, concentrations of sphingomyelin, lecithin, and lysolecithin all were significantly reduced (p less than 0.05; p less than 0.01, and p less than 0.02, respectively). These compositional changes may be potentially atherogenic, because a reduction in the phospholipid content of HDL may impair its capacity to promote the efflux of cholesterol from cells, and the transfer of cholesterol ester from HDL to the larger apo-B-containing lipoproteins is inhibited when their content of FC is increased relative to phospholipid. These previously unrecognized qualitative defects, which are inapparent in the routine estimation of plasma lipids, may compromise reverse cholesterol transport and thereby promote atherogenesis in women with insulin-dependent diabetes mellitus.
mednet.ucla.edu
BACKGROUND: Lecithin has been widely sold as a dietary supplement. 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) is a phospholipid that does not exist in nature and has been used in vitro to study lipid binding. We tested DMPC in vivo in apolipoprotein (apo) E-null mice. METHODS AND RESULTS: DMPC or soy or egg lecithin at 1.0 mg/mL was added to the drinking water of 4-week-old apoE-null female mice. Eight weeks later, HDL cholesterol levels and apoA-I levels were markedly increased in the mice that received DMPC. HDL function was also dramatically improved in the mice receiving DMPC, and there was a significant reduction in aortic lesions (P=0.021) in the DMPC mice but not in those receiving lecithin. Adding 1.0 mg/mL of DMPC to the drinking water of 10-month-old apoE-null female mice for 5 weeks caused regression of aortic sinus lesions (P=0.003). Adding 1.0 mg/mL DMPC to the drinking water of 6-month-old apoE-null male mice for 8 weeks significantly reduced aortic sinus lesion area (P=0.0031) and en face whole aorta lesion area (P=0.001), whereas adding the same concentrations of soy or egg lecithin did not significantly alter lesion area. Jejunal apoA-I synthesis and plasma apoA-I levels were increased 2- to 3-fold in mice receiving DMPC but not soy or egg lecithin. CONCLUSIONS: DMPC (but not lecithin) raises HDL cholesterol and apoA-I, improves HDL function, and prevents lesions or causes their regression in apoE-null mice.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14504179&dopt=Abstract lecithin
Am J Clin Nutr. 1989 Feb;49(2):266-8.
Lecithin intake and serum cholesterol.
Knuiman JT, Beynen AC, Katan MB.
Department of Human Nutrition, Agricultural University, Wageningen, The Netherlands.
To find out whether the consumption of lecithin has a more beneficial effect on serum cholesterol than does the consumption of equivalent amounts of polyunsaturated oils, we scrutinized 24 studies on the effect of supplementary lecithin intakes ranging from 1 to 54 mg/d. Most of the studies lacked an appropriate control group, had a small sample size, or had changes in intake of other foods because of increased energy intake from lecithin. In only four trials were attempts made to balance fatty acid intakes of control and experimental groups. There is no evidence for a specific effect of lecithin on serum cholesterol independent of its linoleic acid content or secondary changes in food intake. The observed lecithin-induced hypocholesterolemic effects found in various studies were artifacts caused by the design and the manner of data analysis, were mediated by other dietary changes, or were due to the linoleic acid present in lecithin.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2916447&dopt=Abstract lecithin
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