Lecithin: benefits, dosage, contraindications

Hypocholesterolemic

Phospholipids exert a hypocholesterolemic effect. Thus, in patients suffering from hypercholesterolemia, supplementation with soy lecithin significantly reduces plasma cholesterol levels. In hypercholesterolemic hamsters and rabbits, supplementation with soy phospholipids increases HDL cholesterol levels and reduces the LDL/HDL ratio, which is a known risk factor for metabolic diseases. These effects would be due to the fact that phospholipids are able to decrease microsomal HMG-CoA reductase activity (an enzyme involved in the cholesterol biosynthesis pathway) and enterocytic absorption of cholesterol. They also increase biliary cholesterol excretion, lipid beta-oxidation and plasma ApoA1 concentration (Apolipoprotein A1 is the main protein component of high-density lipoproteins, HDL, which are anti-atherogenic).

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Metabolic

A study conducted in rats showed that rapeseed lecithin, rich in alpha-linolenic acid (ALA), when added without prior emulsification, was able to induce a dose-dependent increase in the appearance of lipids and ALA in the lymph, which would be associated with an increase in the secretion and size of chylomicrons (lipid particles that transport triglycerides after digestion). As a result, delivery of ALA in the form of phospholipids via rapeseed lecithin would increase its bioavailability, compared with its delivery as triglycerides in an oil. However, the study shows that the beneficial effect of rapeseed lecithin on lipid absorption only becomes significant at supplementation doses (30% of total lipids), much higher than those found in foods, which never exceed 10%. These data validate a dose-dependent effect of plant lecithins on lipid absorption. Regardless of their dose, both lecithins produced changes in the gut microbiota in these mice, increasing the fecal abundance of Clostridium Leptum, a bacterial group described as anti-inflammatory. Rapeseed lecithin would also have a specific effect on bile acid metabolism, promoting the elimination of bile acids, whose accumulation can be toxic. These preclinical data therefore demonstrate that the use of plant lecithins as an ingredient in a balanced diet does not induce any harmful effect on lipid metabolism. Soy and sunflower lecithins would be among the only emulsifiers that do not cause any major deleterious impact on the composition and pro-inflammatory potential of the gut microbiota.

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Hepatoprotective

Animal research findings suggest that lecithin may protect against alcohol-induced liver damage. Furthermore, the liver plays a central role in lipid metabolism and homeostasis. Several preclinical studies have shown that replacing a fraction of dietary triglycerides with plant lecithins was associated with an improved lipid profile in the liver, with a reduction in hepatic triglycerides.

Neurological

Oral intake of lecithin can increase serum choline levels, which is a precursor of acetylcholine. As a source of choline, lecithin was thought to potentially help alleviate symptoms of cholinergic disorders such as Alzheimer's disease and tardive dyskinesia. However, oral lecithin intake does not appear to affect cholinergic neuronal function.

Anti-inflammatory

Supplementation with phosphatidylcholine produced a significant reduction in the development of arthritis in rats, potentially due to inhibition of the neutrophil-mediated inflammatory response. Soy phosphatidylcholine may limit the inflammatory process in the joints in a chronic murine model of rheumatoid arthritis (collagen-induced arthritis) when administered at disease onset. Pretreatment effectively prevented leukocyte adhesion to the endothelial layer and decreased expression of inducible nitric oxide synthase (iNOS), thereby reducing the degree of synovial angiogenesis. Lecithins, therefore, could prove effective in reducing inflammatory reactions in arthritis and similar inflammatory processes.

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