Contains the most effective and safe plant derived lecithin (from non-GMO soy).
The product has been manufactured using high quality pure raw materials and the technology that ensures all their beneficial properties intact, in strict compliance with GMP and TÜV regulations.
Lecithin is a mixture of phospholipids (cholin, inositol, etc.), which are essential for every cell of the human body. Lecithin is an integral part of the cell membranes, the protective sheaths surrounding the brain, muscle and nerve cells.
The word "lecithin" comes from the word lekithos, which is Greek for “egg yolk.” Lecithin was first discovered in 1850 when the French scientist Maurice Gobley isolated the compound from an egg yolk.
A number of studies have shown extraordinary benefits of lecithin for health, especially for cardiovascular, nervous system, and brain functions.
Lecithin plays vital role in maintaining brain functions.
Choline is the precursor to acetylcholine, an important neurotransmitter responsible for normal brain functioning. Acetylcholine is important for many brain functions including memory, so increasing concentration of this neurotransmitter can result in improved memory. Choline is important for the brain development of infants and for the adults during periods of illness or stress. That’s why lecithin is often referred to as "brain food."
Lecithin is essential for the proper functioning of the nervous system.
Lecithin is important in energy production, improves cell oxygen supply, and promotes fat-soluble vitamin A, D, Е and К absorption, which are essential for nourishing every cell in the body.
Various studies indicate that lecithin may positively affect cholesterol and triglyceride levels. Lecithin is a fat emulsifier; it binds with cholesterol and other fats, forming fat-water emulsion, which is then excreted from the body, thus preventing atherosclerosis and other cardiovascular diseases.
Lecithin helps keep the liver healthy. By keeping fats dispersed in water, lecithin prevents these fats from accumulating in the liver. Lecithin is acting as a hepatoprotector, helps in detoxification, may be useful in restoring liver function in a number of ailments including excessive alcohol consumption.
Cholin improves the gallbladder functions, increases the bile secretion; improves bowel movements.
Eggs, liver, soy beans, nuts are all rich with lecithin. One egg for example contains about 400 mg of lecithin, liver (100 g) – 850 mg, oatmeal (100 g) – 650 mg, peanut (100 g) - 113 mg, cheese (100 g) – 100 mg.
There is no universally recognized daily dose of lecithin, but it was calculated that an average person requires between 1,000 and 4,000 mg of lecithinlecithin because of low lecithin content in our diets.
Santegra®’s product Lecithin contains 520 mg of soy lecithin in every capsule. It is established, that lecithin of a vegetable origin is much more effective than lecithin of animal origin.
Lecithin should be a part of everyone’s healthy diet; it is especially useful for elderly people, because lecithin level in the body decreases with age. Lecithin stimulates mental and physical activity, helps fight stress, and enhances vitality.
Per one capsule:
Soy lecithin – 520.0 mg
As a dietary supplement take one capsule with a large glass of water three times daily with meals for 1 month.
Lecithin (often referred to as phophatidylcholine) plays vital roles in many basic biological processes in the body, it is important for the integrity of cellular membranes and overall health. About 30 percent of the brain's dry weight is composed of lecithin. Lecithin also represents nearly 70 percent of fat located within the liver. Until the 1930s, the primary source for commercial lecithin had always been eggs. In 1930 it was found that lecithin could also be obtained from soy. Vegetables now represent the most popular and most bioavailable sources for dietary lecithin. Soybeans, sunflower, rapeseed, grains, wheat germ are the most frequently used plant sources.
Soy lecithin is a byproduct of soybean processing. At first, the soybeans are tempered by keeping them at a consistent temperature and moisture level for approximately seven to 10 days. This has a hydrating effect on the soybeans, loosening it from its hull. Then, the soybeans are cleaned and cracked into small pieces. The cracked beans are separated from the hulls and are heated and pressed into flakes. Next, the flakes undergo a distillation process where the soybean oil is extracted, after which crude soy oil is made to undergo a “degumming” procedure. The sludge that is produced as a result is where soy lecithin comes from. Of course, the sludge would have to undergo another process first, to extract the lecithin.
Lecithin contains three types of phospholipids: phosphatidylcholine, phosphatidylethanolamine, and phosphotidylinositol. Phosphatidylcholine contains choline, which is essential to every living cell in the body and is one of the main components of cell membranes. It seems majority of the health claims about soy lecithin may have something to do with the fact that it is an excellent source of choline.
Pharmacological use of lecithin primarily includes treatments for hypercholesterolemia, neurologic disorders, and liver ailments. Lecithin is also used as an emulsifying and stabilizing agent in the food, pharmaceutical, and cosmetic industries.
Dietary soy lecithin supplementation decreases hyperlipidemia and influences lipid metabolism. Although this product is used by diabetic patients, there are no data about the effect of soy lecithin supplementation on the immune system. The addition of phosphatidylcholine, the main component of lecithin, to a culture of lymphocytes has been reported to alter their function. If phosphatidylcholine changes lymphocyte functions in vitro as previously shown, then it could also affect immune cells in vivo. In the present study, the effect of dietary soy lecithin on macrophage phagocytic capacity and on lymphocyte number in response to concanavalin A (ConA) stimulation was investigated in non-diabetic and alloxan-induced diabetic rats. Supplementation was carried out daily with 2 g kg(-1) b.w. lecithin during 7 days. After that, blood was drawn from fasting rats and peritoneal macrophages and mesenteric lymph node lymphocytes were collected to determine the phospholipid content. Plasma triacylglycerol (TAG), total and HDL cholesterol and glucose levels were also determined. Lymphocytes were stimulated by ConA. The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) dye reduction method and flow cytometry were employed to evaluate lymphocyte metabolism and cell number, respectively. Soy lecithin supplementation significantly increased both macrophage phagocytic capacity (+29%) in non-diabetic rats and the lymphocyte number in diabetic rats (+92%). It is unlikely that plasma lipid levels indirectly affect immune cells, since plasma cholesterol, TAG, or phospholipid content was not modified by lecithin supplementation. In conclusion, lymphocyte and macrophage function were altered by lecithin supplementation, indicating an immunomodulatory effect of phosphatidylcholine. (1)
The current study was designed to investigate the hypocholesterolemic and anti-atherogenic properties of soy lecithin beyond its fatty acid content. In experiment 1, 18 cynomolgus monkeys were divided into three groups of six and fed diets which approximated either the average American diet (AAD), the American Heart Association (AHA) Step I diet, or a modified AHA (mAHA) Step I diet containing 3.4% soy lecithin for 8 weeks. Plasma samples were collected from food-deprived monkeys and analyzed for total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), very low- and low-density lipoprotein cholesterol (non-HDL-C), and triglyceride (TG) concentrations. Group comparisons revealed that monkeys fed the mAHA Step 1 diet had significantly lower plasma TC (-46%) and non-HDL-C (-55%) levels compared to the AAD diet, whereas monkeys fed the AHA Step 1 diet had lesser reductions in plasma TC (-21%) and non-HDL-C (-18%) levels. The monkeys fed the mAHA Step I diet had significantly lower plasma TC (-32%) and non-HDL-C (-45%) compared to the monkeys fed the AHA step diet. Also, only the mAHA Step I diet significantly reduced pre-treatment plasma TC and non-HDL-C levels by - 39 and -51% respectively with no significant effect on plasma HDL-C or TG levels. In experiment 2, 45 hamsters were divided into three groups of 15 and fed the following three modified non-purified diets for 8 weeks: a hypercholesterolemic diet (HCD) containing 10%, coconut oil and 0.05%, cholesterol, HCD plus 3.4%, soy lecithin (+SL), or the HCD with added levels of linoleate and choline equivalent to the +SL diet but no lecithin (-SL). Plasma lipids were determined as in experiment 1 and aortas were perfusion-fixed and Oil Red O stained for morphometric analyses of fatty streak area. Relative to the HCD group, the +SL-treated hamsters had significantly lower plasma TC (-58%), non-HDL-C (-73%) and aortic fatty streak area (-90%). Relative to the -SL group, hamsters fed the +SL diet had significantly lower plasma TC (-33%), non-HDL-C (-50%) and significantly reduced aortic fatty streak area (-79%).
In conclusion, the first experiment suggests that the cholesterol-lowering efficacy of the AHA Step I diet can be enhanced with the addition of soy lecithin without reducing plasma HDL-C levels, whereas the second experiment suggest that the hypocholesterolemic, and in particular, the anti-atherogenic properties of soy lecithin cannot be attributed solely to its linoleate content. (2)
Lecithin has also been used for immune modulation, activating specific and nonspecific defense systems in 20 patients receiving 1 teaspoonful 3 times daily for 30 days. (3) Preliminary results from various clinical trials suggest that lecithinmay be an effective agent in the treatment of various types of alcohol and non-alcohol induced liver damage. (4, 5) For many individuals suffering from liver disorders spawned by toxins, viruses, and disease, phosphatidyl choline has proven more tolerable than choline when used for the enhancement of proper liver functioning.
In one particular mammalian study, a 60 percent phosphatidyl choline supplement was used on test subjects with diets high in alcohol consumption. Both liver fibrosis and cirrhosis were prevented in the test groups receiving a PC supplement. Lecithin may provide certain hepatoprotective effects. (6) Its protective benefits may also be equally effective in organs adversely affected by nonsteroidal anti-inflammatory drug (NSAIDs) treatments. (7)
This experiment (N = 80, college students) employed a double-blind mixed design to test the effect of phosphatidylcholine (PCh) on explicit memory. Dose of placebo and PCh was compared at two levels (10 and 25 g) as was time of testing postingestion (60 and 90 min). With 25 g of PCh, which supplies 3.75 g of choline, significant improvement in explicit memory, as measured by a serial learning task, was observed at 90 min postingestion and slight improvement was observed at 60 min postigestion. Further analyses indicated that this improvement may have been due to the responses of slow learners. This is the first study to test the relationship between a single dose of PCh and explicit memory on normal human subjects. (8)
1. Miranda DT, Batista VG, Grando FC, Paula FM, Felício CA, Rubbo GF, Fernandes LC, Curi R, Nishiyama A. Soy lecithin supplementation alters macrophage phagocytosis and lymphocyte response to concanavalin A: a study in alloxan-induced diabetic rats. Cell Biochem Funct. 2008 Oct 8. [Epub ahead of print]
2. Wilson TA, Meservey CM, Nicolosi RJ. Soy lecithin reduces plasma lipoprotein cholesterol and early atherogenesis in hypercholesterolemic monkeys and hamsters: beyond linoleate. Atherosclerosis. 1998 Sep;140(1):147-53.
3. Pawlik A, et al. Herba Polonica. 1996; 42(1):42-46.
4. Lieber CS, De Carl LM, Mak KM, et al. Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin. Hepatol. 1990; 12:1390-1398.
5. Jenkins PJ, Portmann BP, Eddleston AL, Williams R. Use of polyunsaturated phosphatidylcholine in HbsAg negative chronic active hepatitis: results of prospective double-blind controlled trial. Liver. 1982; 2:7-81.
6. Anand BS, et al. Phospholipid Association Reduces the Gastric Mucosal Toxicity of Aspirin in Human Subjects. Am J Gastroenterol. Jul 1999; 94(7):1818-22.
7. Leyck S, et al. Improvement of the Gastric Tolerance of Non-steroidal Anti-inflammatory Drugs by Polyene Phosphatidylcholine (Phospholipon 100). Eur J Pharmacol. Oct 1985; 117(1):35-42.
8. Ladd SL, Sommer SA, LaBerge S, Toscano W. Effect of phosphatidylcholine on explicit memory. Clin Neuropharmacol. 1993 Dec; 16(6):540-9.