Lipostabil Information ...it's coming soon
10-04-2003 12:33 AM
Lipostabil Information ...it's coming soon
injectable fat killer originaly posted by Pudgy
Lipostabil contain 250 mg Phosphatidylcholine.There are substantial medical research data on Phosphatidylcholine, supporting the beneficient qualities of Phosphatidylcholine
Woodlands Research Healing Center, PA, USA
Phosphatidylcholine (derived from lecithin), a primary dietary source of choline, is composed of a phosphate group, 2 fatty acids, and choline. The composition of essential fatty acids in phosphatidylcholine determines its value in promoting health. When phosphatidylcholine is ingested, most of it is broken down into choline, glycerol free fatty acids, and the phosphate group, rather than being incorporated intact into cellular membranes.
• Although choline can be manufactured in humans from either methionine or serine, it has recently been designated an essential nutrient.
• Choline is required for the proper metabolism of fats; it facilitates the movement of fats in and out of cells. Like Vitamin B12, 5-adenosylmethionine, and Folic Acid, choline acts in the human body as a methyl donor. As such, choline is essential for proper liver function due to its key role in the lipotropic effect, i.e., the export of fat from the liver. In the absence of adequate choline, fats become trapped in the liver, where they block metabolism. Stagnation of fat and bile eventually leads to the development of more serious liver disorders such as cirrhosis.
• Choline is needed for cell membrane integrity because of the critical role it plays in the manufacture of primary components of cell membranes, such as phosphatidylcholine and sphingomyelin.
• Choline is essential in the synthesis of acetylcholine. Choline supplementation increases the accumulation of acetylcholine which plays a crucial role in many brain processes, including memory. (Canty, DJ and Zeisel, SH. Nutr Reviews. 52;327-339, 1994)
• Phosphatidylcholine increases the solubility of cholesterol and thereby decreases cholesterol‘s ability to induce atherosclerosis. Phosphatidylcholine aids in lowering cholesterol levels, removing cholesterol from tissue deposits, and inhibiting platelet aggregation. (Brook, JG, Linn, S, and Aviram, M. Biochem Med Metabol Biol. 35;31-39, 1986.) The high content of linoleic acid in phosphatidylcholine may be responsible for much of the benefit derived from supplementation.
Mode of Action
• Choline acts as a methyl donor, especially in liver function.
• Choline enables synthesis of acetylcholine, phosphatidylcholine and sphingomyelin.
• Choline has recently been designated as an essential nutrient.
Infants and children: 125 to 375 mg/day
Women: 425 mg/day; Pregnant women: 450 mg/day; Breast-feeding women: 500 mg/day
Men: 500 mg/day
• Average intake in the U.S.: Approximately 6 g per day as phosphatidylcholine
• As free choline in vegetables (especially cauliflower and lettuce), whole grains, liver, and soy.
• As lecithin (containing 10-20% phosphatidylcholine) in grains, legumes, meat and egg yolks.
• True choline deficiency appears to be rare or non-existent and has only been induced in a research setting.
• Deficiencies typically present as muscle weakness, tingling in the fingers and toes, weight loss or fatigue.
• Liver and kidney disorders develop when animals are fed a choline-deficient diet.
• Fatty infiltration of the liver and other signs of liver dysfunction develops in humans fed a choline-deficient diet.
• Choline is an essential nutrient for human cells in cell cultures, and humans receiving intravenous feeding with solutions low in choline develop signs of choline deficiency.
(Canty, DJ and Zeisel, SH. Nutr Reviews. 52;327-339, 1994; Zeisel, SH, et al. FASEB J 5;2093-2098, 1991)
Phosphatidylcholine is used in the treatment of a variety of liver disorders, including:
• Acute & Chronic Viral Hepatitis: Chronic viral manifestations severely challenge the liver yet numerous controlled trials have established PC as a safe and potent intervention for infection (Mueting 1972, Hirayama 1980, Yamo1978, Kosina 1981, Jenkins 1982, Visco 1985, Hantak 1990, Ilic and Begic-Janev 1991). Optimal results were achieved in these studies when subjects were maintained on a combination of oral and infused PC utilizing higher doses. Once clinical indicators began returning to normal subjects were maintained on oral doses of PC. In addition to decreases in liver enzymes, serum lipids, immune markers and bilirubin, subjects experienced reversal of fatty degeneration, inflammation, jaundice, liver swelling and fibrosis, per liver biopsy.
• Cirrhosis of the liver
• Decreased bile solubility
• Diabetic fatty liver
• Drug-induced liver damage: The use of anticonvulsant drugs often leads to liver toxicity. Subjects who had received anticonvulsants for an average of five years were assessed by GGT elevation (Hisanaga 1980) and given PC for six months. Positive outcome was consistently achieved in subjects in addition to a decrease in GGT levels.
• Toxic liver damage: (Kuntz 1965) reported remarkable effects with PC in subjects with chemical poisoning and Esslinger (1966) with plant toxin.
• Fatty liver: 650 subjects with varying degrees of liver damage were followed for 5 years. Subjects received intravenous PC at 950 mg along with oral PC (450- 700 mg). When blood parameters returned to normal subjects were shifted to oral PC only. Subjects were categorized as to severity of liver damage: fatty degeneration, acute inflammation, chronic aggressive inflammation, and advanced fibrotic damage. All groups in the study had marked benefit. There was reversal of fatty degeneration in many subjects and in those with acute inflammation PC accelerated recovery by an average of ten days. (Wallnoefer and Hanusch 1973).
• Alcohol-induced liver disease: Studies with baboons have found that phosphatidylcholine supplementation protects against alcohol-induced liver abnormalities and cirrhosis; presumably some of these same effects will be present in humans. Nevertheless, choline salts do not seem to be of any value in the treatment of alcohol-induced liver disease in humans but may be useful in general liver support. (Lieber,CS and Rubin, E. N Engl J Med 280;705-708, 1969)
The health of the membrane is synonymous with the health of the entire organism. Toxins have an affinity for fatty acids; they literally take up residence in the lipid environment and in so doing, weaken and disrupt. The probable result is early apoptosis, premature death of the cell. Generally, normal mitosis provides for new cellular growth to maintain the health of the body, i.e. the previous discussion on photo receptors. However, toxicity's affinity for lipids can easily redistribute toxins and diseased toxic lipids into the new growth. In a healthy state with adequate glutathione and ascorbate to bind the toxins before they take up new residence, the body can keep the bad guys under control. However, if defenses are weak, toxins can continually be redistributed and eventually hide in the CNS and bone where the regeneration process is at a slower pace. The goal of detoxification is to 1) encourage regrowth with a renewed effort at the correct balancing of the essential nutrients, with the exchange of high energy lipids (PUPA and HUP A) to fuel regeneration and the eventual detoxification process; and 2) at the correct time, the inclusion of the toxin removal specialists, ascorbate, chlorella, and if possible IV glutathione.
Detoxification of neurotoxins requires that the cell membrane is nourished with balanced essential fatty acids (4:1, plus HUFAs) and supportive phospholipids. Phosphatidylcholine (PC) is the most abundant phospholipid of the cell membrane and protects the liver, with its 33,000 square meters of membrane, against toxicity and infection. The liver plays a pivotal role in detoxification but due to its fatty acid content and the lipid soluble characteristics of neurotoxins, lipid based interventions are required to impact toxic burdens. Once the liver has been damaged it can no longer metabolize fats normally. Pools of lipids are then deposited within hepatocytes throughout the liver. Beta oxidation of fatty acids is suppressed impairing detoxification and prostaglandin production. Extensive research with PC has revealed that it protects the liver against damage from alcohol, pharmaceuticals, environmental pollutants, xenobiotics and infection due to viral, bacterial and fungal manifestations (Lieber 1994a, 1994b, 1995, 2001a, 2001b).
Hypercholesterolemia and Atherosclerosis
Phosphatidylcholine increases the solubility of cholesterol and thereby decreases its ability to induce atherosclerosis. Phosphatidylcholine also aids in lowering cholesterol levels, removing cholesterol from tissue deposits, and inhibiting platelet aggregation. (Brook, JG, Linn, S, and Aviram, M. Biochem Med Metabol Biol. 35;31-39, 1986.) Here some of the beneficial effects may be attributable to the high content of linoleic acid in phosphatidylcholine.
The phospholipid preparation Lipostabil has been researched for use in the treatment of high cholesterol levels and atherosclerosis. In several trials evaluating this 70% phosphatidylcholine content lecithin product from Germany, total serum cholesterol and triglyceride levels dropped significantly and HDL cholesterol levels improved using dosage ranging from 1.5 g once daily to 3.5 g three timed per day. (Lipostabil. Natterman International GMBH,1990; Wojcicki, J, et al. Phytotherapy Res. 9;597-599, 1995)
A high-concentration phosphatidylcholine preparation, marketed in Germany under the trade name "Essentiale", has produced clinical results consistent enough to gain authorization from the BGA, the German equivalent of the FDA. This form contains 90% phosphatidylcholine, with 50% of the molecule having linoleic acid, the essential fatty acid, bound at the proper position; i.e., the first and second carbon of the glycerol molecule. Using this preparation the standard dosage recommendation is 350 mg three times per day with meals. (Essentiale, Natterman International GMBH, 1989.)
There is evidence that mania is associated with a reduced brain cholinergic activity. Phosphatidylcholine supplementation at levels of 15-30 g/day has been found to exert beneficial effects in the treatment of bipolar depression. (Wutman, R, et al. Nutrition and the Brain. Vol. 5. Raven Press: New York, 1979; Cohen, B, et al. Am J Psychiat 137:242-243, 1980; Cohen, B, et al. Am J Psychiat 139;1162-1164, 1982.)
· The use of phosphatidylcholine may result in significant improvement or amelioration of symptoms in some patients suffering from bipolar depression by increasing brain choline levels. Some researchers believe that one effect of Lithium carbonate, the standard pharmaceutical treatment for bipolar depression, is the promotion of increased acetylcholine activity in the brain. (Jope, R, et al. Am J Psychiat 142;356-358,1985)
Choline supplementation increases the accumulation of acetylcholine within the brain in normal patients so many researchers hypothesized that phosphatidylcholine supplementation would benefit Alzheimer patients. Some research has indicated that increasing acetylcholine content in the brain through supplemental choline might result in improved memory. However, clinical trials using phosphatidylcholine have not produced significant benefits. Studies revealed inconsistent improvements in memory from choline supplementation in both normal and Alzheimer’s patients. Nevertheless, criticisms of these studies and their interpretations have been raised on the grounds that sample size was too small, the dosage of phosphatidylcholine used was too low, and the studies themselves were poorly designed. (Rosenberg, G and Davis, KL. Am J Clin Nutr. 36; 709-720, 1982; Levy, R, et al. Lancet 1;474-476,1982; Sitaram, N, et al. Life Sci 22;1555-1560, 1978.)
Alzheimer’s disease is characterized by a decrease in cholinergic transmission, but the basic defect in cholinergic transmission in Alzheimer’s disease relates to impaired activity of the enzyme acetylcholine transferase, not to a deficiency of choline. Acetylcholine transferase combines choline with an acetyl molecule to form acetylcholine. However, since increased levels of choline do not necessarily increase the activity of this critical enzyme, phosphatidylcholine supplementation will probably not prove efficacious in the majority of patients with Alzheimer’s disease.
In a patient with mild to moderate dementia, the use of a high-quality phosphatidylcholine preparation at a dosage level of 15 to 25 g/day may be beneficial. (Murray, M. p. 140, 1996.)
• Choline is available as a soluble salt, most commonly as either choline bitartrate, citrate, or chloride, or as phosphatidylcholine in lecithin.
• Most commercial forms of lecithin contains only 10-20% phosphatidylcholine.
• Most supplements labeled as "phosphatidylcholine" contain only 35 percent.
• Some newer and more potent preparations contains up to 98 percent phosphatidylcholine. These more pure forms of phosphatidylcholine are preferred since they are associated with fewer gastrointestinal side effects. This is particularly true in the treatment of those conditions that require large doses of phosphatidylcholine (i.e., 15 to 30 grams) because low-concentration forms such as lecithin would be required in such large amounts that side effects would be nearly inevitable.
Intravenous form is also available. The liver is the largest organ of the body and receives the first flush of PC from an infusion. However an exchange of lipids is systemic with every organ, every neuron, every cell sharing the increased PC and the higher performing lipids (HUFAs). It should be expected that improved metabolic performance would also be systemic.
• Using lecithin, the most common form of choline supplementation, with 90 percent phosphatidylcholine, the dosage (three times daily with meals) is:
• 350-500 mg t.i.d. for the treatment of liver disorders;
• 500-900 mg t.i.d. for lowering cholesterol;
• 5,000-10,000 mg q.d. for the treatment of Alzheimer’s disease and bipolar depression.
(Murray, M. p. 141, 1996)
• Choline and phosphatidylcholine are generally well tolerated.
• At doses over 20grams daily, pure choline, but not phosphatidylcholine, will produce a "fishy" odor.
• High doses of lecithin, several grams per day, will produce reduced appetite, nausea, abdominal bloating, gastrointestinal pain and/or diarrhea in some people.
• No toxicity beyond the side effects mentioned above were found in any of the sources cited.
• Phosphatidylcholine is not indicated in patients with depression (unipolar or clinical depression) unless under the supervision of a physician because high-dosage phosphatidylcholine supplementation can worsen depression in some cases.
• Choline works together with other methyl donors and helps the body conserve carnitine and folic acid. (Daily, JW and Sachan, DS. J Nutr 125;1938-1944, 1995; Varela-Mreiras, G, et al. J Nutr Biochem 3;519-522, 1992.)
• Phosphatidylcholine and pantothenic acid are used to form acetylcholine.
Alternative Medicine Review, Vol 7, #2, April, 2002
Phosphatidylcholine (PC) is a phospholipid, one of a primal class of substances ubiquitous among life fonns.1 PC is the predominant phospholipid of all cell membranes and of the circulating blood lipoproteins. It is the main functional constituent of the natural surfactants, and the body's foremost reservoir of choline, an essential nutrient.2 PC is a normal constituent of the bile that facilitates fat emulsification, absorption, and transport, and is recycled via entero-hepatic circulation. Until recently the nomenclature of PC was confused with lecithin, a complex mixture of phospholipids and other lipids. Lecithin preparations enriched in PC at or above 30 percent by weight are considered PC concentrates.
Pharmacokinetics and Metabolism
· Chemically, PC is a glycerophospholipid,3 built on glycerol (CH2OH-CHOH-CH2OH) and substituted at all three carbons. Carbons I and 2 are substituted by fatty acids and carbon 3 by phosphorylcholine. Simplistically, the PC molecule consists of a head-group (phosphorylcholine), a middle piece (glycerol), and two tails (the fatty acids, which vary). Variations in the fatty acids in the tails account for the great variety of PC molecular species in human tissues.
· In vivo, PC is produced via two major pathways.4 In the predominant pathway, two fatty acids (acyl "tails") are added to glycerol phosphate (the "middle piece"), to generate phosphatidic acid (PA). Next, PA is converted to diacylglycerol, after which phosphocholine (the "head-group") is added on from CDP-choline. The second, minor pathway is phosphatidylethanolamine (PE) methylation, in which the phospholipid PE has three methyl groups added to its ethanolamine head-group, thereby converting it into PC.
· Taken orally PC is very well absorbed, up to 90% per 24 hrs when take with meals.
· Postprandially, PC enters the blood gradually and its levels peak over 8-12 hours. During the digestive process, the position-2 fatty acid becomes detached (de-acylation) in the majority of the PC molecules.5 The resulting lyso-PC readily enters intestinal lining cells, and is subsequently re-acylated at position 2. The position-2 fatty acid contributes to membrane fluidity (along with position I), but is preferentially available for eicosanoid generation and signal transduction. The omega-6/omega-3 balance of the PC fatty acids is subject to adjustment via dietary fatty acid intake.6,7
· Choline is most likely an essential nutrient for humans,8 and dietary choline is ingested predominantly as PC. Greater than 98 percent of blood and tissue choline is sequestered in PC, 2 and dietary PC serves as a "slow-release" blood choline source.9 Malnourished individuals with lowered blood choline frequently display liver steatosis and related dysfunctions; these often respond favorably to PC supplementation10.
· Methyl group (-CH3) availability is crucial for protein and nucleic acid synthesis and regulation, phase-two hepatic detoxification, and numerous other biochemical processes involving methyl donation.
· Methyl deficiency induced by restricted choline intake is linked to liver steatosis in humans, and to increased cancer risk in many mammals. PC is an excellent source of methyl groups, supplying up to three per PC molecule.
Mechanisms of Action
PC is the main structural support of cell membranes, the dynamic molecular sheets on which most life processes occur.1 Comprising 40 percent of total membrane phospholipids, PC's presence is important for homeostatic regulation of membrane fluidity. The PC molecules of the outermost cell membrane deliver fatty acids on demand for prostaglandin/eicosanoid cellular messenger functions, and support signal transduction from the cell's exterior to its interior6.
PC is the main lipid constituent of the lipoprotein particles circulating in the blood. The amphipathic properties of PC render it an obligatory micellizing constituent of bile.12,13 PC has surfactant (surface-active) properties that substantially protect the epithelial-luminal interfaces of the lungs and GI tract14,15.
Biochemically, PC is the preferred precursor for certain phospholipids and other biologically important molecules.4 PC also provides antioxidant protection in vivo.16 In animal and human studies, PC protected against a variety of chemical toxins and pharmaceutical adverse effects1.
The best-documented clinical success with PC to date is its significant amelioration of liver damage, probably because liver recovery following damage requires substantial replacement of cell membrane mass. The findings from eight double-blind trials and numerous other clinical reports 1,7 indicate consistently significant clinical benefit, including improvement of enzymatic and other biochemical indicators, faster functional and structural rebuilding of liver tissue, accelerated restoration of subjects' overall well-being, and improved survival following PC treatment.
Alcoholic Hepatic Steatosis and Inflammation
Knuechel conducted a double-blind trial on 40 male subjects with hepatic steatosis (fatty liver) and inflammation linked to alcohol intake.17 Subjects were taken off pharmaceuticals and randomized into two groups; one group received placebo, the other 1,350 mg PC per day by mouth (fortified with B vitamins). Benefits from PC were evident at two weeks, and by the eighth week a wide variety of biochemical liver function measures were significantly improved over placebo.
Three subsequent double-blind trials corroborated these findings. Schuller Perez and San Martin concluded, "It is our view that the use of highly-unsaturated phosphatidylcholine for therapy of alcohol-dependent steatoses is very productive."18 Buchman et al administered PC double-blind to 15 subjects with fatty liver as part of a total parenteral nutrition intravenous feeding regimen, and also obtained significant benefit.19 Other researchers report that subjects with mild to moderate hepatic inflammation benefit the most from PC supplementation.20
In an animal study, baboons were placed on a daily alcohol regimen for up to eight years. Following a blinded trial design, PC was added to the diet of some of the animals. After several years, baboons fed alcohol without PC had progressed to advanced fibrosis, while the PC-supplemented baboons developed fatty liver and mild fibrosis, but did not progress further. After three of the animals were taken off PC and kept on alcohol, they rapidly progressed to extensive; life-terminating liver fibrosis.21
Drug-Induced Liver Damage
In a double-blind trial, 101 tuberculous subjects who had suffered liver damage from rifampin and two other anti-tuberculosis pharmaceuticals received placebo or 1,350 mg of fortified PC daily. After three months, the PC group had significantly lower SGOT and SGPT enzyme levels.22
In a double-blind trial on 30 subjects with progressing liver damage from chronic hepatitis B virus infection (negative for HBsAg), standard immunosuppressive therapy was retained and subjects received either PC (2,300 mg per day) or pla- cebo. At one year, the PC group had clinically stabilized, with significant improvement of liver structure, whereas the placebo group had worsened.23
Sixty subjects positive for hepatitis B (HBsAg-positive) were placed in a fortified PC group (1,350mg per day) or a placebo group for 60 days. From 30 days onward the PC group was clinically improved over placebo, with 50 percent becoming HbsAg-negative, compared to 25 percent of the placebo group.24
In a double-blind trial of 50 subjects, all HBsAg-positive and manifesting extremely severe liver damage verified by biopsy and immunologic testing, the PC group (1,350 mg fortified PC per day) benefited considerably more (p<0.001) than placebo. In the PC group, 80 percent (20 of 25) were judged greatly improved, while 24 percent (6 of 25) moderately improved in the placebo group. Cell-structure, biochemical, immunologic, and hematologic parameters were significantly improved over placebo. Clinical improvement continued well past the end of the one-year trial.25
In a multicenter, double-blind trial, 176 patients with chronic viral hepatitis (B or C) were begun on interferon alpha for 24 weeks then randomized to PC (1.8 g/day) or placebo for 24 weeks. Significantly more patients responded to PC, particularly in the hepatitis C subgroup. In addition, PC supplementation sustained a longer term improvement from hepatitis C over another 24 weeks.26
A long-term, multicenter, double-blind trial of PC for liver disease is ongoing; its results could signal a breakthrough in nutritional management of this life-threatening disease.27
Respiratory Distress Syndrome
The surfactant of premature babies is abnormally low in PC. Treatment with exogenous, mature-profile surfactant (with PC 70-80% of the total phospholipids) is the standard therapy for infants with, or at risk of having, respiratory distress syndrome (RDS). A meta-analysis of clinical trials suggests improved survival and overall better outcome from natural surfactant over synthetic forms.28 In another randomized trial with 78 RDS babies, natural surfactant proved superior after six hours, and by 24 hours normalized the surfactant PC profile.14
Necrotizing Enterocolitis, Gastrointestinal Protection
· As the major intrinsic surfactant of the gastrointestinal tract, PC helps maintain the acid barrier properties of the gastric epithelium. Animal research suggests PC helps protect against the adverse GI effects of aspirin and other non-steroidal anti-inflammatory drugs without blocking their efficacy. 25,29,30 Carlson et al reported a lower incidence of necrotizing enterocolitis in pre-term infants fed with formula high in PC and other phospholipids.31
Central Nervous System Cholinergic Imbalances
In contrast to persistent anecdotal claims, PC failed to benefit cognition in ten double-blind, placebo-controlled trials.32 There are indications the "therapeutic window" for PC might be very narrow,33 which could also explain the disappointing trial results against ataxias, tardive dyskinesia, and other CNS conditions that feature cholinergic imbalances.
Toxicity and Side Effects
PC is freely compatible with other nutrients, and when co-administered may enhance their absorption. Standard toxicological assessments indicate no significant acute or chronic toxicity from PC, as well as no mutagenicity and no teratogenicity. PC is well tolerated at daily intakes of up to 18 grams} Symptoms of intolerance are almost exclusively restricted to GI discomfort - diarrhea, excessive fullness, and nausea.
The therapeutic range of intake is 800- 2,400 mg daily, and 4-6 grams or higher for liver salvage. For subjects with severe liver damage, best results may be obtained by initiating therapy with intravenous and oral PC, then maintaining on oral supplementation after improvement has begun. In cases of liver damage from deathcap mushroom poisoning this procedure has proved lifesaving.34
1. Kidd PM. Dietary phospholipids as anti-aging nutraceuticals. In: Klatz RA, Goldman R, eds. Anti-Aging Medical Therapeutics. Chicago, IL: Health Quest Publications; 2000:283-301.
2. Zeisel SH, Blusztajn JK. Choline and human nutrition. Annu Rev Nutr 1994;14:269-296.
3. Schneider M. Phospholipids. In: Gunstone FD, Padley FB, eds. Lipid Technologies and Applications. New York, NY: Marcel Dekker; 1997:15-30.
4. Kent C. Eukaryotic phospholipid biosynthesis. Annu Rev Biochem 1995;64:315-343.
5. Zierenberg 0, Grundy SM. Intestinal absorption of polyenephosphatidylcholine in man. J Lipid Res 1982;23:1136-1142.
6. Kidd PM. Cell membranes, endothelia, and atherosclerosis -the importance of dietary fatty acid balance. Altern Med Rev 1996;1:148-167.
7. Kidd PM. Phosphatidylcholine, a superior protectant against liver damage. Altern Med Rev 1996;1:258-274.
8. Zeisel SH, Da Costa K, Franklin PD, et al. Choline, an essential nutrient for humans. FASEB 1991;5:2093-2098.
9. Wurtman RJ , Hirsch MI, Growdon JH. Lecithin consumption raises serum free choline levels. Lancet 1977;ii: 68-69.
10. Buchman AL, Dubin MD, Moukarzel AA, et al. Choline deficiency: a cause of hepatic steatosis during parenteral nutrition that can be reversed with intravenous choline supplementation. Hepatology 1995;22:1399-1403.
11. Ghyczy M, Boros M. Electrophilic methyl groups present in the diet ameliorate pathological states induced by reductive and oxidative stress: a hypothesis. Brit J Nutr 2001;85:409-414.
12. Thistle JL, Schoenfield LJ. Bile acid, lecithin, and cholesterol in repeated human duodenal biliary drainage: effect of lecithin feeding. Clin Res 1968;16:450.
13. Toouli J, Jablonski P, Watts JM. Gallstone dissolution in man using cholic acid and lecithin. Lancet 1975;ii: 1124-1126.
14. Lloyd J, Todd DA, John E. Serial phospholipid analysis in pre term infants: comparison of Exosurf and Survanta. Early Human Dev 1999;54:157-168.
15. Dunjic BS, Axelson J. Gastroprotective capability of exogenous phosphatidylcholine in experimentally induced chronic gastric ulcers in rats. Scand J Gastroenterol 1993;28:89-94.
16. Lieber CS, Leo MA. Polyenylphosphatidylcholine decreases alcohol-induced oxidative stress in the baboon. Alcoholism Clin Exp Res 1997;21:375-379.
17. Knuchel F. Double blind study in patients with alcohol-toxic fatty liver. Med Welt 1979;30:411-416.
18. Schuller-Perez A, San Martin FG. Controlled study using multiply-unsaturated phosphatidylcholine in comparison with placebo in the case of alcoholic liver steatosis. Med Welt 1985;72:517~521.
19. Buchman AL, Dubin M, Jenden D, et al. Lecithin increases plasma free choline and decreases hepatic steatosis in long-term total parenteral nutrition patients. Gastroenterology 1992;102:1363-1370.
20. Panos MZ, PoIson R, Johnson R, et al. Activity of polyunsaturated phosphatidylcholine in HBsAg negative (autoimmune) chronic active hepatitis and in acute alcoholic hepatitis. In: Gundermann KJ, SchQmacher R, eds. 50th Anniversary of Phosp*lipid Research (EPL). Bingin-Rhein, Germany: wbn- Verlag; 1990: 103-110.
21. Lieber CS, Robins SJ, Li J, et al. Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon. Gastroenterology 1994;106:152-159.
22. Marpaung H, Tarigan P, Zein LH, et al. Tuberkulostatische kombinations therapie aus INH, RMP und EMH. Therapiewoche 1988;38:734- 740.
23. Jenkins PJ, Portmann HP. Use of polyunsaturated phosphatidylcholine in HBsAg negative chronic active hepatitis: results of prospective double-blind controlled trial. Liver 1982;2:77- 81.
24. Visco G. Polyunsaturated phosphatidylcholine (EPL) associated with vitamin H-complex in the treatment of acute viral hepatitis-H. La Clinica Terapeutica 1985;114:183-188.
25. Ilic V, Hegic-Janev A. Therapy for HHsAg-positive chronically active hepatitis. MedWelt 1991;42:523-525.
26. Niederau C, Strohmeyer G, Heintges T, et al. Polyunsaturated phosphatidylcholine and interferon alpha for treatment of chronic hepatitis H and C: a multicenter, double-blind, placebo-controlled trial. Hepatogastroenterol 1998;45:797-804.
27. Schenker S. Polyunsaturated lecithin and alcoholic liver disease: a magic bullet? Alcoholism Clin Exp Res 1994;18:1286-1288.
28. Halliday HL. Natural vs synthetic surfactants in neonatal respiratory distress syndrome. Drugs 1996;51 :226-;237.
29. Leyck S, Dereu N, Etschenberg E, et al. Improvement of the gastric tolerance of non- steroidal anti-inflammatory drugs by polyene phosphatidylcholine (Phospholipon 100). Eur J PharmacoI1985;117:35-42.
30. Swarm RA, Ashley SW, Soybel Dl, et al. Protective effect of exogenous phospholipid on aspirin-induced gastric mucosal injury. Am J Surg 1987;153:48-53.
31. Carlson SE. Lower incidence of necrotizing enterocolitis in infants fed a preterm formula with egg phospholipids. Pediatr Res 1998;44:491-495.
32. Kidd PM. Unpublished analysis. 1998; El Cerrito, California, USA: email@example.com.
33. Little A, Levy R, Chuaqui-Kidd P, et al. A double-blind, placebo controlled trial of high- dose lecithin in Alzheimer's disease. J Neurol Neurosurg Psychiatr 1985;48:736-742.
34. Esslinger F. Death cap mushroom poisoning: report of clinical experience. Med Welt 1966;19:1057-1063.
Appendix: Food Sources of Choline
Choline and Choline Phospholipid Content of Selected Foods, in Milligrams per Serving Free
Food Serving Choline Lecithin Total Choline
Apple 1 medium 0.39 29.87 4.62
Banana medium 2.85 3.26 3.52
Beef liver 3.5 oz 60.64 3362.55 532.28
Beef steak 3.5 oz. 0.78 466.12 68.75
Butter 1 tsp. 0.02 6.80 1.18
Cauliflower 1/2 cup 6.79 107.06 22.15
Corn oil 1 tbsp. 0.004 0.13 0.03
Coffee 6 oz. 18.59 2.05 19.29
Cucumber 1/2 cup 1.18 3.06 1.74
Egg 1 large 0.22 2009.80 282.32
Ginger ale 12 oz. 0.07 1.11 0.34
Grape juice 6 oz. 8.99 2.11 9.37
Human milk 1 cup 2.10 27.08 10.29
Iceberg lettuce 1 oz. 8.53 2.86 9.06
Infant formula 1 oz. 0.818 2.97 1.38
Lecithin supplement 1 tbsp., 7.5 g. NA 1725 250
Milk whole 1 cup 3.81 27.91 9.64
Orange 1oz. 13.24 107.35 27.91
Potato 1 5.95 25.97 9.75
Tomato 1v 5.50 4.94 6.58
Whole wheat bread 1 slice 2.52 6.57 3.43
(USDA: Composition of Foods. USDA handbook # 8. Washington DC, ARS, USDA, 1976-1986)
LION NUTRITON ROCKS
10-04-2003 12:36 AM
Source: DETOXXBOOK on PhosChol
January 06, 2003
One of the most important biochemical changes regarding aging, is a change in membrane phospholipid composition; the result being that we lose the active life giving highly fluid lipids and replace them with rigid stiff inactive ones. That is how it all comes to an end; how life slows down both in thought and in motion until it is no more and it all happens in the loss of control of the active lipids.
Phosphatidylcholine (PC) is the predominate head group in the outer leaflet of the membrane and is composed of two phospholipid groups opposing each other in a normal bilipid membrane array. PC also tends to incorporate a predominance of HUFAs (highly unsaturated fatty acids), especially arachidonic acid (AA) on the Sn2 position, thus the outer leaflet is composed of a grouping of higher energy lipids than the inner leaflet. In mammalian plasma membranes, the main variation occurs in the relative composition of phosphatidylcholine (PC), and both sphingomyelin (SM) and cholesterol. PC decreases with age while SM and cholesterol increases with age (Barenholz, Schacter 1983). The importance of this shift in the outer membrane is difficult to envision. It involves every cell of the body and every sensory neuron such as, touch, smell, taste, sight, hearing, skin, blood cells, brain neurons, endothelium, alveoli, immune cells, bone cells, etc. It involves the organelles within the cell, such as the mitochondria the peroxisomes and the nuclear membrane. The concept of aging and PC decline is a dramatic shift in the bodies homeostatic ability.
The changes in the relative amounts of PC and SM are especially great in tissues, which have a low phospholipid turnover. For example, plasma membranes associated with the aorta and arterial wall show a 6-fold decrease in PC/SM ratio with aging. SM also increases in several diseases, including atherosclerosis. The SM content can be as high as 70-80% of the total phospholipids in advanced aortic lesion (Barenholz 1982, 1984). Both sphingomyelin (SM) and cholesterol are structurally similar to saturated fats. They are rigid, with the concommittment decline in fluidity and lower metabolic performance. The loss of those dynamic double bonds of the high energy lipids could be the major cause of the aging disease.
Transition Temperatures: The most striking differences between PC and SM derived from biological membranes are (a) the phase transition temperature of the phospholipids and (b) the hydrogen-bonding character of the two phospholipids in a lipid bilayer. Most sphingomyelins have transition temperatures in the physiological temperature range between 30 and 40 Celsius, whereas most naturally occurring PC is well above its transition temperature of 37 C. (Barenholz 1980, 1982, 1984). SM and cholesterol contribute to rigidity of the membrane, while PC has a high affinity for HUFAs, especially AA, with much higher internal energy levels, which as discussed prior with reference to the higher energy of the double bonds, raises the transition temperature.
Heart Myocytes: The relative content of PC to SM in mammalian plasma membranes appears to affect cell functioning significantly. Researchers have recently reported on changes in the lipid composition and activity of primary rat heart myocytes in vitro over time. Measurements of PC and SM content in the cells showed a decline of PC/SM ratio from 5 to ~ 2 in the first three days in culture, and from 2 to ~ 1 over the next 14 days.
The phospholipid changes were accompanied by a dramatic change in heart cell activity, as measured by the beating rate of the cultured cells. Between days 7 and 12 in culture, the beats/minute fell from 160 to about 20, with significant increases in the activities of at least seven enzymes, expressed as Vmax/DNA. One of these enzymes was creatine phosphokinase (CPK), a major intracellular energy transport enzyme, and one which can serve as a PC level indicator.
Phospholipid Exchange: The ability to alter the lipid composition of biological cells by phospholipid exchange provides a means for studying the effect of phospholipid variation on cell function. For example, in the above-discussed myocyte culture system, in which a decline in PC/SM ratio over time is accompanied by a drop in beating frequency, the concerns are (a) whether the original phospholipid composition of the cells can be restored by an exchange of more favorable phospho-lipids, and (b) can the original cell function be restored, i.e. the initial higher beating rate.
There are a number of studies attempting to evaluate the premise of using phosphatidylcholine as a vehicle for phospholipid exchange within cellular membranes. The rat heart myocyte study specifically showed that by infusing PC, a phospholipid exchange increased both PC/SM and PC/cholesterol ratios, thus reversing the abnormal phospholipid composition which occurred in the cultured cells over time. (Yechiel 1985a, 1985b). Interestingly, phospholipid exchange restored cell-beating frequency to its original levels, with the beating frequency showing a jump from 20 to 160 within one day of cell exposure to phosphatidylcholine.
The same phospholipid exchange also led to a reduction in cellular enzymes, such as CPK, which normally increases over time. However, the experiments described were carried out in cell culture, whereby the cells are individually tested for their response to the various phospholipids. However, it is a bit presumptuous, based on in-vitro laboratory experiments that the use of phosphatidylcholine would necessarily lead to similar rates of rejuvenation in humans.
The present focus however, is with the use of phosphatidylcholine (PC) as either a medical intervention using IV therapy, or as a nutritional supplement, with the goal of changing fatty acid composition similar to components of the heart cells of subjects of a younger age. The intravenous administration of PC as a fast infusion, or the use of oral PC should be administered in a protocol sufficient to witness a significant drop in serum creatine phosphokinase (CPK). Both have been used either separately and together, with the oral supplementation as a means of maintaining levels of PC between IVs. IV administration is preferred, when possible, however oral has been documented in the literature to be efficacious. (Lipostabil, Rhone-Poulanc).
Atheroscerosis / Ischemia: An important aspect of the PC treatment program has been the recognition that essential phospholipids rich in phosphatidylcholine are able to reverse age-related changes in phospholipid composition of heart muscle cells in animals. In one series of tests, 18-month-old rats were treated with three doses, administered every three days for six days (three injections), and the animals were sacrificed three days after the final injection. The PC/SM and cholesterol content of heart muscle cells were compared from relatively young animals (three months old) and from untreated 18-month-old animals. The results show that the PC/SM ratio increased by more than twofold with an almost threefold decrease in cholesterol content, reversing the age related shift in both values, as would normally be the alterations experienced with age between three and eighteen months.
The three groups of animals were also tested for heart muscle and serum CPK levels. The changes in lipid composition, which normally occur between three and eighteen months (high SM and cholesterol), were accompanied by approximately threefold increases in both heart muscle cell and serum CPK. After nine days of treatment, heart cell CPK declined about threefold to levels normally seen in 3 month old animals, and serum CPK declined eightfold to a level substantially lower than that in 3 month old animals. The dramatic fall in serum CPK in treated animals thus provides a sensitive indicator of heart lipid changes occurring during treatment.
The above-noted changes in heart cell lipid composition were measured on whole heart homogenates, and therefore represent phospholipid contributions from both myocardial (heart) cells and connective tissue fibroblasts. To confirm that the observed change in phospholipids also reflects changes in myocardial cells, heart cells from three-month-old and eighteen-month-old animals were isolated, cultured under conditions which lead to myocardial reaggregates, then tested for lipid exchange with egg PC. The reaggregates originally showed a decrease in PC/SM ratio and an increase in cholesterol level, when comparing cells from three and eighteen month old animals. These age-related changes were substantially reversed by incubation with egg PC. The results indicate that the observed phospholipid effects seen in heart tissue in vivo are due at least in part to changes in myocardial membrane phospholipids. The effect of the PC treatment program on heart muscle phospholipid concentration is reflected in a number of other physiological changes readily observed in serum samples from the treated individual (animal or human).
Improved Respiratory Function: The use of the PC treatment program can also significantly enhance an animal's ability to withstand respiratory stress. As above, the use of the treatment can easily be monitored by changes in CPK or red blood cell properties. The animal's ability to withstand cardiac stress before and after treatment was measured by a standard lab procedure, in which an animal is placed in a defined-volume chamber, which does not allow gas exchange with the outside. During the course of the test, the depletion of oxygen and accumulation of carbon dioxide reduces the animal's blood pressure gradually to near zero levels. The ability to withstand respiratory stress is measured by the lapse in time in the chamber before the animal's blood pressure drops to near zero.
After three treatments (nine days after the first treatment), 18 month old male rats were able to maintain blood pressure about 50% longer than untreated rats. The treated rats also showed a much slower rate of increase of serum CPK during the test than untreated animals. Blood monitoring throughout the test period showed that both treated and untreated animals maintained comparable levels of blood oxygen and carbon dioxide, indicating that the better performance of treated animals was not merely a blood-gas content effect.
Increasing Longevity: Studies on laboratory animals indicate that treating relatively aged animals with PC infusion over an extended period increases an animals’ lifespan by an average of about 36%. 30-month-old rats were given an initial injection, followed by a second injection 1 week later, and maintenance injections every two months. A group of untreated rats died between ages 32 and 38 months, with an average age of death of about 34 months. The group of treated animals was sacrificed between ages 42 and 48 months.
It is interesting to note that longevity was extended in the treated animals, even though treatment was not begun until a relatively advanced age (32 to 38), actually within a few months of the time the animals would have normally died. This finding indicates that the treatment is effective in reversing age-related changes in lipid composition, even at an advanced age. The approximately 36% increase in longevity indicates that the alteration in lipid composition produced by treatment confers widespread physiological benefits (including, presumably, increased cardiac performance and arterial circulation) which are related to longevity. The increase in longevity, which is achievable in animals, could also result in increase of longevity in humans, assuming that a human lives on the average about 2 years for each month of a laboratory rat, treatment could result in a major increase of longevity equivalent to 25 years. Note: The 36% increase in longevity of the animal could have been improved by permitting a normal expiration period.
Another study examined the effect of treatment on animal longevity. The rats tested were 30-month-old male Sprague-Dawley rats. Since Sprague-Dawley rats normally die between the ages of 24-30 months, the rats tested exhibited some selection for longevity. A test group of six rats were each given PC SuVs, at a dose of between 0.5 and 1g phosphatidylcholine lipid through the tail vein, and similarly dosed after one week, and every two months thereafter, until the animal died of natural causes.
The animals were fed as much as they desired during the treatment period and the usual precautions were taken to avoid animal infection. A second control group of same-aged rats was similarly injected with sterile saline on the same dose schedule. Of the 6 animals in the control group, 2 died at 32 months (two months after the beginning of treatment), 3 died at 34 months, and 1 died at 40 months, giving an average age at death of about 34 months. Of the treated animals, 2 were sacrificed at 44 months, 1 at 45 months, and 3 at 48 months, giving a minimal average age at death of about 46 months.
Increased Male Fertility: Treating relatively old lab animals with this treatment reversed the near-complete loss of competence normally seen in the older male animals. The method is particularly useful for treating older breeding animals. 30 months and older rats received three doses over a 6 day period. Normally male rats at this age are unable to sire litters when placed in the same cage with younger fertile female rats. When untreated rats of this age were individually housed with three female rats, 5-6 months old, only two out of the three females had litters, and in each case the litter was smaller than the usual 10-13 animal litter sired by younger males. Treated rats, by contrast, showed normal male fertility. All of the rats sired litters in all three females, and all of the litter sizes were the normal 10-13 in size.
Difficulty With Animal Studies: It is difficult to extrapolate human reactivity from these animal studies. Rats have a more efficient FA metabolism regarding desaturase and elongase enzyme functions. To determine the final lipid composition of a rat after an infusion of IV PC, into the higher PUFAs and HUFAs, would be onerous to track. It is possible however, to determine the results of a variation in head groups of a PC exchange, but the PUFA lipids in the oral or IV PC are predominantly LA and would be readily metabolized to HUFAs in a rat, in effect, changing the performance relative to humans. In addition, the size of the bolus (1 gram IV) related to humans is in the order of 100:1. Using an IV equivalent would require an infusion of 50 to 100 grams of PC, which is 50 to 100 times the dosage recommended by the pharmaceutical manufacturer. Using an oral equivalent, and based on an absorption rate of oral PC at 20% to an infusion of PC at 100%, a ratio of 1:5, would require the ingestion of ~ 500 capsules at one time ( 900 mg ea.), which is certainly inadvisable.
The majority of the past 20 years of PC research on humans has focused on the positive effects on arteriosclerosis and improving liver enzymes and hepatitis B. The liver receives the first flush of PC from an infusion and receives 25% of the entire blood flow, therefore it was the first examined for potential benefits of a PC exchange. However, an exchange of lipids is systemic with every organ, every neuron and every cell sharing the increased PC and the higher performing lipids (HUFAs). It should be expected that improved metabolic performance would also be systemic.
Also, research has shown that the higher PC levels reached after a 3 month program of PC administration dissipates within 4 months of ceasing infusion or oral supplementation. The ability to maintain PC levels is therefore an energy related rate of change that equates with the higher metabolic rate of youth, but which some portion appears attainable at almost any age. To avail yourself of this exciting PC program, it is therefore necessary to consider a long term maintenance program of both IV and/or PC supplements, once optimum levels are attained from the initial program. The concept of altering an aging membrane is nothing short of exhilarating.
10-04-2003 12:37 AM
Nov 25, 2002 10:38 pm US/Eastern
NEW YORK (CBS) “I don't think any exercise will get rid of these love handles,” says 30-year-old Misty Koons.
But would she be willing to jab the flab?
“I want a quick fix,” replies Misty.
So Koons, a consultant from New Jersey, who says she isn't comfortable with the way she looks chose the latest way to a svelte waistline. CBS 2’s Dr. Mike Rosen has the story.
It's called lipostabil, no, it's not liposuction. It's a cosmetic technique just being introduced in this country, that's been popular in Europe and South America for years.
Lipostabil claims to break down fat deposits with 5-10 injections over 2-3 weeks. But what's in those needles?
“It's basically a molecule that emulsifies fat, it's in everbody's body, it's a natural substance,” says Dr. Soren White.
New York dermatologist Soren White has treated 40 men and women in the last 6 months with lipostabil, “It works on fat deposits resistant to diet or exercise - love handles, abdomen, knees, chins, under the eyes. It's a great thing, works well, easy to do and there are no side effects.”
The cost of each procedure can run anywhere from $350 to $1,000 depending on which part of the body you treat.
“It was easy, painless, pinched in a few places,” adds Misty.
“It's not dramatic on the outside, but for her the way she feels in her clothes will be different,” adds Dr. White.
Just two weeks later, after some minor bruising and swelling, Misty sees results, “As you can see, I can't pinch anymore. I feel like vast improvement.”
But Park Avenue plastic surgeon, Alan Matarasso warns that lipostabil is not FDA approved and still needs to be evaluated.
“We need to know the proper dosage, side effects, how many treatments. No one can tell us now how much drug to use or the long term consequences,” says Dr. Matarasso.
“There was a study published from a dermatologist in Brazil on bulges under the eyes and there were impressive results, no recurrences and no surgery,” responds White.
But Dr. Matarasso contends that liposuction is still the safest, most effective treatment for the permanent reduction of fat, although it may not be for everyone.
“I am more comfortable with lipostabil than with having anesthesia and surgery,” says Michelyn Camen, a 40 something marketing executive who wants lipostabil to melt away her "bra bulges."
“I trained to get rid of this area, and it's resistant, so when I heard about this, I made the call,” says Michelyn.
Meanwhile, Misty is back for treatment number two, “I love it, I worked out, everything is fine. I would rave about it to everyone.”
10-04-2003 12:38 AM
People in the know are talking about the latest (alleged) miracle fat buster gaining popularity, and it’s called Lipostabil. Plug the word Lipostabil into any internet search engine and you’ll net hundreds of hits that match what is being touted as the injectable answer to liposuction. Then it hits you; nearly all of them are penned in a language other than English and originate outside of the United States. Why?
While those seeking a sleeker waistline, less of a double chin, or an end to saddlebags may be chatting up the promise of this fat dissolving elixir, the Food and Drug Administration hasn’t made a peep. In fact, they have yet to receive an application from the maker, Aventis, the gigantic French pharmaceutical company, for approval in the United States.
It is not that the drug itself hasn’t been approved overseas. Lipostabil is phosphatidylcholine, a liquid form of lecithin, an enzyme which occurs naturally in the body. It was first used in the 1950s to dial down climbing cholesterol and triglyceride numbers and is approved for use, according to the manufacturer, in Brazil, Germany, Italy and South America.
It took Brazilian dermatologist, Patricia Rittes, widely credited with pioneering the treatment often called Lipo-Dissolve, to reincarnate the drug as a pathway to physical perfection. After experimental use as an injectable fat-dissolver by doctors overseas such as Rittes, it started to make its way stateside. Thanks to some anecdotal evidence and off label usage, a few doctors in the United States are now injecting surgery-shy but eager patients in order to send their eye bags packing, whittle pudgy upper arms and reduce other areas often too small to treat with liposuction. You may remember that wrinkle busting Retin-A was only FDA approved as an acne treatment for years before it could claim its wrinkle reducing charms. However, doctors were prescribing it to their creased and lined, albeit unblemished, patients for years before it got the FDA stamp of approval. The same is true for Botox. Doctors found it helped reduce the appearance of wrinkles and used it for that off label purpose before it got the FDA go-ahead to claim it could tame wrinkles. But, Retin-A and Botox were FDA approved drugs. Lipostabil is not approved for any use in the United States. Aventis notes that they did not develop the drug for the popular use it’s currently gaining across the globe.
So, how does Lipostabil work? Depending on the area and the desired results, a patient gets injected with the drug at the trouble site or sites spaced over the course of several weeks. A topical anesthetic is used at the injection site. One may experience some side effects like mild swelling and bruising or itching at the injection site. Then the patient waits a couple of weeks and goes back in for another round of shots. After the treatments are over and the swelling subsides, one should find a new, fat free area in its wake thanks to the fat dissolving properties of the drug. Because no official protocols have been established, how many shots you need depends upon what your doctor advises. How much of the drug to use has been determined by trial and error.
You only need a couple of shots to get rid of that stubborn slab of abdominal flab? Sounds fuss free, and it is... sort of. The snag is that we don’t know more than we do know about this treatment. Random calls to dermatologists and other doctors didn’t net a single one who is currently using the drug, although several dermatologists and other doctors have gone on record in the media that they’re performing the treatment. What’s more, testing of the procedure has been limited to just one 30 person (non-peer reviewed, without a control group) study performed in Brazil testing how the drug worked on the small amounts of fat that make up under-eye bags. Photos from the study do show an improvement, but the results have not been duplicated nor scrutinized in other studies.
The American Society for Aesthetic Plastic Surgery has gone so far as to issue a statement questioning the use of Lipostabil adding the only proven method to permanently remove fat deposits is liposuction. The ASAPS also questions how practitioners will evaluate how much fat is to be removed and raises the issues of whether the drug dissolves other tissue as well, how the body will react to the introduction of an increase in a naturally occurring substance and the potential unknown side effects.
For some, the unknown may be offset by what we do know and the promise of dissolving fat. Anecdotal evidence shows it can ditch an inch or more of fat off your waist, arms or thighs and flatten under eye bags or the chin "wattle." Lipostabil injections may also help with the curse of cellulite, the puckering orange-peel skin that plagues 9 out of 10 women. Some doctors are injecting the drug to dissolve this stubborn fat that often shows up on the back of thighs and the buttocks.
How much will the procedure cost you? Figure on $1,000 to $1,500 per session depending on the part of the body being treated (e.g.- the stomach will cost more than the arms). Also, don’t forget you’ll need several, as many as ten, sessions to get the desired results. Don´t expect to just lay out cash for a new physique. Lipostabil is best used for small areas, whereas liposuction can treat larger areas and remove more fat.
Karmen B. Saran
Contributing writer to DERMAdoctor.com
10-04-2003 12:39 AM
Lipostabil concerns- note this is from plastic surgeons who stand to lose alot
however this is still worth reading and considering as with anything ingested , pros and cons.
Press release from the American Society for Aesthetic Plastic Surgery (ASAPS) October 8, 2002
NEW YORK, NY (October 8, 2002) - It is the American Society for Aesthetic Plastic Surgery's (ASAPS') position that, currently, lipoplasty (liposuction) is the only proven method for the permanent reduction of fat deposits. Recently, however, there have been articles in popular consumer magazines describing the injection of phosphatidylcholine, a phospholipid that is known by the trade name of Lipostabil. Claims state that this substance dissolves fat without the need for surgical intervention. ASAPS cautions that the safety and effectiveness of this procedure are unproven.
Licensed physicians may legally offer treatments involving off-label uses of many pharmacologic substances, as long as such substances have been approved by the Food and Drug Administration for other uses and there is no specific prohibition of the intended off-label use. Currently, however, Lipostabil is not approved for any use in this country. In addition, there does not appear to be sufficient scientific and clinical data to substantiate the safety and effectiveness of phosphatidylcholine (Lipostabil) as a fat-dissolving treatment.
Lipostabil was not developed as a fat-dissolving agent. . The only published study using phosphatidylcholine for this purpose treated only 30 patients (on their lower lids), with a maximum follow-up of two years. The published photographs demonstrating visible reduction of the very small amounts of excess fat contained in the lower eyelid seem promising, but the study lacked controls, and the results have yet to be duplicated in other peer-reviewed studies.
Specific questions regarding phosphatidylcholine (Lipostabil) should be answered before its safe use on patients can be assured:
How can it be assured that the appropriate amount of fat - neither too little nor too much -- is dissolved? (It should be noted that current techniques in cosmetic eyelid surgery tend to favor greater preservation of fat tissue in the lower eyelid, with optimal correction often achieved by a combination of minimal fat removal and repositioning or suturing of fatty tissues.)
If phosphatidylcholine dissolves fatty tissue, does it also dissolve other tissue? How is delivery of the substance limited to only the target tissues? While phosphatidylcholine is a naturally occurring compound that is present in the body, what problems might be encountered by adding an uncontrolled amount of the substance?
The injection of phosphatidylcholine into subcutaneous tissues can potentially trigger the release of enzymes (lipases), which break down lipids or act as an emulsifier or detergent to dissolve cell membranes and intracellular fats. Either of these mechanisms may trigger the release of histamines, which tend to produce itching and redness; these may be short-term side effects, but are there also long-term side-effects? Given the chemical makeup of the substance, is there the possibility that side-effects could include leakage of cell membranes or even cell death?
A great deal of the currently published research in aesthetic plastic surgery focuses on the development of minimally invasive procedures that can improve a patient's appearance with fewer risks and shorter recovery than traditional surgery. The way in which safety and effectiveness of new procedures is determined, in preparation for their widespread use in properly selected patients, is through careful scientific and clinical research. Such research is evaluated through publication of results in reputable, peer-reviewed medical journals and presentation of results at medical meetings such as those sponsored by ASAPS and other accredited Continuing Medical Education sponsors.
As the leading society of plastic surgeons certified by the American Board of Plastic Surgery, who specialize in aesthetic (cosmetic) surgery, ASAPS believes that research into new cosmetic surgical and nonsurgical treatments with potential benefits to patients is important and should be conducted responsibly by qualified physicians, according to established scientific and ethical guidelines that are accepted medical practice in this country. If patients are involved in clinical trials of new procedures, they must be provided with adequate data for their full informed consent. The Aesthetic Surgery Research and Education Foundation (ASERF), in conjunction with ASAPS, observes these guidelines in funding research and evaluating new techniques/technology in order to help ensure patient safety and treatment efficacy.
As the leading provider of Continuing Medical Education in cosmetic plastic surgery to board-certified plastic surgeons, ASAPS encourages open-mindedness in regard to any new modalities, but the public must be cautious in regarding such treatments as "harmless" without scientific evidence of their safety and efficacy. It may take some time before important questions about the use of phosphatidylcholine for body contouring are answered by independent researchers.
The American Society for Aesthetic Plastic Surgery (ASAPS) is the leading organization of plastic surgeons certified by the American Board of Plastic Surgery (ABPS) who specialize in cosmetic surgery of the face and the entire body
10-04-2003 01:43 AM
Brewing Anabolic Minds
Let's see if someone can use the search bar at the bottom and dig up some of those doseages used in the injectable studies...
Good find buyb12!
10-04-2003 02:45 AM
here you go
I found an administer plan for Lipostabil that say's to divide 1 vial into 5 injects per side on abs spread out 2 to 3 cm each to cover troubled area. So you would hit .5 ml's spread out over the abs in 10 shots with a slin pin. It say's is moderately painfull for awhile afterwards and to repeat every 3 to 5 day's depending on recovery for 5 sessions.
Effects are noticeable after 3 sessions and by the end there will MARKED fat reduction
10-05-2003 05:41 PM
Running with the Big Boys
Check under Mesotherapy as well.
10-06-2003 12:05 PM
where can you get this stuff?
any guinea pigs out there?
10-09-2003 10:33 PM
lion nutrition may be carring it soon ..we are still on the fence......think I will try it first
10-12-2003 04:48 PM
Is this the same product that was being discussed at elite fitness? Most people just got huge bruises for a few days and very little noticable results.
Similar Forum Threads
By anapolack in forum Anabolics
Last Post: 10-30-2006, 11:38 AM
By anapolack in forum Weight Loss
Last Post: 05-08-2006, 06:50 PM
By anapolack in forum IGF-1/GH
Last Post: 01-13-2006, 07:21 PM
By morfiend in forum Anabolics
Last Post: 06-07-2004, 08:20 AM