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  1. #1
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    I've been thinking of adding PPC to my supp regimen but wasn't crazy about the choices of suppliers until now:



    http://www.jarrow.com/product-380

    Jarrow Poly PC



    You can search PPC or Phoscol (web) for more details.



    NB: this ain't a first tier supplement and I'm not sure I'd add it (depending) unless your regimen is already extensive, or you have specific needs.



    Oh and I have no commercial interests in Jarrow (or anyone else).
    <span style="color:#FF0000"><span style="font-family:Arial Black">THEORY=/REAL WORLD</span></span>

  2. #2
    Senior Member SteveSliwa's Avatar
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    Quote Originally Posted by ScottL' post='445286' date='Dec 30 2007, 08:28 PM
    I've been thinking of adding PPC to my supp regimen but wasn't crazy about the choices of suppliers until now:



    http://www.jarrow.com/product-380

    Jarrow Poly PC



    You can search PPC or Phoscol (web) for more details.



    NB: this ain't a first tier supplement and I'm not sure I'd add it (depending) unless your regimen is already extensive, or you have specific needs.



    Oh and I have no commercial interests in Jarrow (or anyone else).


    LEF produces a 900 mg product at a better retail price.



    Source Naturals also produces it but it's pricey.





    Also Phoschol is the correct name.

  3. #3
    Senior Member SteveSliwa's Avatar
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    More info:





    Overlooked & Overworked

    Preventive maintenance for your stomach, liver and pancreas



    by Karin Granstrom Jordan, MD



    A European soy derivative helps protect vital organs from the effects of toxic overload, obesity, alcohol, aspirin and NSAIDs-and helps maintain a youthful cholesterol profile.



    The aging process, combined with deleterious lifestyle habits, inflicts tremendous damage on our vital organs. NSAIDs and aspirin are toxic to the gut, while alcohol is toxic to the liver and pancreas. Our poor diets too often stress the organs of digestion and metabolism, while contributing to the buildup of arterial plaques. The modern diet and alcohol consumption can also lead to obesity that further promotes liver pathology and cardiovascular disease. One of the best things you can do for your future health is to support and optimize the function of the vital organs compromised by those interrelated stressors-the stomach, liver, pancreas and cardiovascular system.



    PPC Soy derivative

    Phosphatidylcholine (the main component of lecithin) is an integral part of cell membranes, essential for their structural and functional integrity. Cell membranes act like gatekeepers, allowing nutrients into the cells but blocking damaging toxins from gaining entrance. A new extract from soybeans called PPC (polyenylphosphatidylcholine) has been shown to enhance cell membrane function throughout the body.



    PPC is approved for the treatment of chronic liver diseases in many European countries and is actually listed in the Physician's Desk Reference (PDR) of the United States. An accumulating body of research suggests that PPC's umbrella of protection may extend from the liver to the stomach, pancreas and cardiovascular system. PPC is well absorbed in humans and animals when taken orally. There are no known contraindications, side effects or interactions with other drugs, even with consumption of large quantities of PPC.



    It is believed that PPC's protective effect is based on its ability to be incorporated into normal and damaged cell membranes. Animal studies have indicated that PPC, which is a polyunsaturated phosphatidylcholine, becomes incorporated into the membranes of liver cells as a substitute for native saturated phosphatidylcholine molecules (Stoffel W et al 1978). This substitution is shown to result in an increase in membrane fluidity and active transport activity across the membrane. Similarly, PPC is incorporated into blood lipoproteins such as cholesterol, leading to lipid-lowering properties.



    Stomach protection

    The consumption of non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin in our society is greater than any other drug class because of their relative effectiveness in the treatment of pain and inflammation. Recently published evidence shows that those who take NSAIDs have lower risks of Alzheimer's disease, cardiovascular disease and certain cancers. It appears that some of the common diseases of aging are caused by a chronic inflammatory cascade and that daily NSAID ingestion affords considerable protection against these disorders.



    A major concern with NSAID drugs, though, relates to their well-established ability to induce gastrointestinal injury in the forms of erosion, bleeding, ulceration and perforation. Few people realize that GI toxicity from NSAIDs is the most frequent adverse drug event in the U.S., according to some estimates. The facts are alarming (Raskin JB, 1999; Wolfe MM et al., 1999):



    - NSAIDs are used regularly by at least 13 million Americans with arthritic conditions, leading to 16,500 NSAID-related deaths annually (similar to the number of deaths from AIDS).

    - NSAID use increases the relative risk of serious gastrointestinal events three-to-fourfold, and higher for the elderly.

    - 30-60% of chronic NSAID users develop gastroduodenal erosions; 5-30% of chronic users develop ulcers.

    - One third of patients over age 60 with bleeding from peptic ulcers are on NSAIDs.

    - Two thirds of patients over age 60 with GI perforations are on NSAIDs.

    - Over 100,000 people are hospitalized annually in the U.S. for serious GI complications from NSAID use.

    - The mortality rate for patients hospitalized for upper GI bleeding from NSAIDs is 5-10%.

    - GI toxicity from NSAID use is the 15th most common cause of death in the U.S.

    - Advanced age is a primary risk factor for adverse GI events from NSAID use, and the risk increases steadily with age.



    This "silent epidemic" appears without symptoms in up to 40% of cases of NSAID-induced erosive gastritis. While 10-20% of NSAID users have indigestion (dyspepsia), this is not a reliable indicator of mucosal injury. Damage to the gastric epithelium begins within minutes of taking an NSAID, and hemorrhages and erosions follow within hours. In most people the gastric mucosa adapt over time, but studies show that 60-100% of patients on NSAIDs for 1 to 2 weeks develop submucosal hemorrhage, superficial erosions, erythema (inflammation of mucous membranes), or blood in the stool. Moreover, NSAID toxicity extends to the small intestine and large bowel, as manifested in silent ulcerations, colitis-like conditions, and aggravation of inflammatory bowel disease.



    Doses of aspirin as low as 30 mg suppress the production of protective prostaglandins in the gastric mucosa. In addition, aspirin's direct contact with the gastrointestinal tract interferes with the hydrophobic "non-wettable" properties that protect the underlying epithelium from gastric acid and other toxic substances. This characteristic seems to be attributable to an extracellular lining of phospholipids, which are synthesized in surface mucus cells of the stomach. Aspirin and other NSAIDs can rapidly transform the gastric mucosa from a non-wettable to a wettable state, thereby increasing the tissue's susceptibility to the corrosive actions of gastric acid.



    A study on experimentally induced gastric ulcers in rats (Dunjic BS, et al., 1993) showed that mucosal lesions were significantly reduced by a single dose of PPC given before or after the injury factor, which in this study was ethanol or an NSAID.



    A recent clinical trial compared the GI effects of aspirin to those of aspirin complexed with PPC (Anand BS et al., 1999). Sixteen healthy subjects were given either ten doses of aspirin or ten doses of the aspirin/PPC complex over a 72 hour period. After a "washout" period, subjects were switched over to the other medication for a 72 hour period.



    Researchers counted the number of gastroduodenal erosions in each subject. Those taking aspirin had an average of 8.75 erosions, while those taking the aspirin/PPC complex averaged only 2.81 erosions. The protective effect of PPC was most apparent in those who were most susceptible to aspirin injury, and did not interfere with the therapeutic activity of the aspirin.



    (Editors note: The cardio-protective benefits of aspirin are substantial. In addition to reducing abnormal arterial blood clot formation, aspirin suppresses a dangerous pro-inflammatory agent called C-reactive protein. The latest finding about heart attack risk shows that C-reactive protein causes a lethal inflammatory cascade on the inner arterial wall. What happens is that C-reactive protein induces atherosclerotic plaque on the arterial wall to burst open like popcorn, blocking a coronary artery and causing a heart attack. Aspirin specifically suppresses C-reactive protein. Now that PPC supplements are available, taking low-dose aspirin can be made a lot safer for those who take it as a preventive.)



    Cholesterol and angina reduction

    PPC's beneficial effects on blood lipoproteins have been demonstrated in a series of animal and human studies. A clinical trial conducted in St. Petersburg, Russia, (Klimov AN et al., 1995) compared PPC to niacin in angina patients with a hereditary elevation of cholesterol and triglycerides. Niacin is considered a standard treatment for this condition, but adverse effects are fairly common. These include flushing, skin dryness and itching, GI disturbances, elevation of liver enzymes, decline in glucose tolerance, and reduced urinary excretion of uric acid.



    In this study, 100 patients were randomly assigned to receive either PPC or niacin for six months. Patients in both groups were put on a low-fat cholesterol free diet, and any lipid-lowering medications they had been taking were discontinued four weeks before the start of the trial. For the first two weeks of the trial, PPC was given intravenously (500 mg/day); for the remaining five and a half months, patients took 600 mg of PPC in capsules three times a day.



    Both medications reduced the frequency of angina attacks, from 2.3 per week to 0.9 in the niacin group, and from 3.8 to 0.9 in the PPC group. Eight patients (16%) in the niacin group dropped out due to adverse effects of the medication, while the patients in the PPC group were entirely free of side effects. Only the PPC group showed a significant improvement in exercise tolerance. PPC significantly reduced oxidation of apoB lipoprotein, while niacin did not. The two medications improved the overall lipoprotein profile of the patients to a similar extent. PPC lowered total and LDL cholesterol by about 15%, and triglycerides by 32%.



    PPC also raised levels of the "good" HDL cholesterol by 10%. It is fortunate that the researchers looked beneath the surface of this modest increase, where they discovered a fascinating phenomenon.



    HDL and longevity

    It is well known that the most protective subfraction of HDL cholesterol is the one with the largest particles, known as HDL2b. When rhesus monkeys are placed on a calorie restricted diet to slow the aging process, their HDL2b levels increase significantly (Verdery RB et al., 1997). A study of centenarian women provided dramatic evidence of the cardioprotective importance of this subfraction (Barbagallo CM et al., 1998). Lipoprotein profiles of the centenarians were compared to those of healthy middle-aged and elderly women of the same weight. There were no significant differences found between the centenarians and the younger women in the battery of tests, which included plasma lipids, apolipoprotein, and Lp(a)-except in HDL2b and HDL3a levels. While the total HDL levels were about the same, HDL2b levels were significantly increased in the centenarians, and HDL3a levels were significantly decreased, compared to the other groups. The researchers call for further study of the distribution of HDL subfractions as a possible marker of longevity.



    Such a major shift in the distribution of HDL subfractions-from HDL3a to HDL2b-also occurred in the PPC group of the Russian study, but not in the niacin group. Thus, while total HDL levels rose modestly after PPC supplementation, the desirable HDL2b subfraction rose preferentially due to a shift from the 2a and 3a subfractions to the highly antiatherogenic 2b subfraction. Thus PPC may exert an anti-aging effect on the cardiovascular system, a prospect meriting further research.



    High serum lipids are common in diabetic patients (approx. in 50%), and the incidence of coronary heart disease is high. In a double-blind study on the lipoprotein profile in diabetic patients (Kirsten R et al., 1994), 30 non-insulin-dependent diabetics with secondary hyperlipidemia received 2.7 g PPC or placebo daily over a 2-month period. LDL-cholesterol and triglyceride levels decreased significantly when compared with the placebo group, and HDL cholesterol levels increased (see table). In the control group the values did not change throughout the trial.



    Moderate alcohol intake has been shown to improve the lipoprotein profile, and especially to raise HDL cholesterol levels. A study on rats shows that PPC preserves the HDL elevating effect of alcohol, while decreasing LDL and VLDL cholesterol levels after eating (Navder KP et al., 1997).



    However, higher levels of alcohol consumption are toxic to the liver, and increase oxidation of LDL cholesterol. New research on baboons shows that PPC markedly reduces alcohol-induced oxidation of LDL, thus helping to protect against one of the mechanisms that promotes atherosclerosis in heavy drinkers (Navder KP et al., 1999). At the same time, PPC helps protect the liver from alcohol toxicity.



    Fatty liver

    The liver is the largest organ of the body, responsible for metabolizing the food we eat (breaking it down into useful parts) and protecting us from the damaging effects of the numerous toxic compounds that we are exposed to on a daily basis. But what protects the liver so that it can in turn protect the rest of the body? The liver is unfortunately susceptible to toxicity itself, and to an insidious condition called steatosis thought to be a precursor to many serious liver diseases. Steatosis, also called fatty liver, is a common finding in human liver biopsies. It is a condition in which fat has accumulated within liver cells (hepatocytes) without causing any specific symptoms. As we shall discuss, PPC may help correct steatosis.



    Fatty liver as a longstanding chronic condition can occur in association with a wide range of diseases, toxins and drugs, although in clinical practice, the majority of cases are due to alcohol excess, diabetes and obesity. Much less common are occurrences of acute fatty liver during pregnancy and as a response to administration of tetracyclines, acetaminophen and other drugs and toxins.



    Fatty liver had long been believed to be a benign reversible condition. Careful clinical studies, however, demonstrate that fatty liver of either alcoholic or non-alcoholic origin can lead to inflammation, cell death and fibrosis (steatohepatitis), and eventually even cirrhosis. Cirrhosis is the irreversible end result of fibrous scarring, a response of the liver to a variety of long-standing inflammatory, toxic, metabolic and congestive damage.



    Alcohol is by far the commonest cause both of steatosis and cirrhosis in the Western world. However, there is a considerable inter-individual difference in the degree of liver damage produced by excessive alcohol intake. There seem to be no clear correlations between the incidence and severity of fatty liver and either the amount, type or duration of alcohol abuse. It has been unclear why in some individuals steatosis, whatever its etiology, never progresses to steatohepatitis and cirrhosis.



    A growing body of evidence suggests that the oxidation of fat in the liver leads to the development of liver damage, and free radicals have been demonstrated to play an important role in the hepatotoxic effect of many substances. The oxidation of fats takes place through a chain reaction called lipid peroxidation that impairs the anatomical and functional integrity of membranes and creates new toxic substances that further extend the damage. PPC's antioxidant action may help explain its effectiveness in treating fatty liver, as demonstrated by a study carried out in the Czech Republic (Horejsova M and Urban J, 1994).



    This Czech study of 28 women with steatosis of various origins showed PPC to be a highly effective therapy for fatty liver. The women were given PPC along with unsaturated fatty acids and low-dose B vitamins and vitamin E. After six months, ultrasound examinations revealed that eight of the women were free of apparent steatosis, 13 had improved, while the remaining seven showed no change. Abnormal enlargement of the liver (hepatomegaly) was significantly reduced, and the working tissue of the liver (parenchyma) became homogeneous in 10 of the 11 cases where it had been abnormal.



    Lab tests showed highly significant declines in all of the liver enzyme levels measured (ALT, AST, GMT). There were also significant declines in bilirubin, cholesterol and triglycerides. Overall, 54% of the patients in the study improved in all parameters studied, as determined by ultrasound assessment, lab tests and subjective evaluation. Forty-three percent showed improvement in lab tests and subjective evaluation, and only 3.6% did not show any objective improvement.



    Fibrosis, cirrhosis and alcohol

    A characteristic feature of liver disease, regardless of its cause, is the increased deposition of collagen, the connective tissue protein. This increased collagen accumulation could result from enhanced collagen biosynthesis and/or decreased collagen breakdown. PPC appears to increase collagen breakdown by stimulating collagenase activity in hepatic stellate cells preventing the development of fibrosis and cirrhosis (Li J et al., 1992). Several studies have focused on PPC and its effect on collagen and fibrosis.



    A baboon study (Lieber CS et al., 1994) confirmed earlier results (Lieber CS et al., 1990) showing that in the baboon, feeding of ethanol (a form of alcohol) results in hepatic fibrosis and cirrhosis even when associated with an adequate diet. This effect could be prevented by supplementing the diet with a 94-96% pure PPC preparation. None of the eight animals fed alcohol with PPC for up to 6.5 years had progression to fibrosis or cirrhosis as had 10 of 12 unsupplemented baboons, a highly significant difference. Another study (Ma X et al., 1996) revealed that PPC reduces hepatic fibrosis induced by either carbon tetrachloride or human albumin in rats, and that PPC not only prevents the development of fibrosis but accelerates the regression of pre-existing fibrosis. The study further suggested that the protective effect exerted by PPC against fibrosis is due, at least in part to increased collagen breakdown.



    One of the ways PPC helps prevent liver damage from alcohol is by inhibiting an enzyme known as CYP 2E1. Chronic alcohol consumption raises levels of this enzyme, which is involved in the metabolism of alcohol. This leads to oxidative stress and acetaldehyde production, which stresses the antioxidant defense system and depletes glutathione. CYP 2E1 also furthers the production of toxic metabolites from common drugs such as acetaminophen and promotes carcinogenesis. CYP 2E1 inhibitors protect the liver from alcohol-induced damage, but drugs tested for this purpose have been too toxic for practical use. However it has recently been discovered that PPC significantly inhibits CYP 2E1 activity (Lieber CS, 1999; Aleynik MK et al., 1999), providing a potential nontoxic solution to this problem.



    Antioxidant effects

    As we have seen, a key mechanism of PPC action is its antioxidant effect. Despite its rich content of polyunsaturated linoleic acid, PPC has been shown to effectively reduce oxidative stress caused by alcohol in the liver and pancreas, as well as in LDL cholesterol.



    Newly published research (Aleynik SI, Leo MA, Takeshige U et al., 1999) identifies the constituent of PPC primarily responsible for its antioxidant effect. This constituent, DLPC, comprises 40-52% of PPC. The researchers found that the "remarkable" antioxidant effect of PPC on oxidative stress induced in hepatoma cells by arachidonic acid could be accounted for by the DLPC contained in it.



    DLPC appears to be primarily responsible for many of the protective actions of PPC on the liver and pancreas. A new study demonstrates that DLPC stimulates the Kupffer cells of the liver to decrease production of the hepatotoxic tumor necrosis factor-a, while increasing production of the hepatoprotective interleukin-1b (Oneta CM et al., 1999). DLPC also appears to decrease activation of collagen-producing stellate cells in the liver, and to increase collagenase activity and thus collagen breakdown, asdiscussed above.



    The benefits of protection

    Modern living unfortunately involves daily exposure to substances that are toxic to our bodies, which can impose heavy stresses on the vital organs we have discussed. Therefore it is logical to think that all of us can benefit from some kind of support in maintaining the vitality of these organs. In particular, individuals with a substantial alcohol consumption, with obesity, diabetes or with high exposure to NSAIDs or environmental toxins have an even greater reason to take protective measures because of the documented risk of developing serious pathologies.



    Knowing that conventional medicine has very little to offer in the prevention or early treatment of the disorders we have discussed, it seems wise to remember that prevention is the best cure. We are fortunate today to have access to a natural protective remedy that is safe, effective and without significant side effects.



    And it is good to know that protection of the liver, pancreas and stomach is beneficial not only for these vital organs themselves, but for the overall health and vitality of our body.



    Obesity and Steatohepatitis

    Among the causes for non-alcoholic steatohepatitis (NASH), obesity is considered to be the most common. There is evidence to suggest that liver disease actually can be considered a complication of obesity. No major prospective longitudinal studies of NASH have been carried out. It seems, however, that the risk of progression to cirrhosis is generally low for non-obese individuals but significant among obese individuals. There is no predictable correlation between symptoms (or lack of them), abnormality of liver function tests and severity of liver tissue damage.



    In a study of 50 unselected, obese (21-130% above ideal body weight) subjects admitted to the hospital for weight reduction, Braillon et al (1985) found that 10% had normal livers, 48% fatty livers, 26% steatohepatitis, 8% fibrosis and 8% cirrhosis.



    Interestingly, it has been observed among patients with fatty liver related to obesity, that rapid weight loss caused by dieting and intestinal bypass surgery increase the risk for developing steatotohepatitis. The resulting increase in the concentration of fatty acids and/or ketones within the liver severely augments the generation of free radicals (Day CP et al.: 1994).



    A study by Yang et al (1997) indicates that obesity also increases susceptibility to endotoxin-mediated liver injury. Endotoxins are cell wall components produced by intestinal gram-negative bacteria, thought to play a role in liver injury induced by alcohol and other hepatotoxins. Under normal conditions they are absorbed into the portal venous circulation and detoxified in the liver. Hepatic dysfunction will interfere with this clearing mechanism and amplify the negative activities of endotoxin, such as lipid peroxidation, reduced detoxification by the cytochrome P-450 enzymes, and impairment of the immune system.



    Berson et al., 1998 summarizes the insights from the new research on the mechanisms of steatohepatitis well: Its development requires a double hit, the first producing steatosis, the second a source of oxidative stress capable of initiating significant lipid peroxidation. This concept provides a rationale for both the treatment and prevention of disease progression in steatosis of alcoholic and non-alcoholic causes. Management strategies should ideally be directed at reducing the severity of steatosis and at avoiding and removing the triggers of inflammation and fibrosis. Specific treatment modalities for at-risk individuals might include sensible weight reduction, cessation of exposure to toxins and treatment with antioxidants and inhibitors of peroxisomal b-oxidation.



    PPC in hepatitis

    PPC has been found to decrease serum aminotransferases in experimental hepatitis. In 1998, Niederau et al. conducted a multi-center randomized, placebo-controlled clinical study evaluating the effects of PPC in combination with interferon alpha (IFN) in patients suffering from Hepatitis B and C. IFN is the standard treatment for these diseases, however only 50% of patients with Hepatitis B and 20-30% of patients with Hepatitis C respond to this antiviral drug with long-term normalization of serum aminotransferases. Among patients with hepatitis C that do respond to IFN while under treatment, there is at least a 50% relapse rate. Evidently there is a need for more effective treatment.



    In this study 176 patients completed the protocol. All patients were given the same amount of interferon during the 24-week test period. In addition patients were randomly assigned to receive either 1.8 grams per day of PPC or placebo for the same 24 weeks. A biochemical response to therapy was defined as minimum 50% reduction of ALT compared to pre-treatment values.



    The results show that PPC increased the response rate to IFN in chronic viral hepatitis C (71% versus 51 % in the placebo group). Prolonged PPC therapy given to responders 24 weeks beyond the cessation of interferon therapy tended to increase the rate of sustained responses in patients with hepatitis C (41% versus 15%). Hepatitis B patients, however, did not have an improved biochemical response to interferon from PPC. The reason why PPC showed beneficial effect in hepatitis C and not in hepatitis B is not clear and will be further investigated.



    This study suggests that PPC can be a valuable adjunct to IFN treatment of Hepatitis C as well as be of beneficial use after cessation of IFN therapy in order to increase the chance of sustained response to therapy.



    Alcohol and the pancreas

    The pancreas is essential to both digestion and glucose regulation. It secretes digestive enzymes into the duodenum for protein, carbohydrate and fat digestion, and produces large amounts of sodium bicarbonate (as found in baking soda) to neutralize stomach acid in the duodenum. The islets of the pancreas produce insulin and the related hormones glucagon and somatostatin.



    Pancreatitis-inflammation of the pancreas-is caused primarily by overconsumption of alcohol in about 80% of cases. Ethanol causes severe oxidative stress in the pancreas, probably due to increased production of free radicals and depletion of glutathione and other antioxidants. In particular, both alcohol intake and pancreatitis are associated with rises in the CYP 2E1 enzyme in the pancreas.



    The research group that investigated the correction of alcohol-induced liver damage by PPC has recently published research demonstrating the same protective effect in the pancreas (Aleynik SI, Leo MA, Aleynik MK et al., 1999). When rats were given ethanol, markers of oxidative stress in the pancreas rose sharply. However PPC given along with the ethanol prevented this rise, and almost completely alleviated the depletion of pancreatic glutathione caused by ethanol.



    The protective effect of PPC on oxidative stress in the pancreas was even more pronounced than these researchers had observed in the liver of baboons fed alcohol. PPC may protect the pancreas from other causes of oxidative stress; as the authors state, PPC "could provide innocuous but effective and orally active antioxidant therapy, not only as shown before for liver injury, but also, as shown here, for early pancreatic changes."





    References

    Aleynik MK et al.: Polyenylphosphatidylcholine opposes the increase of cytochrome P-4502E1 by ethanol and corrects its iron-induced decrease. Alcohol Clin Exp Res 23(1):96-100, 1999



    Aleynik SI, Leo MA, Aleynik MK et al.: Alcohol-induced pancreatic oxidative stress: Protection by phospholipid repletion. Free Radic Biol Med 26 (5/6): 609-619, 1999



    Aleynik SI, Leo MA, Takeshige U et al.: Dilinoleoylphosphatidylcholine is the active antioxidant of polyenylphosphatidylcholine. J Investig Med 47(9):507-12, 1999



    Anand BS et al.: Phospholipid association reduces the gastric mucosal toxicity of aspirin in human subjects. Am J Gastroenterol 94(7):1818-22, 1999



    Barbagallo CM et al.: Lipoprotein profile and high-density lipoproteins: subfractions distribution in centenarians. Gerontology 44(2):106-10, 1998



    Berson A et al.: Steatohepatitis-inducing drugs cause mitochondrial dysfunction and lipid peroxidation in rat hepatocytes. Gastroenterology 114(4):764-74, 1998



    Biagi PL et al.: The effect of dietary polyenylphosphatidylcholine on microsomal delta-6-desaturase activity, fatty acid composition, and microviscosity in rat liver under oxidative stress. J Nutr Biochem 4: 690-94, 1993



    Braillon A et al.: Liver in obesity. Gut 26(2): 133-39, 1985



    Day CP et al.: The biochemistry of alcohol-induced fatty liver. Biochim Biophys Acta 1215: 33-48, 1994



    Dunjic BS et al.: Gastroprotective capability of exogenous phosphatidylcholine in experimentally induced chronic ulcers in rats. Scand J Gastroenterol; 28: 89-94, 1993



    Fabia R et al.: Effects of phosphatidylcholine on acetic acid-induced colitis in the rat. Digestion 53: 35-44, 1992



    Galli C et al.: Oral polyunsaturated phosphatidylcholine reduces platelet lipid and cholesterol contents in healthy volunteers. Lipids 20(9):561-6, 1985



    Holecek M et al.: Effect of polyunsaturated phosphatidylcholine on liver regeneration onset after hepatectomy in the rat. Arzneimittelforschung 42(3): 337-39, 1992



    Horejsova M and Urban J: The effect of polyene phosphatidylcholine (Essentiale forte) in the treatment of liver steatosis and ultrasound findings--preliminary study. Cas Lek Cesk 133(12):366-9, 1994



    James OFW et al.: Non-alcoholic steatohepatitis (NASH): a disease of emerging identity and importance. J Hepatol 29: 495-501, 1998



    Kesaniemi YA et al.: Effects of dietary polyenylphosphatidylcholine on metabolism of cholesterol and triglycerides in hypertriglyceridemic patients. Am J Clin Nutr 43: 98-107, 1986



    Kirsten R et al.: Polyenylphosphatidylcholine improves the lipoprotein profile in diabetic patients. Int J Clin Pharmacol Ther 32(2): 53-6, 1994



    Klimov AN et al.: "Essential" phospholipids versus nicotinic acid in the treatment of patients with type Iib hyperlipoproteinemia and ischemic heart disease. Cardiovasc Drugs Ther 9(6):779-84, 1995



    Li J et al.: Polyunsaturated lecithin prevents acetaldehyde-mediated hepatic collagen accumulation by stimulating collagenase activity in cultured lipocytes. Hepatology 15(3): 373-381, 1992



    Lichtenberger LM et al.: Non-steroidal anti-inflammatory drugs (NSAIDs) associate with zwitterionic phospholipids: Insight into the mechanism and reversal of NSAID-induced gastrointestinal injury. Nature Medicine 1(2): 154-58, 1995



    Lieber CS et al.: Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin. Hepatology 12(6): 1390-98, 1990



    Lieber CS et al.: Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon. Gastroenterology 106: 152-159, 1994



    Lieber CS: Microsomal ethanol-oxidizing system (MEOS): the first 30 years (1968-1998)--a review. Alcohol Clin Exp Res 23(6):991-1007, 1999



    Ma X et al.: Polyenylphosphatidylcholine attenuates non-alcoholic hepatic fibrosis and accelerates its regression. J Hepatol 24: 604-613, 1996



    Navder KP et al.: Polyenylphosphatidylcholine decreases alcoholic hyperlipemia without affecting the alcohol-induced rise of HDL-cholesterol. Life Sci 61(19): 1907-14, 1997



    Navder KP et al.: Oxidation of LDL in baboons is increased by alcohol and attenuated by polyenylphosphatidylcholine. J Lipid Res 40(6):983-7, 1999



    Niederau C et al.: Polyunsaturated phosphatidylcholine and interferon alpha for treatment of chronic hepatitis B and C: A multi-center, randomized, double-blind, placebo-controlled trial. Hepatogastroenterology 45: 797-804, 1998



    Oneta CM et al.: Dilinoleoylphosphatidylcholine selectively modulateslipopolysaccharide-induced Kupffer cell activation. J Lab Clin Med 134(5):466-70, 1999



    Raskin JB: Gastrointestinal effects of nonsteroidal anti-inflammatory therapy. Am J Med 106(5B), 1999



    Stoffel W et al.: Pleomorphic functions of highly unsaturated phospholipids in biological membranes and serum lipoproteins. Med Welt 29(4): 124-31, 1978



    Verdery RB et al.: Caloric restriction increases HDL2 levels in rhesus monkeys (Macaca mulatta). Am J Physiol 273(4 Pt 1):E714-9, 1997



    Wallace LA et al.: Personal exposures, indoor-outdoor relationships and breath levels of toxic air pollutants measured for 355 persons in New Jersey. EPA 0589, 1989



    Wang XD, Andersson R et al.: Phospholipids prevent enteric bacterial translocation in the early stage of experimental acute liver failure in the rat. Scand J Gastroenterol 29:1117-21, 1994



    Weltman MD et al.: Hepatic cytochrome P450 2E1 is increased in patients with nonalcoholic steatohepatitis. Hepatology 27(1): 128-133, 1998



    Wolfe MM et al.: Gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. NEJM 340(24):1888-99, 1999



    Yamada S et al.: Chronic ethanol consumption alters rat liver plasma membranes and potentiates release of alkaline phosphatase. Gastroenterology 88(6): 1799-806, 1985



    Yang SQ et al.: Obesity increases sensitivity to endotoxin liver injury: Implications for the pathogenesis of steatohepatitis. Proc Natl Acad Sci USA 94: 2557-62, 1997

  4. #4
    Senior Member SteveSliwa's Avatar
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    PPC

    A Key Nutrient That Facilitates Crucial Cellular Processes



    By Bradley Bongiovanni, ND



    Polyenylphosphatidylcholine (PPC), also referred to as phosphatidylcholine, is a fat-soluble nutrient with many health-promoting benefits. These in-clude protecting the liver, sustaining cardiovascular health, and supporting nervous system and gastrointestinal function. Dietary sources of PPC include soybeans, liver, oatmeal, cabbage, cauliflower, egg yolks, meat, and vegetables.



    PPC is an essential component in each of the body’s cell membranes, the dynamic surfaces on which cells carry out many of their biochemical activities. PPC is a phospholipid rich in polyunsaturated fatty acids—particularly linoleic and linolenic acid—that provide fluidity, or flexibility, to the cell membrane, thus facilitating crucial cellular processes.



    Aiding Liver Function

    The liver is one of the body’s most metabolically active organs, and plays a crucial role in detoxifying chemicals, drugs, and hormones. Most metabolic reactions in the liver occur on cell membranes, and thus PPC is a particularly beneficial nutrient for liver health.



    PPC helps protect the liver against the effects of alcohol. In a study in mice, alcohol administration induced numerous changes, depleting the liver-supportive nutrients S-adenosyl-L-methionine (SAMe) and glutathione, as well as increasing lipid peroxidation, a marker of oxidative stress. PPC protected against these effects, restoring levels of SAMe and glutathione, and relieving oxidative stress in the liver.1



    In a study of baboons, PPC helped to prevent alcohol-induced cirrhosis. PPC also helped to prevent two common detrimental effects of alcohol: the formation of fatty liver and the elevation of blood lipid levels.2 In a human study, investigators examined the effects of PPC on heavy alcohol drinkers. While PPC treatment for two years did not affect the progression of liver fibrosis, it did promote favorable changes in blood levels of bilirubin (a liver-produced waste product) and liver transaminases (enzymes that are elevated by liver damage.)3





    Fighting Hepatitis

    In patients with acute viral hepatitis, six weeks of supplementation with PPC helped to speed recovery, though PPC did not hasten recovery from hepatitis secondary to septicemia.4 PPC also appears to benefit patients with chronic hepatitis. In one double-blind study of patients with chronic hepatitis who tested negative for hepatitis B, PPC reduced histological evidence of disease activity. The researchers concluded that PPC may be a useful adjunctive therapy in patients with chronic hepatitis that is inadequately controlled by conventional therapy.5





    Another study examined PPC’s effects when combined with the anti-viral medication interferon on patients with two forms of chronic hepatitis, hepatitis B and hepatitis C. Seventy-one percent of the patients treated with PPC and interferon experienced a biochemical response to therapy (as measured by a 50% or greater decrease in the liver enzyme serum alanine aminotransferase) compared to 56% of the patients treated with interferon alone. PPC was especially effective in increasing the response rate to treatment in hepatitis C patients. The researchers noted that PPC is well tolerated and may be combined with interferon therapy for chronic hepatitis.6



    Improving Heart Health and Brain Function

    PPC’s role in cardiovascular health and cholesterol management has been the subject of extensive study. In combination with diet modifications and regular exercise, PPC can help restore cholesterol and triglycerides to healthier levels. More specifically, PPC may lower coronary risk by helping reduce serum LDL (low-density lipoprotein) levels,7 reducing serum triglycerides,8-10 normalizing platelet function, and favorably influencing plaque volume.11,12 PPC has also been show to decrease the incidence of atherosclerosis-related symptoms such as angina, thus having a powerful effect clinically as well as biochemically.7



    One of PPC’s most important functions is assisting in the formation of acetylcholine, a vital chemical messenger used by cells in the hippocampus and septum, the memory centers of the brain. The choline used by brain neurons mainly comes from dietary sources such as PPC and lecithin. PPC is the preferred dietary source of choline because it is a better delivery form and does not cause unpleasant gastrointestinal side effects associated with choline.13



    PPC may be especially important in advanced age because the brains of older adults take in less choline than those of younger adults.14 PPC may improve some cognitive changes associated with aging. Some evidence suggests that boosting brain levels of choline in older adults can slow or moderately reverse memory deterioration.15,16



    Gastrointestinal and Exercise Benefits

    The stomach’s mucosal tissue lining helps protect it from the high concentrations of acid and digestive enzymes contained within. Without this protection, the stomach wall would be digested just like the food contained within it. PPC is integrated in the gastric lining and protects the stomach from developing ulcerations related to the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen.17 A study of rats suggested that PPC may protect against stress-induced stomach ulcers.18 By helping to heal gastric erosions, PPC may be useful even after an ulcer is already present.19





    Intense or prolonged exercise requires sustained use of the muscle contraction pathways, and may deplete the body’s choline levels. In a group of runners, plasma choline levels dropped by 40% following completion of a marathon. Supplementation with acetylcholine precursors such as PPC may help prevent diminished endurance or performance associated with strenuous exercise.20 Emerging studies indicate that PPC supplementation can help maintain or slightly elevate plasma choline levels during exercise. A plentiful pool of available choline may help enhance athletic performance by assisting in the formation of acetylcholine, which helps relay muscle contraction signals.21



    Dosage and Safety Concerns

    A therapeutic dose of PPC ranges from 1.8 to 2.7 grams per day. PPC has no known contraindications, side effects, or interactions with medications. It also has an excellent safety profile and is generally well tolerated. The most common reported side effect is gas, which is most strongly associated with very high doses, typically 15 grams or more per day. PPC is generally considered safe in pregnancy, and choline requirements appear to be especially high in pregnant and lactating women. Pregnant and lactating women should always consult with their physicians before using PPC or other nutritional supplements.



    References

    1. Aleynik SI, Lieber CS. Polyenylphos-phatidylcholine corrects the alcohol-induced hepatic oxidative stress by restoring s-adenosylmethionine. Alcohol Alcohol. 2003 May;38(3):208-12.



    2. Navder KP, Baraona E, Lieber CS. Polyenylphosphatidylcholine attenuates alcohol-induced fatty liver and hyperlipemia in rats. J Nutr. 1997 Sep;127(9):1800-6.



    3. Lieber CS, Weiss DG, Groszmann R, Paronetto F, Schenker S. II. Veterans Affairs Cooperative Study of polyenylphosphatidylcholine in alcoholic liver disease. Alcohol Clin Exp Res. 2003 Nov;27(11):1765-72.



    4. Atoba MA, Olubuyide IO. The effects of essential phospholipid choline in HBs-Ag negative acute hepatitis. West Afr J Med. 1989 Oct;8(4):284-7.



    5. Jenkins PJ, Portmann BP, Eddleston AL, Williams R. Use of polyunsaturated phosphatidyl choline in HBsAg negative chronic active hepatitis: results of prospective double-blind controlled trial. Liver. 1982 Jun;2(2):77-81.



    6. Niederau C, Strohmeyer G, Heintges T, Peter K, Gopfert E. Polyunsaturated phosphatidyl-choline and interferon alpha for treatment of chronic hepatitis B and C: a multi-center, randomized, double-blind, placebo-controlled trial. Leich Study Group. Hepatogastroenterology. 1998 May;45(21):797-804.



    7. Klimov AN, Konstantinov VO, Lipovetsky BM, et al. “Essential” phospholipids versus nicotinic acid in the treatment of patients with type IIb hyperlipoproteinemia and ischemic heart disease. Cardiovasc Drugs Ther. 1995 Dec;9(6):779-84.



    8. Dobiasova M, Stribrna J, Matousovic K. Effect of polyenoic phospholipid therapy on lecithin cholesterol acyltransferase activity in the human serum. Physiol Bohemoslov. 1988;37(2):165-72.



    9. Navder KP, Baraona E, Lieber CS. Polyenylphosphatidylcholine decreases alcoholic hyperlipemia without affecting the alcohol-induced rise of HDL-cholesterol. Life Sci. 1997;61(19):1907-14.



    10. Kirsten R, Heintz B, Nelson K, et al. Polyenylphosphatidylcholine improves the lipoprotein profile in diabetic patients. Int J Clin Pharmacol Ther. 1994 Feb;32(2):53-6.



    11. Gurevich VS, Bondarenko BB, Mikhailova IA, et al. Evidence of combined therapy of dyslipoproteinemia by HMG-CoA reductase inhibitors and “essential” phospholipids. Clin Ter. 1993 Apr;142(4):329-34.



    12. Khashimov K, Okur F, Orekhov AN, Kurdanov K, Tertov V. [Effect of lipostabil on cholesterol levels in atherosclerotic plaques of the human aorta and the aggregative capacity of thrombocytes (in vitro study)]. Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR. 1988;11(1):95-8.



    13. Hendler SS, Rorvik D, eds. PDR for Nutritional Supplements. 1st ed. Montvale, NJ: Medical Economics Company, Inc: 2001:351-6.



    14. Cohen BM, Renshaw PF, Stoll AL, et al. Decreased brain choline uptake in older adults. An in vivo proton magnetic resonance spectroscopy study. JAMA. 1995 Sep 20;274(11):902-7.



    15. de la ME. Efficacy of CDP-choline in the treatment of senile alterations in memory. Ann NY Acad Sci. 1991;640:233-6.



    16. Secades JJ, Frontera G. CDP-choline: pharmacological and clinical review. Methods Find Exp Clin Pharmacol. 1995 Oct;17 Suppl B1-54.



    17. 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 Pharmacol. 1985 Oct 29;117(1):35-42.



    18. Demirbilek S, Gurses I, Sezgin N, Karaman A, Gurbuz N. Protective effect of polyunsaturated phosphatidylcholine pretreatment on stress ulcer formation in rats. J Pediatric Surg. 2004 Jan;39(1):57-62.



    19. Anand BS, Romero JJ, Sanduja SK, Lichtenberger LM. Phopholipid association reduces the gastric mucosal toxicity of aspirin in human subjects. Am J Gastroenterol. 1999 Jul;94(7):1818-22.



    20. Conlay LA, Sabounjian LA, Wurtman RJ. Exercise and neuromodulators: choline and acetylcholine in marathon runners. Int J Sports Med. 1992 Oct;13 Suppl 1S141-2.



    21. Buchman AL, Awal M, Jenden D, Roch M, Kang SH. The effect of lecithin supplementation on plasma choline concentrations during a marathon. J Am Coll Nutr. 2000 Nov;19(6):768-70.

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    so , for what purposes is it reccomended
    Man on a mission

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    Quote Originally Posted by liorrh' post='445311' date='Dec 30 2007, 11:01 PM
    so , for what purposes is it reccomended


    Antiaging, liver health, brain health, working out etc.



    In a recent study performed by the University of Connecticut at Storrs, and published by Functional Foods and Nutraceuticals in September 2002, researchers examined the influence of PPC on body composition and muscle damage related to repeated resistance training. In a three-week, double blind, placebo-controlled study; nine male subjects took PPC supplements while doing resistance training. Researchers measured muscle damage (creatine, kinase, and malondialdehyde increases) for several days, and had two major discoveries. First, the group taking PPC had no muscle damage on the day after the first day of exercise whereas the placebo group had increased muscle damage lasting up to eight days. Second, the group taking PPC had a significant increase in lean body mass. The bottom line is, polyenylphosphatidylcholine had a favorable effect on lean body mass and recovery from resistance exercise and the effect may become more pronounced over time.

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    I dont have diabetes or liver problems... will it get me hyuge, ripped, help me to live 100000 years, make me super smart or sexy?
    Man on a mission

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    Quote Originally Posted by liorrh' post='445352' date='Dec 31 2007, 07:21 AM
    I dont have diabetes or liver problems... will it get me hyuge, ripped, help me to live 100000 years, make me super smart or sexy?


    Prevention is the best cure.



    I don't think anything can help with those indications for you.

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    WOULD this be a better liver protectant than NAC and/or milk thistle for use while taking methylated oral steroids?
    <div class='quotetop'>QUOTE (Dr. Lats @ Mar 25 2008, 11:43 PM) <{POST_SNAPBACK}></div><div class='quotemain'>more full flaccid penis</div>

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    Quote Originally Posted by SweetDaddyPatty' post='445742' date='Jan 3 2008, 07:00 AM
    WOULD this be a better liver protectant than NAC and/or milk thistle for use while taking methylated oral steroids?


    Yes.

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    Thats an interesting compound;



    I take piracetam during the school year, but I've never tried using it with a choline supplement. ScottL mentions its "not a first tier supplement," so should I invest in phoscol or just go with a bulk choline bitartrate product?



    I imagine with PPC i might be killing two (or more) birds with one stone here.

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    Quote Originally Posted by enemy' post='445831' date='Jan 3 2008, 02:57 PM
    Thats an interesting compound;



    I take piracetam during the school year, but I've never tried using it with a choline supplement. ScottL mentions its "not a first tier supplement," so should I invest in phoscol or just go with a bulk choline bitartrate product?



    I imagine with PPC i might be killing two (or more) birds with one stone here.


    PPC i consider one of the most important antiaging supplements you can take. Very few compounds can reverse/protect against age related cell membrane changes (increased cholesterol/lipofuscin, reduced nutrient intake/phospholipids content in the membrane).





    Probably also a good idea for any steriod user.



    Clin Toxicol (Phila). 2007 Aug 30;:1-10

    Multivitamins and phospholipids complex protects the hepatic cells from androgenic-anabolic-steroids-induced toxicity.



    Pagonis TA, Koukoulis GN, Hadjichristodoulou CS, Toli PN, Angelopoulos NV. Department of Endocrinology, Thessaly University Medical School, Larissa, Greece.



    Introduction. Androgenic-anabolic-steroids (AAS)-induced hepatotoxicity typically occurs with C-17 alkylated oral agents abused by exercising individuals at clinically recommended doses. Injectable compounds appear to have the same risk for hepatotoxicity, but are applied in doses three to six times higher than clinically recommended. AAS users occasionally try to avoid the well-known hepatotoxic effects associated with the abuse of a multitude of AAS agents, by using the pharmaceutical agent compound N a phospholipid/vitamin preparation. Primary Objective. The investigation of the actual hepatoprotective effect of compound N against AAS-induced toxicity. Methodology. This was an observational cohort study of 320 athletes; 160 were AAS users and the other 160 were not abusing any substances. Of the 160 users, 44 were using AAS and compound N (group A), and 116 were using solely AAS (group . The 160 athletes abstaining from substances abuse acted as controls (group C). All athletes were tested for alterations in serum levels of hepatic enzymes. Enzyme levels before the study's onset and after the end of the 8-week AAS regimes were compared among the three groups, in order to delineate the hepatoprotective effect of compound N. Results. Prior to our research all groups showed normal values in all enzymes except creatine kinase (CK). After the 8-week period, CK levels were slightly lower in group A, but without variation in Groups B and C; gamma-Glutamyl Transferase (gammaGT) levels remained normal. Groups A and C had no elevations in any of the enzymes, except CK, while in group B all enzymes' values were elevated above the normal range. The only factor differentiating AAS users in group A from those in group B was the use of compound N, thus the results being suggestive of the compound's detoxification effect. The severity of AAS abuse was positively associated with the degree of changes (Delta values) in all measured enzymes except gammaGT and CK. Conclusions. Previous suggestions that serum hepatic enzyme elevations in exercising AAS abusers are connected to muscle fiber damage rather than the abuse itself, are contradicted by our results. Since all AAS abusing athletes were prone to exhibit elevations in enzymes' values, the mean values of group A were to be similar to those observed in group B, exceeding normal values. The group hepatic enzyme values of group B were significantly higher than the group C (control). Notably, group A did not have any statistically significant difference in the hepatic enzyme values compared to group C. The effect of exercise on these enzymes' elevations was ruled out by the comparability of training regimens and AAS toxicity was correlated to the severity of AAS abuse.

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    --Not a first tier supplement for health promotion.



    --I was wondering about it WRT orals, but I can't speak to the mechanism of oral's effects on the liver and the respective mechanisms of it vs NAC vs milk thistle. Perhaps Steve could explain why PPC is better than the others in offsetting the effects.



    --First tiers would be vitamin c, E, multi with trace minerals, and some form of lipoic acid, green tea, EPA/DHA. Perhaps grape seed extract.



    "PPC i consider one of the most important antiaging supplements you can take."



    I'm sure, but you could say that about 20 things you or I take. Probably depends on one's family history/priorities.



    Steve would it make your first tier if you could only include 5 or 10 things?



    2nd tier supps would include CoQ-10, varoius berry/pomegranite extracts/chocolate (or extracts), curcumin and GLA, I suppose you could throw it in this group (other might put joint supps, adaptogens, or antigoycation agents above it).
    <span style="color:#FF0000"><span style="font-family:Arial Black">THEORY=/REAL WORLD</span></span>

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    Quote Originally Posted by ScottL' post='445863' date='Jan 3 2008, 06:18 PM
    --Not a first tier supplement for health promotion.


    --I was wondering about it WRT orals, but I can't speak to the mechanism of oral's effects on the liver and the respective mechanisms of it vs NAC vs milk thistle. Perhaps Steve could explain why PPC is better than the others in offsetting the effects.


    Research speaks for itself.



    --First tiers would be vitamin c, E, multi with trace minerals, and some form of lipoic acid, green tea, EPA/DHA. Perhaps grape seed extract.


    Essential supplements I don't consider antiaging. R dihydrolipoic acid would be up on my list.



    "PPC i consider one of the most important antiaging supplements you can take."



    I'm sure, but you could say that about 20 things you or I take. Probably depends on one's family history/priorities.


    Cell membrane aging effects everyone this is something everyone should take if they want to protect against it.



    Steve would it make your first tier if you could only include 5 or 10 things?


    For antaging supplements yes. You can't leave out a major aspect of cellular aging.



    2nd tier supps would include CoQ-10, varoius berry/pomegranite extracts/chocolate (or extracts), curcumin and GLA, I suppose you could throw it in this group (other might put joint supps, adaptogens, or antigoycation agents above it).


    Reduced CoQ10 has excellent antiaging effects. Antiglycation agents should be taken by anyone concerned about this aspect of aging.

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    Quote Originally Posted by SteveSliwa' post='445865' date='Jan 3 2008, 06:29 PM
    Research speaks for itself.


    I have not looked, but I assume you must have seen a head-to-head comparison to make that statement. Please cite the research comparing polyenylphosphatidylcholine with NAC and/or Milk Thistle extracts.

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    Quote Originally Posted by Zoalord' post='445872' date='Jan 3 2008, 07:04 PM
    I have not looked, but I assume you must have seen a head-to-head comparison to make that statement. Please cite the research comparing polyenylphosphatidylcholine with NAC and/or Milk Thistle extracts.


    You would have to understand the importance of how each of them work, how liver damage occurs, and the total research of the compounds in liver conditions.

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    OK Steve,



    I've seen your...full regimen. How about you list what you consider:



    --Essential supplements and



    --Important antiaging supplements everyone should take.



    The total list should be finite and shorter than your full regimen ;-)
    <span style="color:#FF0000"><span style="font-family:Arial Black">THEORY=/REAL WORLD</span></span>

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    Quote Originally Posted by ScottL' post='445894' date='Jan 3 2008, 08:31 PM
    OK Steve,



    I've seen your...full regimen. How about you list what you consider:



    --Essential supplements and



    --Important antiaging supplements everyone should take.



    The total list should be finite and shorter than your full regimen ;-)


    I don't have a regimen posted anywhere. Did you forget your coffee today?

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