If you have to take aspirin, or Motrin, if you take it along with lecithin you will drastically reduce your chances of gastrointestinal problems such as bleeding or ulceration. This is good information to pass along. I read about one of these studies in the NYT several years ago and don't know why the information isn't more widely known.
I see the first link below isn't working (I saved it a while back), but its contents are pasted below the link.
uth.tmc.edu
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Lenard M. Licthenberger, Ph.D. (Copyright 1999, UT-Houston Health Science Center)
Lenard M. Lichtenberger, Ph.D., professor of integrative biology, pharmacology and physiology in the UT-Houston Medical School, has been awarded a grant from the Small Business Innovation Research (SBIR) division of the National Institutes of Health to refine his research on producing non-toxic aspirin-like drugs.
Lichtenberger recently completed the first of his clinical trials from research that began in the early 1980s. He discovered that stomachs in both humans and animals have a tendency to create a phospholipid with water-repellant properties called a surfactant lipid. It is this molecule that causes pain and upset stomachs for many people who take aspirin and non-steroidal anti-inflammatories such as Motrin.
“More than one-half of those individuals taking aspirin and anti-inflammatory medicine complain of upper gastrointestinal problems,” says Lichtenberger. “Often these complaints result in even greater medical problems, such as ulcers.”
Lichtenberger developed a method of combining aspirin and lecithin to change the water-repellant property and basically “tie up” the surfactant lipid. This ultimately reduces the toxicity of aspirin and non-steroidal drugs. Recent clinical trials, completed with B.S. Anand, M.D., a gastroenterologist with Baylor College of Medicine, compared patients taking two aspirin three times per day with patients taking the aspirin and lecithin combination during the same time frame. The researchers found there was one third of the amount of erosion in the stomach of those in the lecithin test group....
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lef.org
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.
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ncbi.nlm.nih.gov.
Am J Gastroenterol 1999 Jul;94(7):1818-22 Related Articles, Books, LinkOut
Phospholipid association reduces the gastric mucosal toxicity of aspirin in human subjects.
Anand BS, Romero JJ, Sanduja SK, Lichtenberger LM.
Department of Medicine, Baylor College of Medicine and Houston VA Medical Center, Texas, USA.
OBJECTIVE: In previous studies on rats, we have shown that aspirin (ASA)-induced injury to the gastric mucosa is markedly reduced or completely abolished if ASA is chemically associated with the phospholipid, phosphatidylcholine (PC). We have also shown that the protective effect of PC does not influence the ability of ASA to inhibit mucosal cyclooxygenase (COX) activity in the stomach and other tissues. We therefore sought to assess the effect of PC-associated ASA (ASA/PC) on the gastric mucosa of normal volunteers and to compare the results with the use of ASA alone. METHODS: Sixteen normal healthy subjects were administered ASA or ASA/PC in a randomized, double-blind, crossover study. The subjects received ASA in a dose of 650 mg three times a day for 3 days or an equivalent dose of ASA chemically associated with PC. Endoscopy was performed at baseline and again on the morning of day 4, after the subjects had taken the final dose of the test drug. On both occasions, antral biopsy specimens were obtained for the assessment of mucosal COX activity and prostaglandin concentration. RESULTS: The number (mean +/- SD) of gastric erosions seen with the ASA/PC formulation was significantly less than when ASA was used alone (8.7 +/- 10.7 vs 2.9 +/- 4.3; p < 0.025). A similar trend was seen in the duodenum but the difference was statistically not significant. The antral mucosal COX activity, as well as the level of prostaglandin 6-keto PGF1alpha, were reduced significantly (80-88%) and to a similar extent by both ASA and ASA/PC. CONCLUSIONS: The present study shows that acute aspirin-induced damage to the gastric mucosa can be reduced by chemically associating ASA with PC. The mechanism of mucosal protection provided by this compound is not related to any alteration in the ability of ASA to inhibit mucosal COX activity. We believe this protection is attributable to the maintenance of the defensive hydrophobic barrier of the gastric mucosa.
Publication Types:
Clinical trial
Randomized controlled trial
PMID: 10406241 [PubMed - indexed for MEDLINE]
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ncbi.nlm.nih.gov.
1: Gastroenterology 1996 Oct;111(4):990-5 Related Articles, Books, LinkOut
Comment in:
Gastroenterology. 1996 Oct;111(4):1145-7
Nonsteroidal anti-inflammatory drug and phospholipid prodrugs: combination therapy with antisecretory agents in rats.
Lichtenberger LM, Ulloa C, Romero JJ, Vanous AL, Illich PA, Dial EJ.
Department of Integrative Biology, University of Texas-Houston Medical School, Houston, USA.
BACKGROUND & AIMS: The gastrointestinal side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are reduced by antisecretory agents. The effects of combination therapy on the gastrointestinal toxicity and therapeutic activity of free and phospholipid-associated NSAIDs were investigated in rats. METHODS: Fasted rats, pretreated with either saline or an antisecretory dose of omeprazole, ranitidine, or cimetidine, were intragastrically administered saline, aspirin, or indomethacin. In ulcer models, gastric lesions in aspirin-treated rats and intestinal bleeding in indomethacin-treated rats were measured. For antipyretic and analgesic activity, rectal body temperature in febrile rats and the rats' pain sensitivity to pressure applied to an inflamed limb were measured, respectively. RESULTS: NSAID-induced gastrointestinal ulceration and bleeding were reduced in rats pretreated with antisecretory agents and abolished in rats administered phospholipid-associated NSAIDs in combination with inhibitors of acid secretion. The antipyretic and analgesic activity of both NSAIDs was attenuated in rats pretreated with an antisecretory agent. This pH-dependent block in therapeutic activity was overcome if the NSAID was preassociated with a phospholipid to enhance the drug's lipophilic characteristics. CONCLUSIONS: Combination therapy of antisecretory agents and NSAIDs, chemically associated with phospholipids, has distinct advantages with regard to both low gastrointestinal toxicity and restored therapeutic activity.
PMID: 8831593 [PubMed - indexed for MEDLINE]
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Another Lichtenberger PubMed reference, sort of related:
ncbi.nlm.nih.gov.
1: Biochem Pharmacol 2001 Mar 15;61(6):631-7 Related Articles, Books, LinkOut
Where is the evidence that cyclooxygenase inhibition is the primary cause of nonsteroidal anti-inflammatory drug (NSAID)-induced gastrointestinal injury? Topical injury revisited.
Lichtenberger LM.
Department of Integrative Biology and Pharmacology, The University of Texas Medical School at Houston, 77030, USA. Lenard.M.Lichtenberger@uth.tmc.edu
In this commentary, we take a critical look at the concept that the gastrointestinal (GI) side-effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are due to the ability of these drugs to inhibit cyclooxygenase-1 (COX-1) that is constitutively expressed in the GI mucosa. Indeed, development of the new "super aspirins," such as Celebrex and Vioxx, that selectively inhibit the inducible COX-2, expressed in areas of inflammation, is a direct outgrowth of this concept. We discuss evidence from both the laboratory and the clinic that appears to be inconsistent with the above concept, and cite a number of examples where the depletion of mucosal prostaglandin levels and the development of GI injury can be dissociated. Instead, we revisit the possibility that NSAID-induced GI side-effects are mostly due to the ability of these drugs to topically injure the GI mucosa. We devote the remainder of the commentary to presenting evidence from our and other laboratories that NSAIDs can directly attenuate the surface hydrophobic barrier of the GI mucosa due to their ability to bind to zwitterionic phospholipids, and that even systemically administered NSAIDs that are secreted into the bile may induce GI ulceration and/or bleeding due to phospholipid interactions and the development of topical mucosal injury.
Publication Types:
Review
Review, tutorial
PMID: 11266647 [PubMed - indexed for MEDLINE] ```````````````````````````````````
ncbi.nlm.nih.gov.
1: Gastroenterology 1990 Aug;99(2):311-26 Related Articles, Books, LinkOut
Gastric protective activity of mixtures of saturated polar and neutral lipids in rats.
Lichtenberger LM, Romero JJ, Kao YC, Dial EJ.
Department of Physiology and Cell Biology, University of Texas Medical School, Houston.
It has been shown that intragastric treatment of rats with a suspension of dipalmitoylphosphatidylcholine and tripalmitin at a 1:4 ratio (5 mg lipid/mL per rat) provided rats with highly efficaceous and consistent protection against a variety of ulcerogenic agents and conditions. The gastric protective activity of this mixture was of long duration (t 1/2 approximately 9 hours. In an attempt to understand the mechanism of protection, it was determined that the ulcerogen-induced reduction in gastric surface hydrophobicity was reversed in rats pretreated with the mixture. However, the lipid mixture did not affect the gastric emptying rate and maintained its cytoprotective activity in indomethacin-treated rats. These results indicate that the mixture's protective effect was not mediated by alterations in either gastrointestinal motility or the gastric accumulation of lipids or "cytoprotective" metabolites (prostaglandins). The mixture also appreciably reduced gastric lesion score in response to acid if one or both the lipids was substituted for a metabolically inert ether analogue, suggesting that lipid metabolism makes a negligible contribution to the protective response. Electron microscopic observation indicated that the predominent structure in the mixture is a microemulsion in which a dipalmitoylphosphatidylcholine monolayer encapsulates a tripalmitin core. Last, the improved gastric protective activity of the mixture in comparison to dipalmitoylphosphatidylcholine liposomes is discussed regarding marked differences in the physical structure of the two suspensions and the rate at which lipids in these states adsorb to a surface to enhance its hydrophobic properties.
PMID: 2365185 [PubMed - indexed for MEDLINE] |
