Most recently, I have noted a very large push by pharmaceutical companies hyping products like Anatabine Citrate, with claims such as: Anatabine Citrate is a dietary supplement for anti-inflammatory support of the immune system. Since many disorders, like coronary artery disease, diabetes, asthma, Alzheimer’s, and rheumatoid arthritis, are caused by chronic low-level inflammation, Anatabine Citrate is a potential preventative treatment for these diseases.
Anatabine Citrate is a Nitrogenous compound isolated from Tobacco and cigarette smoke and touted as an alternative to anti-smoking remedies. Maybe you can now smoke yourself to health?
I am always amused by the push by large pharmaceutical companies to come up with new “wonderful†drugs to sell the public at very inflated prices, as alternative to actions that can be taken almost for free, achieving much the same results with very common agents! Recently, there has been a huge push by the world’s pharmaceutical companies to Patent Ayurvedic remedies in India that have been everywhere available at very low cost for centuries. The pharmaceutical companies want Patent rights to these compounds so that they can charge exorbitant fees for products that for centuries have been very low cost.
Anyway, my delayed point is… there actually seems to be a huge benefit to be obtained from serious anti-inflammatory compounds to reduce low-level chronic inflammation or tissue acidosis that seems to come inexorably and increasingly with advancing age. Inflammation or tissue acidosis contributes to every type of age-related deterioration.
There are a very large number of references to the Anti-inflammatory effects of Bicarbonates available by a simple Internet search, for examples:
http://www.ncbi.nlm.nih.gov/pubmed/313351
http://archinte.ama-assn.org/cgi/content/abstract/147/12/2093
http://gut.bmj.com/content/24/9/784.abstract
Why empty your wallet and break your bank to pay for extremely expensive “designer†pharmaceutical compounds to combat chronic acidic inflammation, when all you need are the common Bicarbonates, the most effective of which are found in Dr. Robert O Young's, Young pHorever pHour Salts. To learn more about pHour salts go to:
http://www.phmiracleliving.com/p-221-phour-salts.aspx
References:
Effects of antiinflammatory agents and prostaglandins on acid and bicarbonate secretions in the amphibian-isolated gastric mucosa.
Abstract
Effects of antiinflammatory agents and prostaglandins on H+ and HCO-3 secretions and electrical properties were investigated in the amphibian-isolated gastric mucosa. Gastric HCO-3 transport was studied in Rana temporaria fundus, in which H+ secretion had been inhibited with the histamine H2-receptor antagonists metiamide or cimetidine (10(-3) M), and in Necturus antrum, which secreted HCO-3 spontaneously. Hydrocortisone (100-500 microgram/ml) had no effect on H+ or HCO-3 secretion in the fundus. Indomethacin (10(-4) M) was a considerably more potent inhibitor of HCO-3 secretion than of H+ secretion in the fundus and also inhibited HCO-3 transport in the antrum. Fenclofenac (3 x 10(-3) M) almost abolished fundic HCO-3 transport and also depressed H+ secretion. There was a marked fall in transmucosal potential difference and a decrease in electrical resistance in fenclofenac-treated mucosae whereas indomethacin had less effect on electrical properties at the concentrations used here. The prostaglandins, E2, 16,16-dimethyl E2 and I2 all inhibited H+ secretion but only 16,16-dimethyl E2 stimulated HCO-3 secretion. The inhibitory action of indomethacin on HCO-3 secretion was prevented by co-administration of 16,16-dimethyl PGE2 (10(-6) M). It is proposed that the inhibitory action of nonsteroidal antiinflammatory drugs and the stimulatory action of some prostaglandins on HCO-3 secretion contributes to their ulcerogenic and anti-ulcer actions on the gastric mucosa.
- PMID:
- 313351
- [PubMed - indexed for MEDLINE]
- 2)
Recognition and Response
Arch Intern Med. 1987;147(12):2093-2100.
Abstract
• Gastropathy, recognized as gastric lesional disease ranging from erosions to actual ulcer craters, represents the most ubiquitous significant complication of common nonsteroidal anti-inflammatory drug (salicylate and nonsalicylate) use. Recently, this association has been established as distinct from classic peptic ulcer disease,which is primarily acidmediated, duodenal, and more prevalent in a younger, often male, population. Nonsteroidal anti-inflammatory drug gastropathy is usually antral/prepyloric disease, and research indicates it is mediated through blockade of cyclooxygenase with reduction in cytoprotective gastric prostaglandins. Theprevious literature has been confounded with short-term studies on healthy volunteers and animals that emphasize the resiliency of normal gastric adaptation to heal such gastropathy. Newer long-term studies in patients with arthritis undergoing anti-inflammatory therapy on a sustained basis indicate fatigue of normal adaptation,with persisting gastropathy leading to bleeding and even death. In addition, silent lesions are more common as symptomatology is not synchronous with lesional disease. Since endoscopy is an expensive, not always utilized procedure, it is important to identify the population most at risk for appropriate cytoprotectivemanagement as well as modification of the anti-inflammatory therapy program.
(Arch Intern Med 1987;147:2093-2100)
Author Affiliations
From the Arthritis Center Ltd/Arizona Institute, Phoenix.
Footnotes
Accepted for publication Aug 31, 1987.
Reprint requests to Arthritis Center Ltd/Arizona Institute, 3330 N Second St, Suite 601, Phoenix, AZ 85012 (Dr Roth).
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- Articles
Effects of non-steroidal anti-inflammatory drugs and prostaglandins on alkali secretion by rabbit gastric fundus in vitro
Abstract
The effects of non-steroidal anti-inflammatory drugs and prostaglandins E2 and F2α on the secretory and electrical activity of isolated rabbit fundic mucosa have been studied. Spontaneous acid secretion was inhibited by serosal side application of sodium thiocyanate (6×10−2M) and the resulting alkali secretion measured by pH stat tiration. Serosal side application of indomethacin (10−5M) or aspirin (3×10−3M) inhibited alkali secretion (0·55±0·06 to 0·12±0·06 μmol/cm2/h, n=6, p<0·01 and 0·28±0·06 to 0·11±0·03 μmol/cm2/h, n=7, p<0·02 respectively). Mucosal or serosal side prostaglandin E2 (10−5 to 10−10M) and F2α(10−4 to 10−10M) failed to alter the rate of alkalinisation but secretion was significantly increased by serosal side 16,16-dimethyl-prostaglandin E2 (10−6M) (0·90±0·20 to 1·50±0·30 μmol/cm2/h, n=6, p<0·01). Serosal side application of 10−6M prostaglandin E2 to fundic mucosae pretreated with either aspirin (5×10−3M) or indomethacin (10−5M), to reduce endogenous E2 formation, also failed to alter alkali secretion. Pretreatment of the mucosa with 16,16-dimethyl-E2 (10−6M) abolished the inhibitory effect of indomethacin (10−5M) on alkali secretion (n=6) but did not modify the secretory response to aspirin (3×10−3M) (fall in alkali secretion with aspirin = 81±11% and with aspirin plus 16,16-dimethyl-E2 = 72±10%, n=7). In the doses used, none of the prostaglandins or non-steroidal anti-inflammatory drugs altered transmucosal potential difference or electrical resistance. These results show that the damaging agents, aspirin and indomethacin, both inhibit gastric alkali secretion but that modes of action may differ. The observation that prostaglandins, E2 and F2α failed to increase alkali production suggests that their protective activity against a variety of damaging agents as shown by others, may be mediated by another mechanism.
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