GERD, Esophageal Cancer, Richard Dawson’s Death And How To Naturally Prevent Reflux.

Esophageal cancer affecting the lower esophageus. Insets show the tumor in more detail both before and after placement of a stent. (Photo credit: Wikipedia)

Richard Dawson, of Family Feud, has died of esophageal cancer. Families everywhere take a moment of silence.

So attention is very momentarily on the causes and treatments for esophageal cancer. How often is a person with GERD (acid reflux) likely to get esophageal cancer? (Note: We do not know if Richard Dawson had GERD).

The risk is very low. Following 34,000 people with GERD, only 37 developed esophageal cancer after 7.4 years. That’s a risk of 0.11%. In patients with just GERD (and not other risk factors like alcoholism), out of 7,655 patients only one developed esophageal cancer. (Even less risk). You can read the article at GERD, Inflammation and Esophageal Cancer | dailyRx.

Since GERD is an extremely common disease, it makes sense to look at how we’re treating GERD in the U.S. If you look at GERD over the last century, it has gone from very rare to affecting 25% of the population at some time. (Drugs Today (Barc). 2004 Mar;40 Suppl A:3-8. ) If I did my math right, that means potentially 87,000 cases of esophageal cancer in the U.S. over an eight year period in which GERD played a factor.

Right now we treat GERD with acid reducing medication. So how well does that acid reducing medication reduce the risk of esophageal cancer?

When the esophagus is damaged by acid it begins to show changes in the cells, which may cause them to look more like the cells of the stomach. This change is called Barrett’s esophagus. All the acid reducing medications like proton pump inhibitors (PPIs) help reduce the symptoms of GERD that is associated with Barrett’s esophagus, but “Unfortunately, however, PPIs have no effect on the shortening of Barrett’s esophagus or in preventing the progression to dysplasia and adenocarcinoma.” (J Gastroenterol Hepatol. 2004 Sep;19 Suppl 3:S49-53.)

So even though the person feels like they’ve gotten better and has no symptoms, the changes that move them toward cancer are still taking place. We are, in effect, leaving this potential cancer untreated.

Is it untreatable? Maybe not.

An Indian herb may work as well. ”When compared, bark extract is equipotent to ranitidine but more potent than omeprazole in inhibiting pylorus-ligation induced acid secretion.” In English, that means the bark of this herb works as well as the acid reducing drugs at preventing acid. But wait, there’s more. “It offers gastroprotection against stress ulcer by significantly preventing adhered mucus and endogenous glutathione depletion. It prevents oxidative damage of the gastric mucosa by significantly blocking lipid peroxidation” In other words, it looks like it might undo some of the damage caused by the acid in addition to blocking the acid.

What is this possible treatment? Neem. (Bark or leaf, the seed is a potent insecticide). I wouldn’t take it (or anything) without consulting your doctor. If you can’t consult with your doctor about this sort of thing, it’s honestly time to get a new doctor.

Here’s the abstract:

Life Sci. 2002 Nov 1;71(24):2845-65.

Gastroprotective effect of Neem (Azadirachta indica) bark extract: possible involvement of H(+)-K(+)-ATPase inhibition and scavenging of hydroxyl radical.

Bandyopadhyay U, Biswas K, Chatterjee R, Bandyopadhyay D, Chattopadhyay I, Ganguly CK, Chakraborty T, Bhattacharya K, Banerjee RK.

Source

Department of Physiology, Indian Institute of Chemical Biology, 4, Raja S. C. Mullick road, Kolkata 700032, India.

Abstract

The antisecretory and antiulcer effects of aqueous extract of Neem (Azadirachta indica) bark have been studied along with its mechanism of action, standardisation and safety evaluation. The extract can dose dependently inhibit pylorus-ligation and drug (mercaptomethylimidazole)-induced acid secretion with ED(50) value of 2.7 and 2 mg Kg(-1) b.w. respectively. It is highly potent in dose-dependently blocking gastric ulcer induced by restraint-cold stress and indomethacin with ED(50) value of 1.5 and 1.25 mg Kg(-1) b.w. respectively. When compared, bark extract is equipotent to ranitidine but more potent than omeprazole in inhibiting pylorus-ligation induced acid secretion. In a stress ulcer model, it is more effective than ranitidine but almost equipotent to omeprazole. Bark extract inhibits H(+)-K(+)-ATPase activity in vitro in a concentration dependent manner similar to omeprazole. It offers gastroprotection against stress ulcer by significantly preventing adhered mucus and endogenous glutathione depletion. It prevents oxidative damage of the gastric mucosa by significantly blocking lipid peroxidation and by scavenging the endogenous hydroxyl radical ((z.rad;)OH)-the major causative factor for ulcer. The (z.rad;)OH-mediated oxidative damage of human gastric mucosal DNA is also protected by the extract in vitro. Bark extract is more effective than melatonin, vitamin E, desferrioxamine and alpha-phenyl N-tert butylnitrone, the known antioxidants having antiulcer effect. Standardisation of the bioactive extract by high pressure liquid chromatography indicates that peak 1 of the chromatogram coincides with the major bioactive compound, a phenolic glycoside, isolated from the extract. The pharmacological effects of the bark extract are attributed to a phenolic glycoside which is apparently homogeneous by HPLC and which represents 10% of the raw bark extract. A single dose of 1g of raw extract per kg b.w. (mice) given in one day and application of 0.6g raw extract per kg b.w. per day by oral route over 15 days to a cumulative dose of 9g per kg was well tolerated and was below the LD(50). It is also well tolerated by rats with no significant adverse effect. It is concluded that Neem bark extract has therapeutic potential for the control of gastric hyperacidity and ulcer.