This is true about Asians in Asia. The epidemiology is fascinating. Asian immigrants in the USA do not have the same incidence of gastric cancers, compared to Asians in East Asia proper.
Is it gut bacteria exposure? Alcohol consumption? Other foods, like spicy kimchi? Smoking? I have not looked into it beyond this. Interesting that Korean rates have remained, while rates of stomach cancers have declined in other Asian countries.
Man, when the Zantac stopped working for me I ate so much tums, I’m sure my bones are appreciably denser.
I’d take the cheapest and go from there. With light symptoms there’s statistically very little difference between the common drugs at equivalent doses.
Check out this oldish summary:
"In adults with GERD who have erosive esophagitis:
For complete relief of symptoms at 4 weeks, all PPIs are similarly effective when comparable doses were used.
For time to relief of heart burn, all PPIs are similarly effective.
For rate of healing at 4 and 8 weeks, no differences were found between omeprazole, lansoprazole, pantoprazole, or rabeprazole.
In moderate to severe disease, esomeprazole (40 mg) was more effective at healing esophagitis at 4 and 8 weeks than was either omeprazole (20 mg) or lansoprazole (30 mg).
For preventing relapse in adults with healed esophagitis, there was no difference between omeprazole, lansoprazole, and rabeprazole. "
I haven’t checked out those citations but the summary matches well with local guidelines that I trust.
One type of acid reflux drug associated with doubled incidence of stomach cancer
…you won’t believe which one! Doctors were stunned! [CLICK HERE]
tried prilosec many years ago when it went OTC at the recommendation of the doc as i had been getting by on the OTC zantac or tagament. i got this lovely abdominal rash so that ended that option quite early for me.
Esomeprazole has a much better side-effects profile than omeprazole. About half the side effects come from the unwanted R enantiomer, which has no proton-pump blocking activity. Isolating the S enantiomer gets rid of that half of the side effects without affecting the main effect at all.
Tums have a horrible rebound effect. Look for a magnesium-aluminium antacid instead, you won’t be gulping it nearly as often. In the US, Maalox liquid, or Gelusil (either formulation) are magnesium-aluminum.
I was on omeprazole for I think a month after I’d gotten out of the hospital for a bleeding ulcer. I’ll consider the slightly increased risk of cancer worth it for the decreased risk of the ulcer not healing.
My doctors have me on a PPI indefinitely precisely because after some erosive esophagitis I am at elevated risk for cancer. I could believe the cause and effect is blurred here.
I’m sorry, but unless you can provide a credible source, I call this bullshit. Especially esomeprazole having half the side effects. No way.
I’m having trouble finding a plain head-to-head study with tolerability data. This is the best I came up with, a fairly recent meta-analysis:
https://www.nature.com/articles/srep41021
Altought for a having the word “tolerability” in the title they don’t really give useable information about that.
“In terms of tolerance, the comparison results among active drugs did not reach statistical significance; however, the tolerance was better than the placebo (Fig. 7).”
So very little if any difference? I’d need quart of rum to get the patience to squint through all of that to know how trustworthy it is. A lot of big words though, seems good.
Also they do say this in the conclusion:
"This study indicates that the full/standard doses (40 mg per day) of esomeprazole should be recommended as first-line treatments for GERD in adults based on 4–8 weeks of short-term therapy for healing. Moreover, the full/standard doses (40 mg per day) of omeprazole were associated with the relief of symptoms and were well tolerated. "
You’d think that if there was a major difference in tolerability, it would have come up.
I’d say this is the same enantiomer trick that pharmacetuical companies did with citalopram/escitalopram and loratadine/desloratadine. It’s basically a smoke screen to extend the patents.
As someone overweight, I managed to develop GERD as I gained mass, and PPIs were suggested (but rejected by me) as a workaround. Losing weight plus judicious use of (non-medicinal) Gaviscon when necessary was very successful in reducing the incidence of flare-ups.
Yeah, this is just some random guy speculating, but perhaps the increased incidence of cancer is because the drug made it easier to ignore the reflux and various foods/drinks that would aggravate it?
I was on Nexium for about 5 years, followed by Tecta for another year or two. Then my doctor was on holidays and a locum was in his place, and she told me that if I had tried going without (I had) and experienced a flare up, it was because my body was adapting to not having the drug. If I held out for a few weeks I could see if there was a change.
I immediately stopped taking the drug, and had about a week of awful reflux. Then it went away. Now, unless I am foolish enough to eat more than a little bread, sugar or canned tomatoes in any form, I just don’t get reflux. I have often wondered just how many years I took that fucking drug unnecessarily because it was easier for my doctor to just sign the prescription and send me on my way.
FINALLY! Some common sense.
I’ve suffered from GERD for over a decade. I’m in really good shape (hit the gym or cycle 4-6 times a week), have maybe one drink a week and don’t consume much sugar or pastries. For me it’s an issue from stress and from aging. When I was younger I could eat a lot of anything I wanted, drink lots of beer or other alcohol and not feel any problem. My gastroenterologist wants me to stay on Nexium as a preventative for esophageal cancer.
I’ll take my chances on the side effects, having weaned myself off Nexium and Losec previously and had the GERD issues eventually recurr (dry cough, heartburn when laying on my side etc.).
If you want to get off this type of medication, extend the time between doses by an hour per day until you get to about 36 hours between pills. Then extend the time to every other day for a few days, then every third day. I managed to minimize the reflux backlash pretty successfully this way.
An irony is that PPIs as well as H2 blockers don’t have any effect on reflux per se. They merely reduce the esophageal acid exposure due to reflux. They also don’t impact esophageal Pepsi exposure, which itself may be involved in symptom production.
The only known drug to actually reduce reflux itself is baclofen. But baclofen has its own rather intense side effect profile.
For very severe cases recalcitrant to medicine, there is a new surgical procedure called EndoStim.
The primary problem is that there’s well documented evidence of the statistical connection between long term GI inflammation and development of certain cancers. The fact that people who are on prescription PPI’s tend statistically to be those developing cancers, regardless of H. pylori involvement, is not surprising given that people prescribed PPI’s are likely those with more significant inflammatory disease.
I guess I’ll have to read the article to see if there’s a control for degree of inflammatory disease, or if they managed to isolate PPI use as a single factor (which I’d be surprised if they did). Unless they controlled for degree of inflammation, then this is more correlation than causation…
Yup. Just like:
Sick people tend to be on drugs. It’s not the drugs that make them sick, it’s that the drugs are given because they’re sick.
“Doctors hate them!”
Unlikely. The calcium in Tums is a tightly-bound reaction salt (calcium carbonate), and your body simply can’t use much of it; there’s no real digestive or metabolic mechanism to do so. You’ll still absorb a little bit but it’s NOT an effective calcium supplement, not even close.
I said it mostly in jest, but that’s interesting to know. I probably ought to read up on nutritional chemistry to disabuse myself of old info.
