How your antacid drug is making you sick (Part B)

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  1. Forty2’s avatar

    Well, I am pleased to report that after almost two weeks off PPI meds (Aciphex, after years of Nexium) I am mostly asymptomatic. A few flare-ups here and there but nothing like the disabling OMFG-kill-me-now pain I had years ago when I first went on Nexium. Thanks for the scientific ammo my brain needed to get off this stuff.
    I’m aware that it may take a long time for my gizzard to recover from the PPI onslaught.

  2. Amy’s avatar

    Hi Chris,
    I have really  enjoyed your articles. I have been on a low carb diet for a long time and have seen great results but I am not completely symptom free yet. How long is this process generally? I have not taken HCL partly because I thought is this just another pill I will have to take forever, I do take probiotics.  Do you find that eventually people can stop taking HCL and not have symptoms return? I was on prilosec for seven years! I was also wondering do you find the other symptoms (asthma) that come with reflux go away once the relux is resolved?

  3. Chris Kresser’s avatar

    Final article in the series is up.

    Also, the entire series as well as recommendations for books and offsite articles can be found here.

  4. Chris Kresser’s avatar

    Hi Amy,

    I just published the article on treatment.  Hopefully that will answer your questions.  It can take a while for the bacterial overgrowth to rebalance.  Replacing stomach acid is very important, whether you do it with HCL (preferred), bitters, lemon juice, sauerkraut or apple cider vinegar.

    Some people find that they only need to take HCL for a short time, others continue to use it.  It varies person to person, and depends somewhat on how long they took acid suppressing drugs and the severity of their condition.

  5. Daniel’s avatar

    You’ve done a very solid review of the evidence.  I wish I had never taken PPIs but now I have Barrett’s esophagus, with the result that the conseqeunces of being wrong are greater than just a flare up of heartburn… There is not conclusive proof that PPIs prevent cancer in those with BE, but  most evidence suggests they so.  Thus, for people with BE, PPIs may not be elective.

  6. Chris Kresser’s avatar


    Thanks for making that point. I intended to include a section called “When to seek medical help” at the end of the last article, but forgot! I’ll do it in a couple of hours. What I would have said is that if there’s structural damage to the esophagus, surgery or medication may be necessary – as you have suggested.

  7. Daniel’s avatar

    I think, in principal, controlling reflux should be superior than taking a PPI for cancer prevention in people with BE.  That said, if reflux is recalcitrant (e.g., on account of severe hiatal hernia), skipping the PPIs may be harmful.  Cancer progression in BE seems to be mediated by inflammation and associated oxidative damage.  Acid supression reduces certain markers of inflammation (but not others…) and may have a role in supressing ROS formation (and may have a role in causing ROs formation…).  The best evidence seems to be that the cancer progression rate used to be about 1% per year and now it is .5% per year.  It could just be measurment error, but acid suppression (at minimum) doesn’t seem to hurt (much) as progression to cancer among people with BE on long-term acid suppression is about 0.3% per year according to a 2006 UK study.  Turns out, antioxidants and nitrite scavengers, like vit C and vit E (and melatonin & NAC are promitting too) may do more to prevent cancer than PPIs, at least if the animal and limited human case report evidence is to be trusted.

  8. Chris Kresser’s avatar


    The potential protective effect of PPIs needs to be weighed against the potentially neoplastic effect of insufficient stomach acid and bacterial overgrowth.

    From Effect of Proton Pump Inhibitors on Vitamins and Iron, published in the American Journal of Gastroenterology last year:

    “The ability of ascorbic acid to remove nitrite from gastric juice by converting it to nitric oxide is highly pH dependent.  In gastric juice of pH>4 (which is easily achieved by taking PPIs), the nitrite entering the stomach in swallowed saliva remains as nitrite and causes an increase in gastric juice concentration.

    The original Correa hypothesis of gastric cancer developing in patients with atrophic gastritis hypothesized a central role for the elevated gastric nitrite concentration.”

    This suggests a possible mechanism by which chronic hypochlorhydria could increase the risk of gastric cancer.

    There is also a known link between atrophic gastritis, in association with achlorydria or hypochlorydria, and cancer.  The risk increases with the severity of the problem and the length of time a person has it.  In one Danish study, people with the most severe atrophic gastritis had a four-to-sixfold increased risk of developing gastric cancer.  Perhaps most importantly in the context of this discussion, it took up to seventeen years after achlorhydria was diagnosed for cancer to develop.

    As you have pointed out, there’s no direct proof that PPIs increase cancer risk, and some evidence suggesting the opposite is true.  However, because it can take up to twenty years for cancer to develop, and widespread, chronic use of PPIs is a relatively new phenomenon, I don’t think we can safely conclude that PPIs do not increase cancer risk.

    I also think it’s important to pay attention to the physiological mechanisms involved and the circumstantial evidence, in the absence of direct clinical proof.  There is no doubt that acid suppression promotes bacterial overgrowth, and that bacterial overgrowth promotes production of carcinogenic nitrosamine compounds.  There is also no doubt that acid-suppressing drugs increase both the severity and progression of atrophic gastritis in people with H. pylori infection, and atrophic gastritis is a major risk factor for gastric carcinoma.

    One researcher commented on these risks in 1988, before PPI use became widespread:

    “Until information is available about the effects of powerful gastric secretory inhibitors on the proliferative indices and patterns of the human mucosa, the drugs must be categorized as too dangerous to use therapeutically, especially since the proposed benefits are minimal.”

    It’s certainly not a cut and dry issue, and there is much conflicting evidence.  Still, if there’s any way at all of controlling symptoms without PPI use I think that is the most prudent approach.  I realize this will not always be possible.

  9. Daniel’s avatar

    Excellent points.  It is a dilemma!
    The vit C, nitrite thing is complicated.  There was a very recent mechanistic study that in the presence of 10% fat (almost any meal), vit C actually produces more nitrites in conditions that simulate the stomach.  The idea was that vit C prevents nitrite formation but causes nitric oxide (NO) to be formed which dissolves in fat and then (I think because the NO is insulated from the water-soluble vit C) forms nitrosamines…  Perhaps vit E would help…
    In any case, it’s not clear how much nitrites are involved in the progression to gastric cancer.    This guys thesis is 2 years old but very itneresting.

  10. Daniel’s avatar

    Also, h pylori (which lowers stoach acid) seems to protect against esophageal cancer in people with BE.

  11. Chris Kresser’s avatar


    Thanks for the link.  I’ll check it out – sounds very interesting.

    I think we’re agreed that this is a complex issue with no clear conclusion.  Thanks for your comments!

  12. Daniel’s avatar

    Agreed.  And, thank you for this series.  It is pretty damn good.

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