Give me advice on probiotics
November 8, 2012 11:13 AM Subscribe
I'm taking Augmentin (an antibiotic) for a sinus infection. My doctor said I should also take Florastor, a probiotic, to avoid stomach issues. But won't the Augmentin kill anything that Florastor manages to grow? I know, YANMD, but if you have any experience taking antibiotics and probiotics at the same time, please tell me how that worked for you. Did it help with antibiotic-related tummy trouble?
I definitely found that the probiotics helped stave off the antibiotic-related tummy troubles, and family members and friends who've been on antibiotics for months have said they've helped to shorten any troubles that do start.
Antibiotics killing off our good flora are a big problem that can lead to dangerous things like colitis. They don't kill off All flora in our guts, though, that'd kill us. Probiotics might not help as much as we'd like (because we know surprisingly little about the vast array of healthy gut flora), but they definitely seem to help.
posted by ldthomps at 11:27 AM on November 8, 2012
Antibiotics killing off our good flora are a big problem that can lead to dangerous things like colitis. They don't kill off All flora in our guts, though, that'd kill us. Probiotics might not help as much as we'd like (because we know surprisingly little about the vast array of healthy gut flora), but they definitely seem to help.
posted by ldthomps at 11:27 AM on November 8, 2012
I've taken a probiotic (not Florastor, but something else, I don't remember the name right now) while taking antibiotics. And I found that it helped. I sometimes get diarrhea at the end of a run of antibiotics, and the probiotic seemed to help keep things solid. It works by making the intestinal bacteria come back faster. See here.
posted by bluefly at 11:27 AM on November 8, 2012
posted by bluefly at 11:27 AM on November 8, 2012
A question not answered yet is -- do the antibiotics kill off the probiotics as soon as they're taken? If no, why not?
posted by eas98 at 11:31 AM on November 8, 2012
posted by eas98 at 11:31 AM on November 8, 2012
Best answer: This is a pretty good link. My doctor suggests staggering the probiotic dose to be as far as possible from the antibiotic dose(s) so you get the maximum benefit possible. And taking the probiotics for at least a week after you finish the antibiotics.
Augmentin is great for sinus infections, but I found it really disturbed my stomach. Ginger tea and ginger chews helped some.
posted by Sidhedevil at 11:36 AM on November 8, 2012
Augmentin is great for sinus infections, but I found it really disturbed my stomach. Ginger tea and ginger chews helped some.
posted by Sidhedevil at 11:36 AM on November 8, 2012
Probiotics don't colonise your gut and grow there, any effect you get from them is transitory. The whole recolonising the good bacteria thing turns out to not happen. Probably because of this, often heat killed bacteria gives very similar results as live depending on what you're measuring. So it won't actually matter even if the augmentin is killing whatever in the probiotics (and I'm not sure it does, depends on what kind of bacteria it is specifically targeted towards).
posted by shelleycat at 11:39 AM on November 8, 2012 [1 favorite]
posted by shelleycat at 11:39 AM on November 8, 2012 [1 favorite]
eas, Augmentin targets certain types of bacteria. It will kill those where they appear in the probiotic, but a good probiotic like Florastor has tons of strains of organisms.
posted by Sidhedevil at 11:39 AM on November 8, 2012
posted by Sidhedevil at 11:39 AM on November 8, 2012
I just let the Augmentin have its way with my digestive system, then got right on yogurt once I was done with the course of antibiotics. I didn't want to deal with timing the biotic warriors. And hey, I lost a couple of pounds!
posted by bink at 11:41 AM on November 8, 2012
posted by bink at 11:41 AM on November 8, 2012
Oh and positively effecting gut barrier function is definitely one of the things I've seen similar results for dead vs live bacteria, it's more about the ligands made by the bacteria than growth per se. Reducing diarrhoea is a good thing and will help the microflora balance itself back out again even if the probiotic doing is lost within 24 hours of eating (which it is regardless of if it's dead or alive).
posted by shelleycat at 11:41 AM on November 8, 2012
posted by shelleycat at 11:41 AM on November 8, 2012
I've taken Augmentin twice for some hardcore sinus infections and the first time I took it I underestimated its ability to decimate good flora in the stomach and intestines. The second time around I upped and varied my probiotic intake by like 5 and suffered no ill effects. You'll need to look for live cultures rather than rely just on any probiotic pills, too. You're looking to stave off a major die off in your gut first by taking probiotics concurrently with your augmentin; after that round is done, continue taking probiotics to restore equilibrium.
posted by These Birds of a Feather at 11:43 AM on November 8, 2012 [1 favorite]
posted by These Birds of a Feather at 11:43 AM on November 8, 2012 [1 favorite]
Best answer: Sigh... IAMAMicrobiologist, IAMNYMicrobiologist, and this is neither microbiological nor medical advice. Please always trust your doctor over anything anyone on the internet tells you aside from possibly recommendations to get a new doctor.
The Saccharomyces boulardii in your Florastor is certain to be very insensitive to the antibiotics you are taking, however, there has yet to be any convincing evidence that live pro-biotics have any beneficial effect that the same pro-biotics killed don't also have. The time you take the Florastor in relation to the antibiotics is vanishingly unlikely to have any effect on any efficacy the probiotic may or may not have. Indeed, the most plausible explination for the very minor efficacy that probiotics have been shown to have is that you are feeding your gut microbes easy prey that is easy to eat.
Alternatively you could always make sure you include yoghurt, hefeweizen beer, saurkraut, kimchee, cheese, kombucha, and/or sourcream in your diet - though be careful with beer as people have been shown to experience bad effects with antibiotics similar to ones in your cocktail.
posted by Blasdelb at 12:01 PM on November 8, 2012 [6 favorites]
The Saccharomyces boulardii in your Florastor is certain to be very insensitive to the antibiotics you are taking, however, there has yet to be any convincing evidence that live pro-biotics have any beneficial effect that the same pro-biotics killed don't also have. The time you take the Florastor in relation to the antibiotics is vanishingly unlikely to have any effect on any efficacy the probiotic may or may not have. Indeed, the most plausible explination for the very minor efficacy that probiotics have been shown to have is that you are feeding your gut microbes easy prey that is easy to eat.
Alternatively you could always make sure you include yoghurt, hefeweizen beer, saurkraut, kimchee, cheese, kombucha, and/or sourcream in your diet - though be careful with beer as people have been shown to experience bad effects with antibiotics similar to ones in your cocktail.
posted by Blasdelb at 12:01 PM on November 8, 2012 [6 favorites]
No, the antibiotic probably won't kill all the probiotic bacteria right away. An antibiotic that could make your body entirely free of bacteria would be a very dangerous drug.
Antibiotics selectively kill off or decrease the reproduction rate of some species. Each antibiotic works on a different range of species. They change the balance of species in your body by killing off some species, and giving those that remain the opportunity to grow with less competition. These changes can persist for a long time after antibiotic therapy & cause side effects like diarrhea.
There are a lot of reasons why an antibiotic might not kill a particular species. For example, the chemical in the antibiotic might target the cell wall of bacteria. Some bacteria don't have a cell wall with the chemical targeted by the drug, or they might be able to neutralise the effect of the drug. Some species are in such high numbers in your body that enough survive the therapy and just grow back. Some are in tissues that the drug doesn't penetrate so well. Some are in clumps or films that the drug can't penetrate well. And lots of other reasons!
posted by JeanDupont at 12:07 PM on November 8, 2012
Antibiotics selectively kill off or decrease the reproduction rate of some species. Each antibiotic works on a different range of species. They change the balance of species in your body by killing off some species, and giving those that remain the opportunity to grow with less competition. These changes can persist for a long time after antibiotic therapy & cause side effects like diarrhea.
There are a lot of reasons why an antibiotic might not kill a particular species. For example, the chemical in the antibiotic might target the cell wall of bacteria. Some bacteria don't have a cell wall with the chemical targeted by the drug, or they might be able to neutralise the effect of the drug. Some species are in such high numbers in your body that enough survive the therapy and just grow back. Some are in tissues that the drug doesn't penetrate so well. Some are in clumps or films that the drug can't penetrate well. And lots of other reasons!
posted by JeanDupont at 12:07 PM on November 8, 2012
If you are down for some science, this is the review of note for the strain your doctor prescribed, Systematic review and meta-analysis of Saccharomyces boulardii in adult patients. From the Results section:
Antibiotic-associated diarrhea
Epidemiology of antibiotic-associated diarrhea: The reported incidence of antibiotic-associated diarrhea (AAD) ranges from 12/100 000 to 34/100[122] depending upon the type of antibiotic, host factors (age, health status, etc.), etiology, hospitalization status and presence of a nosocomial outbreak. The highest frequency of AAD is found (26%-60%) during healthcare associated outbreaks, when susceptible patients are clustered by time, exposure and proximity[123]. Healthcare associated (hospital, long-term care facilities, nursing homes) outbreaks of AAD are to be expected because inciting agents (antibiotics), infectious agents and a susceptible patient population are intermixed. Historically, most cases of AAD were reported in hospitalized patients[122]. More recently, although AAD still occurs in hospital settings, rates of 6-33/100 have been reported in outpatient populations[124,125] and lower rates (12/100 000 to 14/100) in non-hospitalized adults[126,127]. Lower rates observed in outpatients may be due to their generally higher health status compared with hospitalized patients and also to the lack of exposure to nosocomial pathogens that commonly contaminate hospital environments. Higher incidences are still found in healthcare associated pediatric and adult patients (ranging from 5-34/100 patients)[128-130].
The clinical presentation of AAD may be mild (uncomplicated diarrhea) or more severe (colitis), or result in toxic megacolon or death[122]. The onset of AAD may occur while the patient is on antibiotics, but delayed-onset AAD is more common[122]. In addition, the onset of AAD may vary according to the type of antibiotic. Elmer et al[131] found a variable time of onset using the hamster model of AAD and different types of antibiotics. Early onset of AAD was associated with clindamycin, amoxicillin and ampicillin, while delayed-onset AAD was associated with erythromycin, ciprofloxacin and clarithromycin. Consequences of AAD may result in extended hospital stays, increased medical care costs and increased diagnostic procedures[122,132]. Prevention of AAD has rested on discontinuing the inciting antibiotic or switching to an antibiotic with a narrower spectrum of action, but there are no other current effective preventive measures for AAD.
Efficacy evidence for AAD: There have been ten randomized controlled trials in adults using S. boulardii for the prevention of AAD (Table (Table22)[37,42,44,54,55,58,133-136]. These studies have used a variety of daily doses, durations of treatment, length of follow-up and types of patient population. Of the ten controlled trials, 8 (80%) showed significant efficacy for the prevention of AAD compared with controls. One of the earliest trials by Adam et al[37], randomized 388 hospitalized patients to 200 mg of S. boulardii [4 × 109 cfu (colony forming units)/d] or placebo for seven days and found a significant reduction in AAD in the S. boulardii group (4.5%) compared with the controls (17.5%, P < 0.05). The protective effect of S. boulardii was confirmed in later studies. Monteiro et al[55] enrolled 240 patients receiving oral antibiotics and found significantly fewer patients randomized to S. boulardii developed AAD (15.7%) compared with placebo (27.7%, P < 0.05). McFarland et al[54] enrolled 193 hospitalized patients receiving beta-lactam antibiotics and randomized them to either 1 g of S. boulardii or placebo for the duration of the antibiotic treatment plus three additional days. Significantly fewer patients developed AAD while on the beta-lactam antibiotics or in the seven week follow-up period when given S. boulardii (7.2%, P < 0.05) compared with 14.6% of those given placebo. This study confirmed an earlier study by Surawicz et al[58] of 180 hospitalized adults randomized to either S. boulardii or placebo for the duration of their antibiotic treatment plus an additional two weeks. Of the 23% patients who were contacted 2-3 wk after the study, only one patient given placebo developed delayed-onset AAD. Only 9.5% of those randomized to S. boulardii developed AAD compared with 21.8% of those on placebo (P < 0.05). Can et al[135] enrolled 151 adult inpatients receiving various types of antibiotics, who were then randomized to S. boulardii or placebo for the duration of the antibiotic treatment. Significantly fewer patients (1.4%, P < 0.05) of those given S. boulardii developed AAD compared with the control group (9.0%). Three trials have been in conducted in patients with H. pylori infections receiving triple therapy (usually two antibiotics and an acid suppressor), which is associated with a high rate of AAD development. Duman et al[44] enrolled 389 patients with peptic ulcer or non-ulcer dyspepsia in nine hospitals in Turkey to observe if lower rates of side-effects could be achieved. This study compared 204 patients who received 1 g of S. boulardii (2 × 1010/d for 2 wk) and triple therapy with 185 controls, who received only the triple therapy. Of the 389 patients, 376 completed the treatment phase and the four-week follow-up. Significantly fewer patients given S. boulardii (6.9%) developed AAD compared with the control group (15.6%, P = 0.007). Two other randomized controlled trials in adult patients receiving triple therapy for H. pylori infections were conducted and both showed a significant reduction in AAD for those treated with S. boulardii. Cremonini et al[134] randomized 85 H. pylori carriers to placebo, L. rhamnosus GG, S. boulardii or a mix of L. acidophilus and Bifidobacterium lactis and found significantly fewer patients developed AAD in only the S. boulardii group (5%, P = 0.05) compared with placebo (30%). Cindoruk et al[42] also found a significant reduction in AAD in adult patients treated with triple therapy for H. pylori infections for those randomized to S. boulardii (14.5%, P < 0.05) compared with placebo (30.6%). None of these trials reported any adverse reactions associated with S. boulardii.
posted by Blasdelb at 12:33 PM on November 8, 2012
Antibiotic-associated diarrhea
Epidemiology of antibiotic-associated diarrhea: The reported incidence of antibiotic-associated diarrhea (AAD) ranges from 12/100 000 to 34/100[122] depending upon the type of antibiotic, host factors (age, health status, etc.), etiology, hospitalization status and presence of a nosocomial outbreak. The highest frequency of AAD is found (26%-60%) during healthcare associated outbreaks, when susceptible patients are clustered by time, exposure and proximity[123]. Healthcare associated (hospital, long-term care facilities, nursing homes) outbreaks of AAD are to be expected because inciting agents (antibiotics), infectious agents and a susceptible patient population are intermixed. Historically, most cases of AAD were reported in hospitalized patients[122]. More recently, although AAD still occurs in hospital settings, rates of 6-33/100 have been reported in outpatient populations[124,125] and lower rates (12/100 000 to 14/100) in non-hospitalized adults[126,127]. Lower rates observed in outpatients may be due to their generally higher health status compared with hospitalized patients and also to the lack of exposure to nosocomial pathogens that commonly contaminate hospital environments. Higher incidences are still found in healthcare associated pediatric and adult patients (ranging from 5-34/100 patients)[128-130].
The clinical presentation of AAD may be mild (uncomplicated diarrhea) or more severe (colitis), or result in toxic megacolon or death[122]. The onset of AAD may occur while the patient is on antibiotics, but delayed-onset AAD is more common[122]. In addition, the onset of AAD may vary according to the type of antibiotic. Elmer et al[131] found a variable time of onset using the hamster model of AAD and different types of antibiotics. Early onset of AAD was associated with clindamycin, amoxicillin and ampicillin, while delayed-onset AAD was associated with erythromycin, ciprofloxacin and clarithromycin. Consequences of AAD may result in extended hospital stays, increased medical care costs and increased diagnostic procedures[122,132]. Prevention of AAD has rested on discontinuing the inciting antibiotic or switching to an antibiotic with a narrower spectrum of action, but there are no other current effective preventive measures for AAD.
Efficacy evidence for AAD: There have been ten randomized controlled trials in adults using S. boulardii for the prevention of AAD (Table (Table22)[37,42,44,54,55,58,133-136]. These studies have used a variety of daily doses, durations of treatment, length of follow-up and types of patient population. Of the ten controlled trials, 8 (80%) showed significant efficacy for the prevention of AAD compared with controls. One of the earliest trials by Adam et al[37], randomized 388 hospitalized patients to 200 mg of S. boulardii [4 × 109 cfu (colony forming units)/d] or placebo for seven days and found a significant reduction in AAD in the S. boulardii group (4.5%) compared with the controls (17.5%, P < 0.05). The protective effect of S. boulardii was confirmed in later studies. Monteiro et al[55] enrolled 240 patients receiving oral antibiotics and found significantly fewer patients randomized to S. boulardii developed AAD (15.7%) compared with placebo (27.7%, P < 0.05). McFarland et al[54] enrolled 193 hospitalized patients receiving beta-lactam antibiotics and randomized them to either 1 g of S. boulardii or placebo for the duration of the antibiotic treatment plus three additional days. Significantly fewer patients developed AAD while on the beta-lactam antibiotics or in the seven week follow-up period when given S. boulardii (7.2%, P < 0.05) compared with 14.6% of those given placebo. This study confirmed an earlier study by Surawicz et al[58] of 180 hospitalized adults randomized to either S. boulardii or placebo for the duration of their antibiotic treatment plus an additional two weeks. Of the 23% patients who were contacted 2-3 wk after the study, only one patient given placebo developed delayed-onset AAD. Only 9.5% of those randomized to S. boulardii developed AAD compared with 21.8% of those on placebo (P < 0.05). Can et al[135] enrolled 151 adult inpatients receiving various types of antibiotics, who were then randomized to S. boulardii or placebo for the duration of the antibiotic treatment. Significantly fewer patients (1.4%, P < 0.05) of those given S. boulardii developed AAD compared with the control group (9.0%). Three trials have been in conducted in patients with H. pylori infections receiving triple therapy (usually two antibiotics and an acid suppressor), which is associated with a high rate of AAD development. Duman et al[44] enrolled 389 patients with peptic ulcer or non-ulcer dyspepsia in nine hospitals in Turkey to observe if lower rates of side-effects could be achieved. This study compared 204 patients who received 1 g of S. boulardii (2 × 1010/d for 2 wk) and triple therapy with 185 controls, who received only the triple therapy. Of the 389 patients, 376 completed the treatment phase and the four-week follow-up. Significantly fewer patients given S. boulardii (6.9%) developed AAD compared with the control group (15.6%, P = 0.007). Two other randomized controlled trials in adult patients receiving triple therapy for H. pylori infections were conducted and both showed a significant reduction in AAD for those treated with S. boulardii. Cremonini et al[134] randomized 85 H. pylori carriers to placebo, L. rhamnosus GG, S. boulardii or a mix of L. acidophilus and Bifidobacterium lactis and found significantly fewer patients developed AAD in only the S. boulardii group (5%, P = 0.05) compared with placebo (30%). Cindoruk et al[42] also found a significant reduction in AAD in adult patients treated with triple therapy for H. pylori infections for those randomized to S. boulardii (14.5%, P < 0.05) compared with placebo (30.6%). None of these trials reported any adverse reactions associated with S. boulardii.
posted by Blasdelb at 12:33 PM on November 8, 2012
Personal first-hand experience with taking antibiotics and also eating organic yogurt to help combat the tummy problems:
Persistent use of a probiotic while on antibiotics seemed to develop somewhat antibiotic resistent gut flora for me. I have taken Augmentin specifically. But I have also taken stronger antibiotics with side effects like really, extremely severe diarrhea and also "kills some small percentage of patients".
YMMV, of course.
posted by Michele in California at 3:00 PM on November 8, 2012
Persistent use of a probiotic while on antibiotics seemed to develop somewhat antibiotic resistent gut flora for me. I have taken Augmentin specifically. But I have also taken stronger antibiotics with side effects like really, extremely severe diarrhea and also "kills some small percentage of patients".
YMMV, of course.
posted by Michele in California at 3:00 PM on November 8, 2012
Augmentin is a combination of an anti-bacterial antibiotic (amoxicillin) and a substance (clavulanic acid) which blocks an enzyme which confers resistance to amoxiillin on bacteria which can produce that enzyme.
Saccharomyces boulardii, on the other hand, is a tropical yeast related to brewer's yeast, not a bacterium, and as such, amoxicillin has no activity against it as far as I know.
posted by jamjam at 4:53 PM on November 8, 2012
Saccharomyces boulardii, on the other hand, is a tropical yeast related to brewer's yeast, not a bacterium, and as such, amoxicillin has no activity against it as far as I know.
posted by jamjam at 4:53 PM on November 8, 2012
When I take antibiotics, I also take a probiotic because otherwise, I get a yeast infection that makes me feel like I'm going to die.
posted by kat518 at 7:11 PM on November 8, 2012
posted by kat518 at 7:11 PM on November 8, 2012
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And without the Florastor the good bugs will grow back eventually, but you'll likely get a yeast infection in the interim.
posted by tilde at 11:16 AM on November 8, 2012 [1 favorite]