MetaPhlAn Metagenomic

What to do if taking ANTIBIOTICS, MICROBIOME

Summary:  Antibiotics carpet bomb the microbiome. Here’s important things to do if you must take an antibiotic as noted in this article by Dr. Robynne Chutkan, MD and gastroenterologist,  see bio below. I’ve adapted the list to include the How-To-Do details.  Realize that the gist of the steps below you should ALWAYS be doing, not just during times you take antibiotics.  But be particularly diligent and persistent following these steps if you must take an antibiotic in order to try to counteract the antibiotics, microbiome, nuke!  For even more guidance on what to do before and after taking antibiotics, Dr. Mark Hyman’s recommendations from his article, Here’s the Downside of Antibiotics Your Doctor Might Not Tell You,  has been added.  Last,  the studies looking at antibiotics and Culturelle, VSL #3, and Saccharomyces boulardii or Florastor(®), as well as their precautions, are included.

A word of caution concerning the FODMAP and Resistant Starch prong on the below gut preservation list:

FODMAP and resistant starch are part of the preservation strategy since both build up the diversity and richness of the microbiome.  This is especially important for antibiotic dosing as the antibiotics nuke the microbiome; Caution though with FODMAPs… many with gut dysfunction have a hard time eating those. If you haven’t been eating FODMAPs, start slow and see if your gut can tolerate them. The goal of the FODMAP diet is to learn your individual tolerance for FODMAPs and NOT to eliminate them from your diet.  Healing the gut using healing diet tenets and lifestyle supports the microbiome and will increase what you can consume FODMAP wise!

Antibiotics, microbiome and preservation — adapted from this article by Dr. Robynne Chutkan, MD

1. Take a probiotic during and after antibiotics (continue for at least one month after finishing antibiotics). [Consume the probiotic two hours before and two hours after the antibiotic.]  Probiotics containing strains of Lactobacillus and Bifidobacterium are the most useful, as well as those containing the beneficial yeast Saccharomyces boulardii.  Note though that bifidobacterium, in the SCD/GAPS world, seems to be contradicted due to overgrowth concerns and here.  It’s controversial however; UMass IBD-AID permits this strain; see An anti-inflammatory diet as treatment for inflammatory bowel disease: a case series report.  Whole food probiotics to consider for a crowding out pathogen purpose to help preserve the beneficial microbiome constituency, are lactose-free SCD yogurt, live sauerkrauts, Kimchi, pickles, etc. such as:

If you ask your doctor about CDiff risk with the antibiotic being prescribed, often they’ll tell you it is rare (not true by the way; it’s currently an epidemic, read the post ANTIBIOTIC RESISTANCE AND MICROBIOME COMPETITIVE CROWDING OUT CONCEPTS) and then they’ll immediately prescribe Florastor(®) (which likely won’t be covered by you insurance but it costs under $20 in my area). Also concerning, only 9.6% of academic medical centers stocked Culturelle and Florastor according to this study which is detailed below.  Florastor(®) is S.Boulardii, which actually is a yeast, not a bacteria.  The article, Saccharomyces boulardii CNCM I-745 supports regeneration of the intestinal microbiota after diarrheic dysbiosis – a reviewis extraordinarily important .  It has a gut mucosal focus, and anyone thinking about taking S.boulardii should read it… more than once… to realize the potential of this yeast.  This article, along with other Saccharomyces boulardii  or Florastor(®) studies, is excerpted below as is information on Saccharomyces boulardii  or Florastor(®) precautions.

2. Eat PREBIOTIC foods (called FODMAPs and RESISTANT STARCH) to support your gut microbes. Foods high in fiber and resistant starch feed your microbes and help to promote species diversity and richness, which can decrease dramatically after a course of antibiotics. A Convenient FODMAPs Food list from Food Washington Post and from Monash University “Low FODMAP Diet” book and app (by Sue Shepherd and Dr. Peter Gibson, MD) follows. “High” FODMAP foods promote species diversity and richness.  The limits noted are threshold levels where consumption above those levels, may not be tolerable for some. 

High-FODMAPs protein: Legumes (chickpeas, broad beans, butter beans, kidney beans), lentils over ½ cup. Low-FODMAPs protein: Meat, fish, chicken, tofu ( I don’t recommend soy especially if you are a Westerner since many lack the microbial bacterial enzymes to properly digest soy).

High-FODMAPs vegetables: Garlic, leeks, onions, asparagus, cabbage, brussels sprouts, beets, artichokes, sugar snap peas, peas over 1/3 cup, celery, sweet corn, mushrooms, sweet potatoes over ½ cup, cauliflower, broccoli, cooked and then cooled potatoes, spinach over 15 leaves, zucchini over ¾ cup. Low-FODMAPs vegetables: Green beans, carrots, cucumbers, lettuce, tomatoes.

High-FODMAPs fruit and nuts: Avocados, apricots, apples, mangoes, pears, peaches, plums, pineapple over 1 slice, dates, pomegranate seeds over ½ cup, cranberries over 1 Tbsp, cherries over 3, watermelon, cashews, dried fruits, green bananas, green plantains. Pistachios, cashews and greater than 10 almonds or walnuts. Chia and flax seed both if over 1 Tbsp. Low-FODMAPs fruit and nuts: Ripe spotted bananas, oranges, grapes.

High-FODMAPs cereals, grains, breads, pastas: Wheat products, barley, rye. Low-FODMAPs cereals, grains, breads and pastas: Gluten-free bread and pastas, oats, rice, quinoa.

High-FODMAPs dairy products: Soft cheeses, cow’s milk, cream, ice cream, commercial yogurt, kefir (if not lactose-free). Low-FODMAPs dairy products: Lactose-free milk and yogurt, hard cheese.

High-FODMAPs sweeteners and bakery type products: Cocoa powder and anything ending in “ol” (such as sorbitol) on the ingredient label, honey and many fruits (see above).   NOTE:  I don’t recommend consuming the “ol” artificial sweeteners as they were found to alter microbial metabolic pathways that are linked to host susceptibility to metabolic disease, induced dysbiosis, and glucose intolerance in healthy human subjects, see the Nature article here).

3. Drink ginger tea it has a soothing effect on the digestive system and can help to reduce gas and bloating associated with taking an antibiotic. Tip:  Thinly slice ginger root on the diagonal and freeze in single layers. It’s easy to pull out a few slices to steep in filtered water. You can do the same with turmeric root, and even add in peppermint and spearmint leaves for a even greater gut healing anti-inflammatory friendly treat.

4. Skip the acid suppression drugs. Read the post HEARTBURN DRUGS, DEMENTIA, ALZHEIMER’S RISK FOR ALL? T2D, IS IT THE CANARY IN THE COAL MINE!?!   Blocking stomach acid while taking an antibiotic leaves you vulnerable to overgrowth of pathogenic bacteria like Cdiff that can lead to a serious antibiotic resistant infection. [Contact your doctor to] stop acid suppressing drugs seventy-two hours before and while taking antibiotics to allow levels of stomach acid to return to normal. In fact, acid suppression drugs can cause dysbiosis downstream (including SIBO — read the above HEARTBURN post) and hopefully, as you journey through whole, clean, low toxin, nutrient dense, and anti-inflammatory foods you’ll stop needing them entirely.

NOTE:  The above antibiotic microbiome preservation section was adapted from Dr. Robynne Chutkan’s article: “5 Medications That Can Seriously Bloat You.”

Dr. Mark Hyman’s article, Here’s the Downside of Antibiotics Your Doctor Might Not Tell You, recommends the following before and after taking antibiotics. Dr. Hyman is the Medical Director at Cleveland Clinic’s Center for Functional Medicine.

  1. First, add in the good stuff. Eat a low-glycemic, whole-foods diet and take quality probiotics and prebiotics.
    • A high-quality, multi-strain probiotic helps populate your gut with beneficial bacteria.
    • Prebiotics, a form of soluble fiber, which also helps feed good bugs, which can be found in onions, garlic, resistant starch, sweet potatoes, dandelion greens and jicama.
    • Resistant Starch.  I like to supplement with my favorite resistant starch found in Bob’s Red Mill Unmodified Potato Starch. I suggest adding about 1 teaspoon to a glass of water.  Unlike regular starch, your small intestine doesn’t absorb potato starch. Instead, your gut bacteria process it, creating molecules that help balance blood sugar and healthy gut flora. In other words, when you consume resistant starch, it “resists” digestion and does not spike blood sugar or insulin.
  2. Then, focus on gut repair – especially after you’re finished using antibiotics. Utilize gut-healing nutrients including L-glutamine, omega-3 fats, vitamin A and zinc to repair your gut lining so it can resume its normal, natural functions. The use of digestive enzymes can help you digest your food better.
  3. That’s it … pretty simple but with amazing results.  If you’ve ever used antibiotics, did you use prebiotics, probiotics, healing foods, or other nutrients to help recover?

Culturelle, VSL #3, and Saccharomyces boulardii or Florastor(®) related studies

Conclusion:  There may be some benefit in using S boulardii for treatment and secondary prevention in patients experiencing recurrent CDI in conjunction with a particular concurrent antibiotic treatment. Because only a small number of studies address the primary prevention of CDI, more research is required before any changes in practice can be recommended with regard to using S boulardii prophylactically. The risks of administering S boulardii seem to be minimal compared with placebo, but because of case reports of potential morbidity secondary to serious fungemia, the use of this yeast agent should be considered on a case-by-case basis.

Its action is based on multiple mechanisms, including immunological effects, pathogen-binding and antitoxinic effects, as well as effects on digestive enzymes…  Correlated with these effects, but also due to its inherent properties, S. boulardii is able to create a favorable growth environment for the beneficial intestinal microbiota, while constituting extra protection to the host mucus layer and mucosa…Several human studies as well as animal models demonstrate that treatment with S. boulardii in dysbiosis leads to the faster reestablishment of a healthy microbiome. The most relevant effects of S. boulardii on the fecal composition include an increase of short chain fatty acid-producing bacteria (along with a rise in short chain fatty acids), especially of Lachnospiraceae and Ruminococcaceae, as well as an increase in Bacteroidaceae and Prevotellaceae.  

S. boulardii is absent from the natural gut microbiota. If administered, it achieves steady-state concentrations in the colon within 3 days and is cleared from the stools 2–5 days after discontinuation.56,57 In mice, S. boulardii reached 107 colony forming units (CFU)/g of feces in a steady state, when 5×108 CFU was administered daily. When the administration was stopped, the yeast still numbered 7.3×106 CFU/g 3 days later, but was undetectable after 1 week.58

Compared with bacterial probiotics, the yeast cells of S. boulardii have the following advantages: they are antibiotic resistant due to their fungal nature, and they do not exchange DNA, eg, resistance genes with bacteria.53

Prebiotic effect.  The cell wall material of S. boulardii is composed of glucans, mannoproteins, and chitin, which serve as excellent substrates for microbial fermentation, especially for various SCFA producers. This helps explain the increase in butyrate and other SCFA produced within the colon after S. boulardii administration.95,96

Elimination of bacterial toxins, pathogen binding, and growth inhibition of microbial pathogens. S. boulardii produces factors that neutralize bacterial toxins and modulate host cell signaling pathways implicated in proinflammatory response during bacterial infection.53 For example, S. boulardii releases a protease that cleaves C. difficile toxins;101 also, S. boulardii can inactivate cholera toxin102 and dephosphorylate lipopolysaccharides from Escherichia coli O55B5.103

In addition, a direct binding to some pathogens is possible: strains of E. coli, Salmonella typhimurium, and S. typhi adhere to the surface of S. boulardii, thus preventing adhesion to and invasion of the host.104106 Moreover, S. boulardii can inhibit the growth of a number of microbial pathogens like S. typhimurium107and C. albicans.108

Physical barrier effect and colonization resistance. The presence of an intact mucus layer is pivotal to the protection of the intestinal mucosa against bacterial infiltration.15  It can be hypothesized that the sticky outer mucus surface offers the opportunity for S. boulardii to grow and build protective interlaced layers, making it even more difficult for pathogenic strains to reach the mucosa.19

In the healthy situation, commensals have been shown to limit pathogen colonization by competing for metabolites, thereby leading to “colonization resistance.”109 Similarly, S. boulardii – by its mere presence and/or its metabolic activity – may hinder potentially harmful bacteria from occupying a niche at the exposed mucosa. At the same time, S. boulardii itself is not competitive enough to keep this position for long, once habitual/essential bacteria regenerate. Yet its makeshift function may give the host further opportunities to rebuild the mucus layer by reducing the pressure from the potentially harmful microbiota. Studies are needed to verify this hypothesis.

Although the use of S. cerevisiae (eg, S. boulardii CNCM I-745) is considered safe, an increased number of S. cerevisiae infections (fungemia) have been observed in critically ill and/or immunocompromised patients.59 Interestingly, virulence seems to be associated with an enhanced tolerance to oxidative stress 60 as well as increased copy numbers of genes of the purine nucleotide synthesis pathway, which in turn increase survival rates in the bloodstream of the host.61 However, in order to cause fungemia, S. cerevisiae first needs to cross the intestinal barrier and reach the bloodstream in sufficient numbers.

Clinical efficacy of Saccharomyces boulardii as a probiotic in acute gastrointestinal conditions: Antibiotic-associated diarrhea, Clostridium difficile infection,  Helicobacter pylori infection, and Acute, persistent, enteral nutrition-related feeding, and travelers diarrhea.

Clinical efficacy of Saccharomyces boulardii as a probiotic in chronic diseases (IBD, IBS, Parasitic, HIV diarrhea)

Although no probiotics were supported by a strong evidence base, both Culturelle and Florastor appear to be supported by more evidence compared to Lactinex and VSL #3, which had low/no evidence to moderate evidence base for all of the indications identified. Only 27.2% and 9.6% of academic medical centers stocked Culturelle and Florastor, respectively, whereas 51% of academic medical centers stocked at least 1 probiotic that was supported by low/no evidence. These results suggest that a majority of academic medical centers stock a probiotic that lacks a reliable evidence base.

Seven studies out of the 24 RCTs identified were related to Florastor use (Table A2). Of those studies, 1 was related to the use of Florastor for rotaviral diarrhea, 4 for antibiotic-associated diarrhea, and 2 for CDD recurrence. The risk of bias in these studies ranged from low to high. While 29% of the studies were found to have a low risk of bias, 57% had an unknown risk of bias, and 14% had a high risk of bias.2228

A majority (57%) of the evidence identified evaluated the use of Florastor in antibiotic- associated diarrhea. Three (75%) of these studies showed a statistically significant benefit for decreasing the incidence of antibiotic-associated diarrhea, while 1 (25%) did not report a statistically significant benefit. Additionally, 1 (25%) study showed a statistically significant benefit for decreasing hospitalization duration, 1 (25%) showed no benefit, and 2 (50%) studies did not evaluate duration of hospitalization.2326Overall, Florastor had a moderate evidence base for antibiotic-associated diarrhea.

Of the 2 RCTs identified regarding the use of Florastor for Clostridium difficile–associated disease (CDD) recurrence, 1 study showed a statistically significant benefit for decreasing the incidence of CDD recurrence in patients with recurrent CDD, while that same study found no benefit in those with an initial CDD. The other study showed no benefit for the use of Florastor in CDD recurrence in patients who received vancomycin or metronidazole.27,28 Overall, Florastor had a moderate evidence base for CDD recurrence.

There was 1 RCT identified for the use of Florastor in rotaviral diarrhea. This RCT showed a statistically significant benefit for decreasing the incidence and duration of rotaviral diarrhea. Overall, Florastor had a moderate evidence base for rotaviral diarrhea.22

Florastor(®) Precautions

The article, Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders notes that caution should be taken when using S.boularii in patients with risk factors for adverse events, such as immunocompromised patients. That is concerning since actually a lot of folks take immuno-suppression drugs. Some studies such as this, discuss the risk as “reports of fungemia in both immunocompromised and immunocompetent patients. The reports also suggest increased risk for fungemia in patients with central venous catheters and the critically ill (6). These patients, however, are at higher risk of developing CDI and its associated complications. Therefore, this patient population may benefit from preventive therapy.”  Check with your doctor if there are other patient circumstances with increased risk. There are also special precautionary situations noted on the Florastor website FAQ: Do not use Florastor if you are currently using a central line or port. Central lines include short- and long-term central venous catheters (CVCs) and peripherally inserted central catheters (PICCs). Do not use Florastor if you are allergic to any of its components (especially yeast). 

Dr. Chutkan’s bio,  Gastroenterologist and Wellness Expert:

A member of the faculty at Georgetown Hospital since 1997, Dr Chutkan founded the Digestive Center for Women (DCW) in 2004, an integrative gastroenterology practice that includes nutritional therapy, stress reducing techniques such as meditation, biofeedback and counseling, as well as gastrointestinal procedures like endoscopy, colonoscopy, and video capsule endoscopy. In addition to digestive disorders in women, her clinical areas of interest include alterations in gut bacteria (dysbiosis), inflammatory bowel diseases, irritable bowel syndrome, and food as medicine. She is a recognized leader in gastroenterology both nationally and internationally and Washingtonian magazine has consistently named her one of the top doctors in her field. Board certified in Gastroenterology, Dr Chutkan serves on numerous committees and boards and is actively involved in patient and physician education. She is a past Governing Board member of the American Society for Gastrointestinal Endoscopy (ASGE) and former Chair of their Training Committee and Public Relations Committee. She is the author of the bestselling book Gutbliss, and the newly released The Microbiome Solution, and has lectured extensively throughout the United States and Europe.  Mount Sinai Hospital, GI fellowship, Columbia College of Physicians & Surgeons, MD, Yale University, BS.

In health through awareness,






Last updated: February 9, 2017 at 7:30 am  to add Dr. Mark Hyman’s recommendations for what to do before and after taking antibiotics, excerpted from his article, Here’s the Downside of Antibiotics Your Doctor Might Not Tell You.

Prior update Oct 11, 2016 added clarification in the FODMAP section that “”High” FODMAP foods promote species diversity and richness.  The limits noted are threshold levels where consumption above those levels, may not be tolerable for some.”  Prior updates updated the title to “What to do if taking ANTIBIOTICS, MICROBIOME”.  Prior title was “Antibiotics, Microbiome, and Preservation”.  The visual readout compatibility of excerpted studies was also updated.



4 thoughts on “What to do if taking ANTIBIOTICS, MICROBIOME”

  1. Infectious Diseases / Bacteria / Viruses
    Immune System / Vaccines
    Pharmacy / Pharmacist
    Public Health
    One course of antibiotics disrupts gut microbiome for a year, 2015,

    Antibiotics and microbiome: Microbiome diversity in feces was significantly reduced for up to 4 months in participants taking clindamycin and up to 12 months in those taking ciprofloxacin.
    Amoxicillin had no significant effect on microbiome diversity in either the gut or oral cavity, but it was associated with the greatest number of antibiotic-resistant genes.

    The microorganisms in participants’ feces were severely affected by most antibiotics for months. In particular, researchers saw a decline in the abundance of health-associated species that produce butyrate, a substance that inhibits inflammation, cancer formation and stress in the gut. The drugs were found to enrich genes associated with antibiotic resistance and to severely affect microbial diversity in the gut for months after exposure. By contrast, microorganisms in the oral cavity and saliva showed signs of recovery in as little as a few weeks after drug exposure.

    “Antibiotics should only be used when really, really necessary. Even a single antibiotic treatment in healthy individuals contributes to the risk of resistance development and leads to long-lasting detrimental shifts in the gut microbiome. Certainly we cannot live or survive without antibiotics; that’s out of the question. But there are situations when we should not use them, like when there are no evidence-based reasons.”

  2. Probiotics in the prevention of antibiotic-associated diarrhoea and Clostridium difficile infection, 2011

    Antibiotics and probiotics: L. rhamnosus GG, S. boulardii and two mixtures, one containing L. casei DN-114 001 and the other Lactobacillus acidophilus CL1285, all have good evidence of efficacy in preventing AAD in clinical trials, but evidence of feasibility and efficacy in routine practice is required. The evidence for prevention and treatment of CDAD is currently equivocal. There may be other strains that have equal or better efficacy and research is required to establish which strains are the best to use.

Now I'd like to hear your thoughts... comments are always welcome!