It's well known, and verified by published research, that vitamin D deficiency during pregnancy can be associated with adverse outcomes, such as preterm birth, gestational diabetes, and low birth weight. So it doesn't take much of a stretch of the imagination to rationalize that vitamin D supplementation during pregnancy might provide benefits. And indeed, even the new guidelines of the Endocrine Society recommend that pregnant people should take supplemental vitamin D above the recommended intake levels of the Institutes of Medicine (IOM), because of the potential to reduce the risk of pre-eclampsia, intra-uterine mortality, preterm birth, small-for-gestational age birth, and neonatal mortality (Press release, 2024, June 03).1

As a result, many of us have doubted the accuracy of the findings that have been published regarding most of the recently published research articles, because they invariably claim to find that taking supplemental vitamin D provides no benefits. So it was rather surprising to see that some British researchers have recently published the results of a study that showed that taking additional vitamin D during pregnancy provides significant benefits above and beyond those suggested by the IOM (Moon, et al., 2024).2

Unlike most vitamin D studies, this study by researchers at the University of Southampton, took a different approach for studying benefits of vitamin D supplementation. They found that children whose mothers took daily vitamin D supplements during pregnancy had stronger bones, with higher bone mineral density.

In the study, assessments made at age four showed improved bone health in these children. And follow-up assessments made at age seven also showed significant improvements in bone health. This implies that vitamin D supplementation contributes to a lasting increase in calcium and mineral content in bones, reinforcing the value of maternal vitamin D as a preventative measure against future bone health issues, including osteoporosis.

This suggests that epigenetic mechanisms may also be involved in the impact of vitamin D supplementation on bone outcomes later in childhood, although this has not yet been verified by research. In other words, although vitamin D supplementation by their mothers during gestation cannot change their genetics, it may change the way certain genes are expressed during their developmental years. Consider that the vitamin D receptor (VDR) is a nuclear, ligand-dependent transcription factor. When activated by the active form of vitamin D (1,25[OH]2D3), it regulates the expression of more than 900 genes in the body that play a role in a huge variety of chemical and physiological functions.

The results of this study add weight to those guidelines by verifying how supplemental vitamin D during pregnancy reduces the risk of bone-related health issues for newborns and developing children later in life, such as fractures and osteoporosis, this approach could contribute to reducing healthcare costs associated with bone health.

Beyond bone health, earlier findings from the trial indicated that vitamin D supplementation during pregnancy may reduce the likelihood of atopic conditions like eczema in infants up to a year old, showing vitamin D's potential to impact immune health. And the trial also verified that mothers receiving supplemental vitamin D were more likely to have spontaneous vaginal deliveries, potentially reducing the need for medical interventions during childbirth.

1. Press release. (2024, June 03). Endocrine Society Guideline recommends healthy adults under the age of 75 take the recommended daily allowance of vitamin D. Endocrine Society, Retrieved from https://www.endocrine.org/news-and-advocacy/news-room/2024/endocrine-society-recommends-healthy-adults-take-the-recommended-daily-allowance-of-vitamin-d

2. Moon, R. J., D’ Angelo, S., Curtis, E. M., Ward, K. A., Crozier, S. R., Schoenmakers, I., . . . Prentice, A. (2024). Pregnancy vitamin D supplementation and offspring bone mineral density in childhood follow-up of a randomized controlled trial. The American Journal of Clinical Nutrition, 120(5), 1134. Retrieved from https://pubmed.ncbi.nlm.nih.gov/39306330/

For decades we've noted that pregnancy significantly affects the clinical symptoms of microscopic colitis (MC) patients. Many patients who are currently in a flare, tend to experience a remission as their pregnancy progresses. And occasionally, the reverse occurs. In other words, patients who are in remission, experience a relapse of symptoms as their pregnancy develops. Theories about why this happens have usually focused on hormonal changes that occur during pregnancy.

And indeed, the hormonal changes that occur with pregnancy are numerous and relatively complex. Beginning 6 to 12 days after fertilization, trophoblast tissue in embryos (this tissue will eventually be part of the placenta) produces the chemical human chorionic gonadotropin (hCG), which promotes the production of progesterone and estrogen until the placenta takes over. Production of hCG peaks at around 10 weeks. hCG frequently triggers the symptoms of morning sickness.

As the pregnancy proceeds, many additional hormones are eventually produced to enhance the development of the fetus. And soon after these hormonal changes begin, the symptoms status changes for many MC patients, so it seemed logical that the hormonal changes might be the primary reason for the sudden remission of symptoms for some patients, and relapse of symptoms for others.

Enlarged villi and increased intestinal surface area enhance the uptake of essential nutrients, including sugars, proteins, and fats. And slowed food flow through the intestine due to the structural changes further optimizes nutrient absorption.​

The research showed that in mice lacking the RANK/RANKL pathway, the failure of intestinal adaptation led to altered milk composition. Babies born to such mothers exhibited reduced weight and glucose intolerance under metabolic stress, indicating transgenerational health effects.

The study showed that the intestinal expansion is reversed after lactation ends, providing a dynamic physiological adaptation, rather than a permanent change.​

Although this study was primarily conducted on mice, findings from human intestinal studies suggest that similar mechanisms should be applicable to humans.

Since this hasn't been specifically studied by any formal research projects, we can only speculate. However, it's well known that pregnancy itself is an inflammatory state due to the fact that the placenta produces cytokines that are capable of worsening the symptoms of IBD during pregnancy.

According to Doctor Daniel Stein, of RMA of New York, during pregnancy, the immune system must strike a delicate balance to support the developing baby while preventing its rejection as a foreign entity (Stein, 2020, October 26).3 One key component of this process involves T-lymphocytes (T-cells), which have distinct roles in the immune response. Cytotoxic T cells identify and destroy infected cells, while T-helper cells regulate other immune cells. These T-helper cells are further divided into subtypes with contrasting functions:​

TH1 cells produce cytokines that activate and enhance immune cell activity, promoting inflammation.
TH2 cells produce cytokines that suppress the immune response, reducing inflammation and preventing aggressive immune activity.

For a pregnancy to progress without complications, the balance between these cells is critical. A higher ratio of TH2 to TH1 cytokines is necessary to suppress excessive immune responses and avoid the rejection of the embryo.

Additionally, T regulatory cells (Tregs) play a crucial role in promoting the implantation of the embryo and facilitating the placenta's integration into the uterine wall. These cells help maintain immune tolerance to the fetus. Studies have shown that women with recurrent miscarriages or unexplained infertility often have reduced levels of T regulatory cells, highlighting their importance in supporting a healthy pregnancy.

This relatively critical balance between T cells may allow sufficient leeway for the inflammation level associated with pregnancy to overwhelm the state of remission associated with MC, to cause a relapse of MC symptoms. And although this hasn't been documented by research, it's possible that MC might have an effect on the balance between TH1 and TH2 cells under certain circumstances.

The reason why they're especially important is because if we are reacting, we have a malabsorption problem, and even if we're in remission, we're on a restricted diet, which may result in the development of deficiencies in certain vitamins and minerals, if not properly supplemented.​

Adequate nutrition is critical for not only a developing fetus, but the mother-to-be, also. And this is often a problem for mothers who do not have an IBD, making proper supplementation especially important for MC patients. Magnesium is particularly important. Many of us struggle to keep our magnesium reserves at a safe level, and adequate magnesium is especially critical during gestation.

In fact, Dr. Carolyn Dean, author of "The Magnesium Miracle", suggests that increasing magnesium reserves early on during pregnancy can help to prevent morning sickness, although that opinion isn't shared by most physicians.

1. Hashash, J, G. and Kanen S. (2015). Pregnancy and Inflammatory Bowel Disease. Gastroenterology & Hepatology, 11(2), pp 96–102. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC4836574/

2. Onji, M., Sigl, V., Lendl, T., Novatchkova, M., Ullate-Agote, A., Andersson-Rolf, A., , , Penninger, J. M. (2024). RANK drives structured intestinal epithelial expansion during pregnancy. Nature, Retrieved from https://www.nature.com/articles/s41586-024-08284-1

3. Stein, D. E. (2020, October 26). The Immune System and Pregnancy: How Your Body Can Turn on Itself. RMA of New York, retrieved from https://www.rmany.com/blog/the-immune-system-and-pregnancy-how-your-body-can-turn-on-itself

For years, antibiotics have been suspected of contributing to the development of microscopic colitis (MC). However, a major new study suggests this link may be overstated, and possibly a result of diagnostic bias, rather than a true biological effect.​

Researchers from the Karolinska Institutet in Sweden conducted a nationwide, self-controlled case series study examining 2,393 individuals aged 65 and older who were prescribed antibiotics and later diagnosed with biopsy-confirmed MC between 2007 and 2017.

The study was published in Alimentary Pharmacology & Therapeutics and also summarized by an online Medscape article under the headline “Antibiotics Getting False Blame for Colitis” (Szilcz. Wastesson, Bergman, Johnell, and Ludvigsson, 2025; Rai, 2025, February 21).”1, 2 The study found that:

​

• During antibiotic treatment there was a 44% increased risk of a diagnosis of MC (adjusted incidence rate ratio [aIRR] = 1.44)
• In the 3–12 months following-treatment, there was a 19% increased risk (aIRR = 1.19)
• The short-term risk (during the first 3 months after treatment) was modest or statistically insignificant

Antibiotics are frequently implicated because they commonly cause chronic, watery, nonbloody diarrhea, suggestive of MC. And because of this characteristic, subsequent investigation frequently uncovers pre-existing, asymptomatic cases of MC.

• 10 to 15% result in a diagnosis of MC.
• 30 to 50% have no visible or microscopic inflammation. This is often diagnosed as "functional diarrhea" or irritable bowel syndrome with diarrhea (IBS-D).
• 5 to 10% are found to be due to other microscopic abnormalities, including nonspecific colitis, drug-induced changes, or early IBD.
• 5 to 10% are found to have macroscopic inflammation, including Crohn's disease or ulcerative colitis (UC), with mucosal changes visible during the colonoscopy.
• 5 to 10% result in other diagnoses, including ischemic colitis, bile acid diarrhea, radiation colitis, or eosinophilic colitis.
• 10 to 15% result in nonspecific findings, or mild histologic changes, which may show subtle lymphocytic infiltration, mild edema, or inflammation without clear diagnostic criteria.
• 1 to 5% are found to have "infectious colitis" (this is often diagnosed by's stool tests, not colonoscopy)
• 1 to 2% may be attributed to colorectal cancer or polyps, although this is a somewhat rare cause of watery diarrhea, unless the tumor is large or secretory.

So based on the statistics, if antibiotics trigger chronic, watery, nonbloody diarrhea, it's not surprising that gastroenterologists might expect to find MC. But obviously a large portion of people with chronic diarrhea (30 to 50%) will have a completely normal colonoscopy, with normal, or near-normal biopsies, resulting in a diagnosis of IBS-D, functional diarrhea, medication -induced diarrhea (for example, metformin, SSRIs, PPIs, magnesium) or bile acid diarrhea (underdiagnosed unless specifically tested).

While it was shown that antibiotics do not cause MC, the study also found that antibiotic associated GI symptoms may lead to additional colonoscopies, thereby increasing the chance of detecting pre-existing MC.

Did the study prove that antibiotics cannot trigger symptomatic flares in previously asymptomatic MC? Well, no, because it didn't test that directly. What it did show was that the rise in MC diagnoses after antibiotic use was matched by a rise in normal colon biopsies, which implies that the antibiotics themselves may not be causing new disease, but rather unmasking existing conditions, by provoking the symptoms of diarrhea.

In other words, the study suggests that antibiotics might provoke symptoms in someone who has asymptomatic or subclinical MC, which then leads to investigation, and a diagnosis of MC. But there's no clear evidence that antibiotics cause MC where it did not exist previously, and no clear evidence that antibiotics convert asymptomatic MC into active disease (this was not specifically investigated).

Medications such as NSAIDs, SSRIs, and PPIs have also long been considered to be possible causes for the development of MC. In view of the findings of this large, well-controlled study that determined the long-held assumption that antibiotics are a significant cause of MC to be without merit, will research soon show that medications such as NSAIDs, SSRIs and PPIs do not cause MC, either?

Probably not, because unlike antibiotics (which don't generally cause chronic inflammation) NSAIDs, SSRIs, and PPIs can definitely cause chronic inflammation, and chronic inflammation commonly causes the development of MC.

1. Szilcz, M. Wastesson, J. W., Bergman, D., Johnell, K. and Ludvigsson, J. F. (2025). Antibiotic Use and Risk of Microscopic Colitis in Older Adults: A Nationwide Self-Controlled Case Series Study. Alimentary Pharmacology and Therapeutics, Retrieved from https://onlinelibrary.wiley.com/doi/10.1111/apt.70028

2. Rai, A. (2025, February 21). Antibiotics Getting False Blame for Colitis, Study Finds. Medscape, Retrieved from https://www.medscape.com/viewarticle/antibiotics-getting-false-blame-colitis-study-finds-2025a10004j5?ecd=mkm_ret_250418_mscpmrk_idhiv_antibiotic_etid7362030&uac=95382HN&impID=7362030

Caffeine appears to be the major pharmacologically active compound in coffee, and it's considered to be a mild central nervous system stimulant. Chlorogenic acids determine most of the taste of coffee, providing a range of flavor, depending on the concentration. And they're believed to be the source of the unpleasant taste that can be associated with prolonged brewing.​

Caffeine and chlorogenic acids enhance stress adaptation, reduce inflammation, improve metabolic health, and preserve cellular mechanisms crucial for aging, such as genomic stability (basically defined as the prevention of errors from DNA replication) and proteostasis (the process that regulates proteins within the cell in order to maintain the health of both the cell and the organism itself). And coffee acts as a "normalizer", stabilizing physiological symptoms rather than merely being a psychostimulant.

Another possible issue that might have caused results to be skewed is the possibility that individuals with certain pre-existing conditions (such as hypertension, arrhythmias, or digestive disorders) may avoid drinking coffee.​

And while caffeine and chlorogenic acids are the most studied components, coffee contains thousands of bioactive compounds with uncertain individual contributions to health benefits. It's unknown whether any of these compounds have any effects on issues such as stem cells and tissue regeneration.

Consistent epidemiological trends suggest that coffee can improve longevity and reduce age-related diseases, although causation remains uncertain. Coffee may transition from being seen as a stimulant or indulgence, to a health-promoting beverage, and moderate coffee consumption could be considered part of a healthy lifestyle, especially for aging populations.​

While coffee may offer health benefits, it's not a cure-all. Benefits likely depend on individual health, genetics, and lifestyle factors. Excessive consumption or consumption by those with contraindications (such as anxiety, insomnia, or heart conditions) may counteract potential benefits.

That's a fair question, in view of the general recommendations by most doctors that IBD patients should avoid drinking coffee. But as most of us have found, as long as we don't add anything to the coffee that's contraindicated for MC patients, if coffee didn't cause major digestive system problems for us before we developed MC, then it shouldn't cause any major problems after we develop MC.

And even if it doesn't turn out to be the fountain of youth for us, it's definitely one of life's little pleasures that most of us would rather not eliminate from our daily routine. It gives us something to look forward to every morning, and adds to our enjoyment of life. And if it's actually improving our health, and extending our longevity in the process, how could that not be a good thing?

That said, that doesn't mean that all of us can safely drink 3 cups of coffee every morning, especially while we're still recovering. We all have to determine our boundaries as we fine tune our diet, and coffee is no exception. Consequently, most of us will find that our coffee drinking has to be adapted to our own individual needs.

1. Jackson, J. (2024, December 9). Industry-funded study suggests coffee really is the fountain of youth. Medical Xpress, Retrieved from https://medicalxpress.com/news/2024-12-industry-funded-coffee-fountain-youth.html?utm_source=nwletter&utm_medium=email&utm_campaign=daily-nwletter

2. Lopes, C. R. and Cunha, R. A. (2024). Impact of coffee intake on human aging: Epidemiology and cellular mechanisms. Ageing Research Reviews, 102, 102581. Retrieved from https://www.sciencedirect.com/science/article/pii/S1568163724003994?via%3Dihub

Recently published research shows that antibiotics damage the protective mucus layer (of the epithelia) in the intestine, independent of microbiota changes (Sawaed, et al., 2024).1 This appears to be an important discovery for microscopic colitis (MC) patients, as MC, like other IBDs, involves chronic inflammation of the intestinal lining. The disruption of the mucosal barrier (by an antibiotic treatment) could potentially worsen MC symptoms by exposing the intestinal epithelium to bacteria, triggering immune responses and exacerbating inflammation. Most of us are well aware of this problem, and many of us have been aware of it for many years. But now, the medical community is officially aware of it, also.​

For many years after MC was first medically described, researchers suspected that IBD (especially Crohn's disease) might be caused by a bacterium similar to the one that causes Johne's disease in ruminants (Mycobacterium avium subspecies paratuberculosis [MAP]). But no research studies have ever been able to prove that connection. While this new discovery supports the probable role of pathogenic bacteria in the actual physical damage to the mucosal barrier (that initiates the development of IBD), the smoking gun that provides the opportunity for those bacteria to gain access to the mucosal barrier has been shown to be the use of antibiotics.​

Depending on the details of the particular health issue that is prompting our doctor to make that recommendation, there may be some leeway in the choice of antibiotics. But if the reason for using an antibiotic is a life or death matter, there may not be much leeway — we may just have to do what we have to do, and hope for the best.

Let's consider two categories for these antibiotic selections that are least likely to trigger a reaction for MC patients.

1. Narrow-Spectrum Antibiotics — Narrow-spectrum antibiotics target specific bacteria and tend to have less impact on the gut and systemic health compared to broad-spectrum antibiotics. This makes them a safer option for MC patients. However, their safety still depends on the specific drug and individual response. They are effective for targeted bacterial infections, but their utility is limited to bacteria they are specifically designed to treat. For infections that involve resistant bacteria or multiple types, their efficacy may be lower.

2. Penicillin Derivatives (for example, Amoxicillin, Amoxicillin-Clavulanate) — Penicillin derivatives like amoxicillin are generally well-tolerated and are considered among the safer antibiotics for people with gut issues, including MC. However, combinations like amoxicillin-clavulanate (Augmentin) may cause “mild” gastrointestinal disturbances, so they should be used cautiously. Penicillin derivatives are highly effective for a broad range of bacterial infections, including respiratory, skin, and soft tissue infections. Amoxicillin, in particular, is a first-line treatment for many infections.

Despite that endorsement based on theoretical considerations, it should be noted that our shared experiences on our discussion forum suggest that amoxicillin causes many of us to react with diarrhea, although that doesn't necessarily mean that the antibiotic is triggering an MC reaction. Diarrhea is a labeled side effect of many, possibly most, antibiotics.

3. Cefuroxime — Cefuroxime is a second-generation cephalosporin with a relatively narrow spectrum of activity. While safer than some broad-spectrum cephalosporins, it can still have moderate effects on the gut, so it should be used with caution by MC patients. It is effective against respiratory tract infections, skin infections, and urinary tract infections (UTIs). It’s not as broad-spectrum as other cephalosporins but remains a reliable option for many bacterial infections.

4. Macrolides (for example, azithromycin, clarithromycin) — Macrolides are often used in penicillin-allergic patients and have a lower impact on the gut microbiome compared to some other antibiotic classes. They are generally considered safer for MC patients, but prolonged use can still pose some risks to gut health. Macrolides are effective for respiratory infections, certain skin infections, and atypical bacterial infections. Azithromycin is particularly known for its shorter duration of therapy and fewer side effects.

5. Nitrofurantoin — Nitrofurantoin is minimally absorbed in the gut, meaning it has limited systemic effects, including on the gastrointestinal system. This makes it a very safe choice for MC patients, especially when treating urinary tract infections (UTIs). Nitrofurantoin is highly effective for treating UTIs but is not useful for infections outside the urinary tract, which limits its broader applicability.

6. Rifaximin — Rifaximin is minimally absorbed systemically and acts locally in the gut. It is often used to treat conditions like irritable bowel syndrome (IBS) and small intestinal bacterial overgrowth (SIBO) without significantly disrupting the gut microbiome. It’s considered one of the safest antibiotics for gut-sensitive patients, including those with MC. Rifaximin is highly effective for gastrointestinal-related infections but is not a broad-spectrum antibiotic for systemic infections. Its use is mainly limited to gut infections and conditions like traveler’s diarrhea or hepatic encephalopathy.

When rifaximin first became available, many gastroenterologists were prescribing this antibiotic as a treatment for MC. And for some patients, it did indeed seem to control the symptoms for a week or two. But following that brief respite, symptoms virtually always returned. It was originally labeled for "traveler's diarrhea", and that's probably it's best use.

7. Fluoroquinolones (for example, levofloxacin, ciprofloxacin) — Fluoroquinolones are associated with a range of serious side effects, including risks of tendinitis, and neuropathy. Fluoroquinolones are broad-spectrum antibiotics that are highly effective against a wide range of infections, including respiratory, urinary, and gastrointestinal infections. However, their high efficacy comes with significant safety trade-offs, especially for long-term or recurrent use. Note that the U.S. Food and Drug Administration (FDA) has imposed regulations that require black box warnings against the possibility of tendon or neurological damage due to the use of fluoroquinolones (Tanne, 2008, July 19).2​

Note that these are also included in the "theoretically safe" category above, but they have been found to be safe for most of us by our personal experiences.

​So please don't write the warnings off as "trivial". Ciprofloxacin (similar to the other fluoroquinolones) depletes magnesium, and as we have learned in the school of hard knocks, magnesium deficiency opens the door to many adverse consequences. Similarly, magnesium diminishes the effectiveness of Cipro. Therefore, although it's important for us to replenish our magnesium reserves while we're taking Cipro, we have to be careful not to take the Cipro and a magnesium supplement at the same time, because if we do, each one will antagonize the other. In other words, we need to allow enough time after taking Cipro for it to be absorbed into our bloodstream, before taking any magnesium supplements.

Although the following viewpoint has never been proven by medical research, (because it has never been trialed or researched), epidemiological evidence suggests that the risks reflected in the black box warnings regarding the use of fluoroquinolones, are due to the effects of magnesium deficiency.​

Consequently, it appears that individuals who use any of the fluoroquinolones are at risk of tendon damage, or neurological damage, for example, if they allow their magnesium level to be depleted. Those who maintain an adequate magnesium level, don't appear to have an increased risk of tendon or neurological damage. But please remember that since this has never been proven by medical research, it must be regarded strictly as speculation. And just as there are never any guarantees that published medical research findings are valid proof that a medication will work well for everyone, there certainly are no guarantees that any statement based on speculation is valid for everyone (or anyone, for that matter).

1. Topical Antibiotics (First Choice)
​

• Mupirocin
• Bacitracin and Neomycin
  
  

2. Oral Antibiotics (When Topicals Are Not Sufficient)

• Ciprofloxacin (not for patients who are magnesium deficient)Azithromycin
• Cephalexin
• Clindamycin
• Sulfamethoxazole-Trimethoprim (Bactrim) (particularly skin infections caused by MRSA)​

1. Pre-Surgical Prophylactic Antibiotics

• Cefazolin (Ancef)
• Cefuroxime

​2. For Penicillin-Allergic Patients

• Clindamycin
• Vancomycin

3. Metronidazole
4. Ampicillin-Sulbactam (Unasyn)
5. Gentamicin

1. Sawaed, J., Zelik, L., Levin, Y., Feeney, R., Naama, M., Gordon. A., . . . Bel. S. (2024). Antibiotics damage the colonic mucus barrier in a microbiota-independent manner. Science Advances, 10(37), p 4119. Retrieved from https://www.science.org/doi/10.1126/sciadv.adp4119

2. Tanne, J. H. (2008, July 19). FDA adds "black box" warning label to fluoroquinolone antibiotics. BMJ, 337(7662), a816. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2483892/