Personally, I have long held the opinion that many of us have pancreatic inflammation associated with our microscopic colitis (MC), especially if our disease is not put into remission promptly. Decades ago, when I developed MC, I'm reasonably certain that I had an inflamed pancreas, because I obviously didn't have the enzymes needed to properly digest my food (and I had several of the symptoms mentioned below). Back then, it rarely occurred to gastroenterologists to even test for pancreatic insufficiency. But there was no reason to be concerned, because those enzyme deficiencies were slowly resolved after I eliminated the foods from my diet that were causing my immune system to produce antibodies.

And I've always felt that it's typical for problems caused by an inflamed pancreas to resolve for most of us, when our MC is put into remission. But these days, gastroenterologists are beginning to diagnose pancreatitis in MC, and other inflammatory bowel disease (IBD) patients with increasing frequency. And although the pancreatitis is associated with the IBD, they choose to treat it as if it were a separate issue. But is the extra cost and inconvenience experienced by the patient worth it? Let's consider the facts

Common IBD medications such as azathioprine, 6-mercaptopurine, and some biologics,can trigger acute pancreatitis, typically within 90 days of initiation (Wikipedia, n.d.).3 Especially in Chron's disease (due to terminal ileal disease), gallstone formation can cause acute pancreatitis, independent of medications (Antonini, Pezzilli, Angelelli, and Macarri, 2016). Note that similar to Crohn's disease, MC typically concentrates the highest concentration of inflammation in the ileum, in many (possibly most) cases.

But remember, all the studies cited here excluded MC patients, so we can only make an educated guess as to whether MC has a greater or lesser chance of causing pancreatic inflammation. But based on our own experiences, as evidenced by the shared experiences found in the database of the discussion and support forum associated with the Microscopic Colitis Foundation, a relatively high percentage of us appear to have issues associated with an inflamed pancreas when our disease is in a flare.​

The evidence suggests that in most cases,especially when pancreatitis is directly linked to medications, gallstones, or autoimmune causes, pancreatic inflammation resolves alongside IBD remission, or after the offending factor is removed. In a cohort of ulcerative colitis (UC) patients, those who developed type 2 autoimmune pancreatitis were typically treated with corticosteroids (Kim et al., 2017).4 All patients recovered uneventfully, with no recurrence during follow-up (median 28 months), even while UC remained in remission.​

In cases where pancreatitis appears as an extra-intestinal manifestation of IBD (described above), especially in Crohn’s disease, some studies show that pancreatic complications improve in tandem with bowel inflammation, although specific remission data is limited (Daniluk et al., 2023).5 This pediatric research also indicates that elevation in pancreatic enzyme levels frequently subsides once IBD goes into remission, supporting a parallel disease course.

Unfortunately, that's not an easy question to answer. The best answer may be, "It depends".
With or without diagnosis and treatment, pancreatitis will usually resolve when MC goes into remission. And because intestinal healing is slow, due to stem cell damage caused by the chronic inflammation, digestive system healing time is going to be slow, with or without any intervention, including diet changes.

That said, in cases where weight loss due to incomplete digestion is a major problem, treating pancreatitis (assuming that it's causing significant digestive enzyme deficiencies) may be beneficial, for several reasons:

Incomplete digestion causes:

• Watery diarrhea
• ​Malabsorption
• Fatty stools (steatorrhea
• Gas generation, bloating, and urgency
  

​Treating pancreatitis could help restore digestive enzyme output, improve nutrient absorption, and reduce diarrhea or urgency, (if pancreatic insufficiency is a contributing factor).

if the treatment introduces gut-disrupting medications (for example, PPIs, antibiotics, or NSAIDs), it may slow down healing or reactivate inflammation, or even cause an MC flare. Treatments such as:

1. Enzyme replacement therapy (for example, pancrelipase):

• Is usually safe and often beneficial in chronic or subclinical pancreatitis
• Rarely causes flares unless additives (such as lactose or artificial coloring) are problematic for sensitive MC patients

2. Steroids (for example, prednisone or budesonide),
Used for autoimmune pancreatitis or severe flares could either help or hurt:

• May help both conditions by suppressing immune overactivity
• But long-term use or tapering can destabilize MC if not managed carefully

3. Antibiotics (for example, if used for infected pancreatic necrosis):

• Certain antibiotics are known to cause or exacerbate microscopic colitis(for example, amoxicillin, cephalosporins, macrolides)
• Could trigger an MC flare in susceptible patients, especially if used without a clear need

4. NSAIDs (sometimes used for pain):

• Well-documented triggers for MC
• Should be avoided whenever possible

5. Changes in diet:

• Pancreatitis treatment often involves a low-fat diet, which may already be part of an MC patient’s routine
• ​But introducing new processed low-fat foods could inadvertently include triggers (due to gums, additives, soy, gluten, casein, or some other allergen)

It's quite plausible, and in some cases likely, that microscopic colitis (MC) patients with severe, unexplained weight loss may have underlying pancreatic insufficiency or pancreatitis, especially if they exhibit certain overlapping symptoms. This connection is often underdiagnosed or overlooked in clinical practice (gastroenterologists tend to view MC treatment as a one-size-fits-all situation. A connection between MC and pancreatitis (or pancreatic insufficiency) makes sense in this situation because there can be:

1. Shared mechanisms of inflammation:

• Both MC and pancreatitis may be driven by immune system dysregulation, including autoimmune syndromes, mast cell activation, or lymphocytic infiltration.
• Some IBD-related cases (especially Crohn’s) are associated with autoimmune pancreatitis, and similar patterns may apply in MC, despite not being studied by dedicated research projects.

2. Malabsorption and weight loss

Pancreatic insufficiency causes fat malabsorption, which leads to:

• Steatorrhea (greasy, floating stools)
• Deficiencies in fat-soluble vitamins (A, D, E, K)
• Muscle wasting and progressive weight loss
• These symptoms can mimic or compound MC, making it difficult to separate the causes without specific testing.

3. Overlapping symptoms

• Chronic watery diarrhea
• Weight loss
• Abdominal pain (esp. upper)
• Fatty, foul-smelling stools
• Nutrient deficiencies

For most of us, whether or not our pancreas might be inflamed because of the inflammation caused by our MC, is irrelevant, due to the fact that after we put our MC into remission, any pancreatic issues will probably be automatically resolved. But for those of us who have severe weight loss, or despite having MC in remission for many months, are still unable to gain any weight (assuming that more than enough calories are being ingested), treating a pancreatitis issue could be beneficial. It might be time to ask our gastroenterologist to test for pancreatitis.

1. Antonini, F., Pezzilli, R., Angelelli, L., and Macarri, G. (2016). Pancreatic disorders in inflammatory bowel disease. World Journal of Gastrointestinal Pathophysiology, 7(3), pp 276–282. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC4981767/

2. Massironi, S., Fanetti, I., Viganò, C., Pirola, L., Fichera, M., Cristoferi, L., . . . Danese, S. (2022). Systematic review-pancreatic involvement in inflammatory bowel disease. Alimentary Pharmacology & Therapeutics, 55(12), pp 1478–1491. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC9322673/

3. Wikipedia, (n.d.). Chron's disease. Wikipedia, Retrieved from https://en.wikipedia.org/wiki/Crohn%27s_disease

4. Kim, J. W., Hwang, S. W., Park, S. H., Song, T. J., Kim, M-H., Lee, H.-S., . . . Yang, S.-K (2017). Clinical course of ulcerative colitis patients who develop acute pancreatitis. World Journal of Gastroenterology, 23(19), pp 3505–3512. Retrieved from https://www.wjgnet.com/1007-9327/full/v23/i19/3505.htm

5. Daniluk, U., Krawiec, P., Pac-Kożuchowska, E., Dembiński, Ł., Bukowski, J. S., Banaszkiewicz, A., , , , Lebensztejn, D. M. (2023). Pancreatic Involvement in the Course of Inflammatory Bowel Disease in Children—A Multi-Center Study. Journal of Clinical Medicine, 12(13), 4174. Retrieved from https://www.mdpi.com/2077-0383/12/13/4174

A study analyzing data from nearly 30,000 Americans shows how restrictive dieting can increase depressive symptoms, with particularly pronounced effects in men and individuals with higher body mass index (BMI) (Menniti, Meshkat, Lin, Lou, Reichelt, and Bhat, 2025).1 Published in BMJ Nutrition, Prevention & Health, this research challenges common assumptions about the universal benefits of calorie restriction, and suggests a need for more personalized approaches to dietary interventions.

who participated in the US National Health and Nutrition Examination Survey (NHANES) between 2007 and 2018. Participants completed comprehensive dietary assessments alongside the Patient Health Questionnaire-9 (PHQ-9), a validated tool for measuring depression severity. This cross-sectional approach provided researchers with substantial data to examine the relationships between restrictive dietary patterns and mental health outcomes across various populations.

The study specifically focused on two main types of dietary restriction: calorie-restrictive diets (limiting overall energy intake) and nutrient-restrictive diets (eliminating specific food groups or nutrients). These patterns were compared against individuals following no specific dietary restrictions to identify potential mental health consequences of common dieting approaches.

The results showed a clear association between restrictive dieting and increased depressive symptoms. Overall, individuals following calorie-restrictive diets showed a 0.29 point increase in PHQ-9 depression scores compared to those not following any specific diet. While this might seem modest, it represents a measurable shift toward more significant depressive symptoms across large populations.
​
The study identified 2,508 participants (7.79% of the total sample) who self-reported symptoms of depression, providing a substantial cohort for analyzing the relationship between dietary patterns and mental health outcomes. This prevalence aligns with national depression statistics, suggesting that the findings of the study are representative of the broader American population.

Men demonstrated particularly pronounced susceptibility to diet-related mental health effects. Male participants following restrictive diets showed higher somatic symptom scores (physical manifestations of depression such as fatigue, sleep disturbances, and appetite changes) compared to men not following specific diets. Additionally, men on nutrient-restrictive diets experienced a 0.40 point increase in cognitive related symptom scores, including mood changes, concentration difficulties, and negative thought patterns.

This gender disparity may reflect several factors. Men typically have higher baseline caloric and nutritional requirements due to greater muscle mass and metabolic demands. When these needs aren't met through restrictive dieting, the physiological stress may manifest more readily as depressive symptoms. Additionally, men may be less likely to recognize or address the emotional impacts of dietary changes, allowing symptoms to accumulate before being acknowledged.

The finding that men experience more somatic symptoms aligns with broader research showing that depression in men often presents differently than in women, with physical symptoms sometimes predominating over emotional ones. This pattern suggests that healthcare providers should be particularly vigilant for depression symptoms in male patients undertaking restrictive diets.

Individuals with elevated BMI showed increased vulnerability to diet-related depressive symptoms. Overweight participants following calorie-restrictive diets experienced a 0.46 point increase in PHQ-9 scores, while those on nutrient-restrictive diets showed an even more substantial 0.61 point increase. These findings are particularly concerning given that overweight individuals are often specifically encouraged to pursue restrictive dieting for health benefits.

This relationship may reflect the complex interplay between weight stigma, diet culture pressures, and the psychological stress of restriction. Individuals with higher BMI often face societal pressure to diet and may experience shame or guilt around food choices, potentially amplifying the mental health impacts of dietary restriction. Additionally, the metabolic changes associated with calorie restriction, including alterations in hormones like leptin and ghrelin, may have more pronounced effects on mood regulation in individuals with higher baseline weight.

since those most likely to be prescribed restrictive diets for health benefits may be the most vulnerable to the associated mental health consequences. This finding underscores the need for careful monitoring and potentially alternative approaches for weight management in higher BMI populations. And it certainly helps to explain why the GLP-1 medications are so popular, despite their numerous side effect risks.

The relationship between dietary restriction and depression likely involves multiple interconnected pathways. Calorie restriction can lead to significant physiological changes, including alterations in neurotransmitter production, hormone regulation, and blood sugar stability, and all of these factors directly influence mood and cognitive function.

Nutritional deficiencies common in restrictive diets may particularly impact brain function. Essential nutrients including omega-3 fatty acids, B vitamins, vitamin D, and minerals like zinc and magnesium play crucial roles in neurotransmitter synthesis and neural protection. When restrictive diets eliminate entire food groups or severely limit caloric intake, these critical nutrients may become insufficient to support optimal brain function.

The psychological stress of restriction itself compounds these physiological effects. Food restriction can increase cortisol production, trigger anxiety around food choices, and create cognitive burden from constant dietary monitoring. These psychological stressors may be particularly burdensome for individuals already managing weight-related stigma or pressure to achieve unrealistic body standards.

Although the research findings didn't consider this, a degree in psychiatry is certainly not needed for anyone to recognize that the association with depression enhancing factors such as adverse neurotransmitter production, hormone regulation, and blood sugar stability, is almost surely the main reason why most patients who attempt-restricted diets are unable to maintain them in the long run. Apparently, those few who are able to successfully follow a restricted diet for the long term are unusually dedicated individuals who are able to “soldier through” despite oppressive symptoms that finally overwhelm most people.

Reviews of randomized controlled trials show that only 20–35% of dieters maintain strict adherence for 1 year, and roughly 10–20% sustain meaningful calorie restriction and weight loss for 2–5 years.​

The fact that such a small percentage of dieters are able to stick with a restricted diet for the long term, suggests that virtually everyone experiences these symptoms to at least some extent. That doesn't bode well for the future of dieting to accomplish the goal of weight loss. Yet physicians continue to recommend dieting and patients continue to attempt to follow that advice.

Obviously most healthcare providers may need to reconsider their procedures for prescribing or recommending restrictive diets. The research suggests that dietary interventions should be tailored, based on patient sex, and BMI status, with special monitoring for depressive symptoms in high-risk groups, such as men and individuals with elevated BMI.

Rather than severe calorie restriction, gradual reductions in caloric intake while maintaining nutritional adequacy may minimize mental health risks. Emphasizing food quality over quantity, incorporating regular physical activity, and addressing psychological relationships with food may provide more sustainable and mentally healthy approaches to dietary change.

Hundreds of diets have been promoted over the decades, but they've all been vulnerable to the limiting factors highlighted by this study. While nutrient-restricted diets will continue to be effective for treating autoimmune diseases such as IBD, calorie-restricted diets will continue to be doomed to fail, unless some sort of honest-to-goodness research breakthrough occurs.

1. Menniti, G., Meshkat, S., Lin, Q., Lou, W., Reichelt, A., and Bhat, V. (2025). Mental health consequences of dietary restriction: increased depressive symptoms in biological men and populations with elevated BMI. BMJ Nutrition, Prevention & Health, (8). Retrieved from https://nutrition.bmj.com/content/8/1/10

Our primary method for measuring blood pressure remains essentially unchanged since the early 1900s. The basic framework, developed by Scipione Riva-Rocci in 1896, and refined by Dr. Nikolai Korotkoff in 1905, still forms the foundation of both manual and automated systems used today. While we've added automation, digital displays, and smartphone connectivity, the core measurement principle hasn't evolved to address the fundamental accuracy limitations that have persisted for over a century.​

This technological stagnation becomes particularly problematic when we consider how much medical decision-making relies on blood pressure readings. Unlike many diagnostic tests that serve as rough indicators, blood pressure measurements directly drive treatment thresholds, medication dosing, and risk stratification. Physicians rely on them as if they were "gospel". Yet the underlying technology predates the invention of the airplane.

Beyond the inherent limitations of the measurement technology itself, numerous factors can introduce additional errors that compound the problem:​

Patient preparation failures are endemic. Ideally, patients should sit quietly for at least five minutes before measurement, yet this rarely happens in busy clinical settings. Even talking during measurement can raise systolic pressure by 10–15 mm Hg. During clinic appointments, medical assistants spend most of their time asking questions of patients to fulfill the requirements of the mandated electronic health records (EHR) system, then they immediately take blood pressure readings without allowing additional time for the patient to relax.

Positioning errors are commonplace. Crossed legs or dangling feet can raise systolic BP by 2-8 mm Hg, while unsupported arms or backs increase readings further. A full bladder common in medical appointments can add another 10-15 mm Hg.

Cuff sizing problems remain widespread despite decades of awareness. Too-small cuffs overestimate pressure, while too-large cuffs underestimate it. With the increasing prevalence of obesity and the sex-based fit issues described above, proper cuff selection has become more critical and more challenging.

Environmental and behavioral factors introduce additional variables. Recent caffeine, nicotine, or alcohol consumption, physical activity, cold environments, and the well-known "white coat syndrome" all skew readings in unpredictable directions.

When multiple error sources combine, a stressed, improperly positioned patient with an ill-fitting cuff measured by an inadequately calibrated device — the cumulative error can be substantial enough to completely alter treatment decisions.

Research reveals a disconnect between how blood pressure measurements are supposed to work and how they actually perform in clinical practice. While cardiologists and experienced clinicians understand these limitations and typically require multiple readings across different settings before making treatment decisions, the broader healthcare system often treats individual readings as definitive.​

Dr. Khashayar Hematpour, a cardiologist at UTHealth Houston, notes that specialists "already know you don't diagnose and treat hypertension based on one or two readings in the office." However, this understanding hasn't consistently translated to practice across all healthcare settings, particularly in primary care environments where time pressures and workflow demands may prioritize efficiency over measurement precision.

These accuracy limitations raise fundamental questions about how we should interpret and use blood pressure readings. If stress-related blood pressure elevations are associated with significantly increased mortality risk due to cardiovascular events, why do we focus primarily on resting readings? Perhaps the variability we've been trying to eliminate actually contains valuable diagnostic information.​

Some researchers suggest that blood pressure reactivity — how much pressure rises in response to stress, medical environments, or daily activities, may be more predictive of future cardiovascular events than carefully controlled resting measurements. This would represent a paradigm shift from viewing measurement variability as error to recognizing it as clinically relevant data.

Addressing blood pressure measurement accuracy requires action on multiple fronts. In the immediate term, healthcare systems need better protocols for measurement standardization, including proper patient preparation, cuff sizing, and positioning. Calibration schedules for automated devices need enforcement, and staff training on proper technique requires reinforcement.

More fundamentally, we need measurement technologies designed for 21st-century medicine rather than adapted from 19th-century innovations. Emerging cuffless technologies using optical sensors, tonometry (measuring pressures inside the eye), or pulse transit time show promise, though none yet match cuff-based accuracy across all patient populations.​

And probably most importantly, clinical guidelines need updating to reflect the reality of measurement variability. Rather than treating different measurement methods as interchangeable, we need method-specific reference ranges and treatment thresholds that account for the systematic differences research has now clearly documented.

Blood pressure measurement accuracy matters because hypertension is both common and consequential. As a "silent killer" that often produces no symptoms until catastrophic events occur, accurate measurement represents our primary defense against cardiovascular disease. When that defense is compromised by measurement inaccuracy, the health consequences ripple through entire populations.

The current situation represents a critical gap between the precision medical decision-making requires and the accuracy our measurement tools actually provide. Closing this gap, through better technology, improved protocols, or more nuanced interpretation of existing measurements, represents one of the most important opportunities for improving cardiovascular care quality and outcomes.

Until we address these fundamental accuracy limitations, millions of patients worldwide will continue receiving treatment decisions based on measurements that may be systematically wrong. For a diagnostic test performed billions of times annually, even small improvements in accuracy could prevent countless heart attacks, strokes, and premature deaths while avoiding the costs and side effects of unnecessary treatment for others.​

One thing stands out — the technology that measures our blood pressure hasn't kept pace with our understanding of cardiovascular disease. Surely we're capable of developing the technology to bridge that gap.

1. Yeh, J-T., Huang, C-J., Lee, C-W., Chen, Y-J., Huang, S-L., Wang, W-T., . . . Cheng, H-M. (2025). Agreement Between Different Types of Blood Pressure Monitoring: A Systematic Review and Network Meta-analysis. Annals of Internal Medicine, Retrieved from https://www.acpjournals.org/doi/10.7326/ANNALS-24-02142

2. Spriano, P. (2025, August 04). Why Your Arm Shape Skews Blood Pressure Readings. Medscape, Retrieved from https://www.medscape.com/viewarticle/why-your-arm-shape-skews-blood-pressure-readings-2025a1000kno