Guest Case Study: A Young Female with Chronic Diarrhea Responds Well to Basic Gut Support

GUEST CASE STUDY PROVIDED BY: SCOTT SPIRIDIGLIOZZI, ND
SUPERVISING CLINICIAN: ROB ABBOTT, MD

Patient Info:

• Susan is 21 year old female college student
• Previous Dx
  • n/a
• Rx
  • Omeprazole 20 mg as needed for abdominal pain
  • Oral Contraceptive Pill (OCP)
• Chief Complaints
  • Urgent Diarrhea – 2-4x/day
  • Bloating – Daily
  • Abdominal Pain – Daily and significant
  • Belching – Daily
  • Nausea – happens about once per week, mild
• Other Symptoms
  • Eczema
  • Asthma
  • Fatigue

Visit 1 (Day 1) – History and Exam:

• Initial Impression:
  • Susan is a 21 yo college female who presents on a zoom call appearing quite tired with a flat affect
• Rx
  • Omeprazole 20 mg prn
  • OCP
• Previous Testing
  • Abdominal Ultrasound – WNL
  • OPx3 Stool Test – WNL
• Onset
  • Began 3 months ago from the time of our first visit. Prior to the onset of her symptoms, she was asymptomatic.
  • She then developed urgent diarrhea, abdominal pain, bloating and belching. Fatigue has also increased.
  • Stools were loose, unformed, and multiple times per day.
  • She reported moving into a new college apartment from a previous home approximately one month prior to her GI symptom development
  • Additionally, she reported some significant water damage in the new apartment soon after her move in.
• Family History
  • Not significant
• Prior Treatments
  • Omeprazole for epigastric abdominal pain, which brings on some symptomatic relief. Takes a few times per week.
• Assessment
  • In evaluating her new onset symptoms, I am suspecting that her change in dietary habits coinciding with a move into the college apartment – eating more processed, nutrient poor foods is behind most of her GI complaints.
  • It is also interesting to note the water damage to her apartment building that could be an additional contributor to her symptoms.
• DDX
  • Food intolerances/sensitivities
  • IBS-D
  • Dysbiosis
  • SIBO
  • Celiac disease
• Prognosis
  • Good to Excellent
• Initial Testing
  • CBC, CMP, Iron Panel, Vitamin D, B12, Celiac Panel
  • Stool Calprotectin and Fecal Occult Blood
  • Food sensitivity test – Patient Requested
• Rationale
  • Given her looser stools and fatigue, I would like to assess for potential anemia, electrolyte disturbances, and common nutritional deficiencies.
  • As she was consuming gluten-containing foods, I also suggested completing a screen for celiac disease.
  • While unlikely, I wanted to rule out microscopic blood in her stool or an inflammatory process more suggestive of IBD. I did not feel her symptoms warranted further, more expensive functional stool testing at this point in time.
  • The patient insisted on food sensitivity testing. I expressed the limited clinical utility of this type of testing, however, I obliged her request.
• Initial Recommendations
  • 1-3 day bone broth fast prior to starting the paleo diet
  • Paleo diet
  • Triple probiotic therapy
    • Saccharomyces boulardii
      
      
    • Bifido/Lacto
      
    • Soil-Based Probiotic
      
  • Digestive Enzymes by Designs for Health: 1 capsule per meal
    
• Rationale
  • With regards to the diet, I expressed to her that she would likely benefit from a more nutrient-dense, less processed way of eating. I shared that the elimination period is not a “forever diet,” but a mini-experiment to see how her body responded. I encouraged her to try her best, but avoid the need to be 100% perfect and that she should give the dietary experiment at least 3 weeks.
  • In suggesting the Paleo template over a Paleo low FODMAP template, I recognized the patient would likely be more successful with a less restrictive diet given her current living situation.
  • I love this dietary approach with college students because it is more practical and helps to minimize anxiety or create unnecessary restrictions.
  • In addition to the dietary template, I felt that she would benefit from some initial GI supportive therapies, most notably triple probiotics and a trial of digestive enzymes. There was no indication at this time for the use of herbal or prescription antimicrobials or a more complicated GI treatment.

Visit 2 (3 Weeks Later) – Lab Review and First Follow-Up Visit

• Subjective Assessment:
  • Abdominal pain upon awakening: 70% improved
  • Loose stool: 40% improved
  • Nausea: Resolved
  • Stool Urgency: 40% improved
  • Bloating: Slightly improved
• Additional Notes:
  • Patient notified me that they found mold in their apartment as determined by an IEP. She stopped taking her PPI as she no longer had symptomatic needs or previously noted benefits.
• Lab Interpretation:
  • Normal Calprotectin
  • Negative occult blood
  • Negative celiac profile
  • 25 – Vitamin D: 13
  • B12: 330 (Low normal)
  • US BioTek Food Sensitivity IgG Testing Results
    • 3 and 4 Reactivity Foods: Chestnuts, Cane Sugar, Chocolate/Cocoa Bean, Candida Albicans
    • 2 Reactivity Foods: Oats, Wheat, Almonds, Banana, Cantaloupe, Figs, Mushrooms, Baker’s/Brewers Yeast
    • 1 Reactivity Foods: Dairy
• Diagnosis:
  • Vitamin D Deficiency
  • IBS-D
  • Dietary mismatch
• Impression:
  • Overall, after just a few weeks of making dietary changes and starting some probiotics, she has noticed multiple positive improvements in her symptoms. I am suspecting she is suffering primarily from dysbiosis and dietary mismatch. Her Vitamin D is remarkably low, likely secondary to her geographic location, the winter season, increased time indoors, and a lack of previous supplementation.
  • Her food sensitivity testing is clinically unremarkable as expected. It’s possible some of the fungal elements that are positive on her testing are connected to underlying gut dysbiosis and environmental – mold exposures.
• Recommendations:
  • Continue Paleo given her progress to date
  • Vitamin D: 10,000 IU for 30 days, then reduce to 2,000 IU once/day
  • Temporarily move out of apartment if possible
  • Increase doses of each probiotic
  • I encouraged her to seek alternatives to daily consumed foods noted on her testing (any benefit derived from this would likely be related to removing high carbohydrate content foods or psychologically driven “safety” from the avoidance of “allergic” foods).
  • I suggested she could consider the avoidance of fermented foods to see if this has any further impact on her symptoms.
  • Follow up in 4 weeks

Visit 3 (1 Week Later) – Follow-Up Message

• Susan notified me that upon increasing the triple probiotics, she experienced a worsening in abdominal pain. I suggested decreasing her probiotics back to previous levels with the additional consideration of the cessation of boulardii. In following these recommendations she reported that the worsening of her symptoms resolved and she returned to her previous state of improved health.

Visit 4 (3 Weeks Later) – Follow-Up Visit

• Subjective Assessment:
  • Abdominal Pain: Resolved
  • Urgency for BM: 80% improved
  • Bloating: 75% improved
  • Nausea: No recurrences
  • Eczema: Improved
  • Asthma: Improved
  • Energy: Much better
• Additional Notes:
  • Susan has not taken Omeprazole in weeks. She also moved out of her apartment and moved back in with her parents.
• Impression:
  • Susan appears to have responded well to the modified triple probiotic therapy and moving out of the apartment with suspected environmental toxicity. The combination of a nutrient dense elimination diet with supportive gut therapies appears to have facilitated improvement in her GI symptoms. I am also mindful that she could have likely seen some improvements simply with the passage of time.

Visit 5 (1 Week Later) – Follow-Up Message

• Subjective Assessment:
  • Susan notified me that she started experiencing more belching than usual.
• Recommendations:
  • Increase Digestive Enzymes
  • Avoid cold beverages with foods
  • Chew food more thoroughly before swallowing
• Impression:
  • I feel Susan could do well with some basic troubleshooting focused more on situational eating behaviors than significant modifications to her treatment recommendations.
  • She notified me following these recommendations to state that she experienced relief primarily from the lifestyle changes focused on limiting  cold beverages with meals and chewing food more thoroughly.

Clinician’s Comments

Clinical Rule: Focus on restoring gut health and the basic avoidance of environmental triggers or toxicity BEFORE any extensive testing or intricate treatments focused on mold.

• I was super excited to share this case because of how beautifully the patient responded to basic gut support and also the avoidance of a moldy environment.
• In retrospect, I realized that once we found out she had mold in her living environment, we could have easily gone down the mold rabbit-hole leading to a urine mycotoxin test followed by mycotoxin-specific treatments which could have taken months and led to unnecessary financial expenditure and treatment.
• By focusing on her symptoms, which were mainly GI in nature, and starting with the basic avoidance of the moldy environment, we implemented supportive dietary and probiotic treatments that led to dramatic improvements across multiple symptom domains.
• It is also important to appreciate how basic lifestyle modifications such as chewing food more thoroughly and cold water avoidance during meals can be low risk and effective treatments for GI symptoms.
• Scott demonstrates another great example of how a cost-effective and gut-based treatment approach can lead to positive clinical outcomes. It is greatly encouraging to see more clinicians adopting more conservative and value-based treatments and achieving significant clinical success. Scott’s case also demonstrates the importance of following a flexible, but systematic treatment hierarchy to prevent excessive treatments and the overdiagnosis of severe mold toxicity.

Clinical Review: The Role of Fungal-Based Testing in GI Conditions

Clinical Question

Does routine testing using various fungal-based markers offer value for clinicians treating patients with GI conditions?

Clinical Topics Examined

1. Fungal Dysbiosis
2. Candida Overgrowth
3. Anti-Saccharomyces Cerevisiae Antibodies (ASCA)
4. Serum Candida Antibodies

Essential Clinical Points

• Fungal dysbiosis and disturbed interactions between gut bacteria and gut fungus have been identified in patients with IBS-D and IBS symptoms overall.
• Despite this association, fecal mycobiome testing (with machine algorithm assessment) as well as older antibody and culture testing methodologies DO NOT appear to offer significant additional clinical value for the diagnosis of IBS-D.
• Candida overgrowth (as measured by stool culture) is more common in individuals with antibiotic associated diarrhea than in healthy controls.
• Presence of ASCA in pediatric patients with Crohn’s Disease is associated with a WORSE prognosis and a higher likelihood for more intensive treatment including surgery.
• Patients with ASCA are MORE LIKELY to have autoantibodies to other barrier (intestinal and blood-brain) associated proteins compared to healthy controls.
• IgG antibodies to yeast elements IS UNLIKELY to clinically differentiate patients with IBS from healthy controls.
• Candida IgG antibodies are found more often in pediatric patients with autism spectrum disorder (with and without GI symptoms) than healthy developing controls.

What We Are Exploring at Our Center

• Our clinic will be exploring the utility of a combination of PCR stool and serum antibody testing for patients with chronic GI conditions such as IBS. We hope to identify any associations between treatment response and the presence/change of PCR or antibody levels.

1. Fungal Dysbiosis

Clinical Take Home:

• Fungal dysbiosis and disturbed interactions between gut bacteria and gut fungus have been identified in patients with IBS-D and IBS symptoms
• Despite this association, fecal mycobiome testing (with machine algorithm assessment) DOES NOT appear to offer additional clinical value for the diagnosis of IBS-D.
• The use of herbal or prescription antifungals WITHOUT specific testing is a clinically viable treatment for patients with IBS or visceral hypersensitivity.

Research into the gut mycobiome and its connection with IBS is evolving, but is in its early stages.

The Potential Role of Gut Mycobiome in Irritable Bowel Syndrome

• “The study on the contribution of gut mycobiome to IBS is yet in its infancy, and numerous problems remain to be addressed. For instance, the associations between gut mycobiome with the classification, differential diagnosis, and relapse of IBS are all subjects that merit further study.”

Several researchers have identified fungal dysbiosis and disturbed interactions between constituent bacteria and fungal elements via genetic sequencing analysis of stool samples.

Gut fungal dysbiosis and altered bacterial-fungal interaction in patients with diarrhea-predominant irritable bowel syndrome: An explorative study

• “Gut fungal dysbiosis and altered bacterial-fungal interactions were present in patients with D-IBS, and gut fungi could be used to diagnose D-IBS.”

Identifying (if present) a distinct (disturbed) gut mycobiome in patients with IBS, however, does not appear to carry much clinical utility.

The fecal mycobiome in patients with Irritable Bowel Syndrome

• “As a putative biomarker of IBS, the predictive power of the fecal mycobiome in machine learning models was significantly better than random but insufficient for clinical diagnosis. The mycobiome presents limited therapeutic and diagnostic potential for IBS, despite co-variation with bacterial components which do offer such potential.”

There is mechanistic potential (from rat models) for the use of various antifungals to treat visceral hypersensitivity in patients with IBS given the correlations with fungal dysbiosis. Patient level data from our clinic suggests that certain patients with IBS respond well to herbal antimicrobials with antifungal properties as well as antifungal medications.

Intestinal Fungal Dysbiosis is Associated with Visceral Hypersensitivity in Patients with Irritable Bowel Syndrome and Rats

• “In an analysis of patients with IBS and controls, we associated fungal dysbiosis with IBS. In studies of rats, we found fungi to promote visceral hypersensitivity, which could be reduced by administration of fungicides, soluble β-glucans, or a SYK inhibitor. The intestinal fungi might therefore be manipulated for treatment of IBS-related visceral hypersensitivity.”

2. Candida Overgrowth:

Clinical Take Home:

• Candida overgrowth (as measured by stool culture) is more common in individuals with antibiotic associated diarrhea than in healthy controls.

Candida overgrowth as measured by stool culture appears to be more common in individuals with antibiotic associated diarrhea than in healthy controls. It is important to note that the Candida overgrowth appears mechanistically to be the RESULT of rather than the cause of the diarrhea.

Role of Candida and Antibiotic-associated diarrhea

• “In control subjects, Candida positivity and overgrowth were less common than in all other groups. Data indicate that elevated Candida counts are a result of antibiotic treatment or diarrhea rather than a cause of AAD.”

3. Anti-Saccharomyces Cerevisiae Antibodies (ASCA):

Clinical Take Home:

• Presence of ASCA in pediatric patients with Crohn’s Disease is associated with a WORSE prognosis and a higher likelihood for more intensive treatment including surgery.
• Supplementation with boulardii in patients with ASCA + Crohn’s Disease appears safe and may be an efficacious treatment in combination with Lacto/Bifido probiotics.
• Patients with ASCA are MORE LIKELY to have autoantibodies to other barrier (intestinal and blood-brain) associated proteins compared to healthy controls.

Anti-saccharomyces cerevisiae antibodies (ASCA) have routinely been used as a SPECIFIC marker for Crohn’s Disease. A recent systematic review with consensus statements from a pediatric gastroenterology organization suggested that ASCA positivity was associated with an increased prevalence of severe – penetrating disease and the need for surgery.

Predicting Outcomes in Pediatric Crohn’s Disease for Management Optimization: Systematic Review and Consensus Statements From the Pediatric Inflammatory Bowel Disease-Ahead Program

• “Prognostic factors for surgery included CD diagnosis during adolescence, growth impairment, NOD2/CARD15 polymorphisms, disease behavior, and positive anti-Saccharomyces cerevisiae antibody status.”
• Older age at presentation, small bowel disease, serology (anti-Saccharomyces cerevisiae antibody, antiflagellin, and OmpC), NOD2/CARD15 polymorphisms, perianal disease, and ethnicity were risk factors for penetrating (B3) and/or stenotic disease (B2)”

There has been concern for the use of S. boulardii probiotics in Crohn’s Disease given the near 100% homology between S. boulardii and S. cerevisiae. Pilot examinations looking at the effects of S. boulardii on ASCA presence and titers in individuals with Crohn’s Disease have been reassuring and a recent meta-analysis even suggested trends for benefits with combination probiotic therapy (Lacto/Bifido + S. boulardii) in those of Crohn’s Disease.

Probiotics are a good choice in remission of inflammatory bowel diseases: A meta-analysis and systematic review

• “Combination of Saccharomyces boulardii, Lactobacillus, and VSL#3 probiotics in CD had also a trend for efficiency (p = 0.057).”

Saccharomyces Boulardii in Crohn’s Disease: Effect on Anti-Saccharomyces Cerevisiae Antibodies and Intestinal Permeability

• “Based on the present study, we believe the intake of boulardii in CD patients is safe and does not induce antibodies against S. cerevisiae.”
• “We can conclude that although both species share up to 100% sequence homology, they do not appear to induce antibodies in CD patients.”

Prominent functional medicine researchers Aristo Vojdani (Cyrex Laboratories) and Datis Kharrazian sought to examine the association between certain barrier (intestinal and blood-brain) auto-antibodies and ASCA.

Cyrex has popularized testing for various autoantibodies including two antibodies to elements of astrocytes that may be associated with increased blood-brain permeability (S100B, and aquaporin-4) as well as antibodies to aspects of the intestinal barrier – tight junctions (zonulin+occludin). As you will see below in the conclusions, the “blood-brain” barrier proteins S100B and aquaporin-4 are also present in the enteric nervous system and cannot be solely thought of as blood-brain barrier proteins.

Their study from ~100 ASCA positive blood samples did demonstrate a higher prevalence of barrier protein autoantibodies compared to ~ 200 healthy controls.

The authors then make some fairly liberal conclusions about the mechanisms of LPS disrupting barrier proteins and the need to screen for various antibodies in those with Inflammatory Bowel Disease (with ASCA) in order to “abrogate” disease symptoms in IBS (not IBD).

I suggest that their study may have identified a signature or pattern of inflammation with potential barrier protein autoimmunity that may be more common in the setting of inflammatory bowel disease with ASCA.

Their research DOES NOT AND CANNOT suggest that testing for various barrier protein antibodies and antibodies to LPS will significantly alter clinical management with any of the most common and widely available treatments for individuals with GI conditions including IBD and IBS.

Correlation between Antibodies to Bacterial Lipopolysaccharides and Barrier Proteins in Sera Positive for ASCA and ANCA

• “Results show significant elevation in antibodies in about 30% of ASCA- and ANCA-positive sera and demonstrate positive linear relationships between these antibodies.
• “Additionally, since S100B and AQP4 is expressed not only in the BBB but also in the enteric nervous system, we cannot at this point determine whether the antibodies we detected against S100B and AQP4 originated from the brain or the enteric nerve system. Therefore, S100B or AQP4-mediated inflammatory effects are not limited to the brain, but their over-expression and the immune response mounted against them may also be associated with the onset and maintenance of inflammation in the gut [102,103].”

4. Serum Candida Antibodies

Take Home:

• IgG antibodies to yeast elements IS UNLIKELY to clinically differentiate patients with IBS from healthy controls.
• Candida IgG antibodies are found more often in pediatric patients with autism spectrum disorder (with and without GI symptoms) than healthy developing controls.

There is ongoing debate and research about the utility of candida antibody testing to evaluate fungal-based pathology outside of overt, systemic candidiasis. It has been argued that the presence of serum candida antibodies stems from pathological intestinal permeability and represents a primary GI condition that may involve elements of fungal and bacterial dysbiosis.

“Candida Albicans Interactions With The Host: Crossing The Intestinal Epithelial Barrier”

• “Overwhelming evidence suggests that the gastrointestinal tract is the main source of disseminated Albicans infections. Major risk factors for disseminated candidiasis include damage to the mucosal intestinal barrier, immune dysfunction, and dysbiosis of the resident microbiota.”

A 2012 case control study examining the presence of IgG yeast sensitivity as well as additional IgG food antibodies in IBS patients versus healthy controls, however, DID NOT find clear correlations between IBS and any of the food or yeast sensitivities examined.

IgG and IgG4 antibodies in subjects with irritable bowel syndrome: A case control study in the general population

• “Our findings suggest that IgG-and IgG4-mediated food and yeast hypersensitivity in IBS is unlikely. IgG antibodies against food and yeast may reflect the diet.”

A 2018 study examining the presence of IgG candida antibodies in children with autism spectrum disorder (ASD) found significantly higher rates of candida antibodies in children with ASD as compared to healthy developing controls. Around 50% of the children with ASD and candida antibodies had notable GI symptoms.

Anti-Candida Albicans IgG Antibodies in Children with Autism Spectrum Disorders

• “Plasma anti- Albicans antibody positivity was found in 36.5% (19/52) of children with ASD. Anti-C. Albicans antibodies in typically developing controls were (14.3%; 4/28).”
• “GI dysfunction was found in about half of the ASD children who were positive for anti-Candida This study provides evidence of a new microbial risk factor for ASD.”

Rapid-Fire Research: Ultra-Concise Summaries of Noteworthy Studies

Effects of select dietary supplements on the prevention and treatment of viral respiratory tract infections: A systematic review of randomized controlled trials

https://pubmed.ncbi.nlm.nih.gov/33858268/

• Systematic Review containing 39 trials, ~17,000 participants
• Vitamin D appears helpful, with main signals in those with overt deficiency
  • “Vitamin D supplementation (400 to 4000 IU/day) appears to improve the health outcomes with viral respiratory tract infections (RTIs) across cohorts particularly in those with vitamin D deficiency.”
• Synbiotics with lactobacillus species carry some potential for prevention
  • “Select lactobacillus strains (casei, paracasei, coryniformis, acidophilus, fermentum, plantarum, and rhamnosus) and prebiotics (short-chain fructooligosaccharides or galactooligosaccharides) are the most widely used dietary supplements with potentially positive effects on prevention treatment of viral RTIs.”
• Beta-glucans may help to decrease symptoms/days of symptoms of RTI’s
  • “Yeast beta-glucan supplementation (250 to 900 mg/day) may be associated with decreased RTIs symptoms such as the number of days with the common cold or flu symptoms.”
• The flavonoid Quercetin also appears to be a reasonable option for addressing RTI’s
  • “Quercetin supplementation (500 to 1000 mg/day) may decrease the incidence and duration of upper respiratory tract infections.”

Synbiotics containing lactobacillus based probiotics, beta-glucans, quercetin, and maintaining Vitamin D sufficiency all appear to be reasonable options for preventing and mitigating symptoms of viral respiratory tract infections Given the nature and understood properties of these supplements, it appears that much of the benefit is derived from modulation of the gut microbiome or improved gut – immune health as a whole.

Preventing Respiratory Tract Infections by Synbiotic Interventions: A Systematic Review and Meta-Analysis of Randomized Controlled Trial

https://pubmed.ncbi.nlm.nih.gov/31996911/

• Systematic Review containing 16 studies with a total of >10,000 participants
• Synbiotics are a safe and potentially effective preventative strategy for viral respiratory tract infections. While the preventative effect is not substantial, given their safety and minimal risks, synbiotics are reasonable supplement considerations for most individuals
  • “Overall, synbiotic interventions reduced the incidence rate of RTIs by 16% (95% CI: 4%, 27%) and the proportion of participants experiencing RTIs by 16% (95% CI: 5%, 26%).”

Practitioner Tip

How to Help Frustrated Patients

We have all dealt with extremely frustrated patients. Patients can be frustrated by the lack of progress they make with our recommended treatments or by elements of the patient experience (backordered supplements, inability to get a question answered by the support staff, rescheduled appointments, etc). It can be easy to feel defensive when patients express their frustration during their visit, especially if it is regarding something primarily out of your control as a clinician. These encounters can easily derail into non-therapeutic outcomes leaving both provider and patient feeling frustrated or hurt. Given the challenges these types of visits present, I want to provide you with a framework for approaching these visits that empowers you and gives you concrete language and actions to take to decrease the likelihood of non-therapeutic outcomes.

1. Recognize the patient is frustrated and listen to their expression of this frustration

Step 1 is a mindfulness and recognition step. It may seem simple, but we must observe and recognize that the patient is frustrated so we do not react or project back from a place of defensive hurt. We must also seek to avoid taking the expression personally, especially when the expression of frustration contains more hurtful language or a lack of respect for you as an individual.

2. Acknowledge to the patient you see/hear their frustration

This is an important step where after recognizing and receiving their frustration, you directly say back to the patient something like

“I can hear that you are frustrated with …., I am also frustrated we haven’t made the progress we have desired.”

If the patient hasn’t clearly demonstrated that they are in a frustrated state, but you are sensing this from their body language/tone of voice, this can also be an opportunity to share what you are hearing and feeling with examples such as

“I get that sense that you are feeling frustrated with your progress …”

3. Seek clarity in understanding the precise nature of the patients frustration

In direct continuation from Step 2, we can jump right into seeking clarity behind the exact nature of their frustration. While we may sense or know they are frustrated with their progress, this is the opportune time, right after acknowledging you see their frustration, to ascertain precisely what is most frustrating to them. You can use phrases such as

“Can you help me to understand what is causing you the most frustration or suffering?

“It would help me as we seek to move forward to understand clearly what is causing you the most frustration. Would you mind sharing with me a little more about what is causing you the most frustration?”

From this space, we can strengthen the therapeutic alliance and lay the groundwork for building a plan of action for moving forward (Step 4).

4. Make a therapeutic plan of action for moving forward

If you recognize somewhere in Steps 1-3 that an apology or an expression of this nature is warranted and helpful, please provide it to the patient. I often find this can naturally flow after Step 3 after you have received clarity about their greatest source of frustration and ascertained how a precise apology may be used therapeutically.

In this step, you can again remind the patient of your intentions for helping them to feel better as quickly as possible (reasonably so). An example of language you can use is

“Thank you for sharing your frustrations and this information with me. I recognize this work is challenging and it’s hard when the outcomes of our work are not guaranteed or realized. It is my goal for you to feel better as quickly as possible and I want to work together to get you there. Based on what you have shared today and what we have tried so far, I feel our next steps could involve … What do you think about this plan?”

It can be easy to overlook the importance of our efforts to contain our patients’ emotions and frustrations and simply judge our skills as clinicians by our acumen interpreting labs or prescribing medications and supplements, but oftentimes the greatest benefits (or greatest harm minimizations) come from tactful and compassionate communication with our patients during times of increased emotion or frustration.