High Health Care Costs: Plenty of Blame to Go Around

Zack Cooper, NY Times, 5/4/26. This Is the Biggest Culprit for High Health Care Spending.

An excerpt:

Responding to the wrongdoing of insurers is imperative, but it won’t do much to address the unsustainable cost of health care. We are directing our anger at the part of the system that is most visible and frustrating (insurers’ restrictions on care) while ignoring the part of the health system that is most responsible for high costs and economic pain: hospital prices…

Hospitals in the United States earn $29,000 on average for a replacement covered by private insurance and $16,000 for one covered by Medicare. In Germany, the public system of nonprofit insurers, which covers 90 percent of the population, pays hospitals $9,400.

Hospital prices are the leading driver of the 320 percent increase in insurance premiums that Americans have experienced over the past 25 years. Since 2000, prices at hospitals have grown faster than prices in virtually any other sector of the economy. They have grown three times as fast as inflation and twice as fast as prescription drugs and doctor visits.

The reason hospital prices are so high: hospitals’ accumulation of market power, which brings them more bargaining heft when they negotiate prices with insurers. Since 2000, there have been more than 1,300 hospital mergers among the nation’s approximately 5,000 hospitals. When hospitals that were once competitors merge, prices go up, often by double-digit percentages, with no measurable improvement in patient outcomes. Even though we rely on competition to determine hospital prices, 21 percent of hospitals are effectively monopolies — they have no competitor within a 30-minute drive — and an additional 24 percent face only one competitor…

If hospital prices are such a key driver of rising costs, why aren’t elected officials doing more about them? Partly the answer is politics. Hospitals are the largest or second-largest employer in many counties in America, and a formidable lobbying force — spending more than $100 million annually in Washington, often more than health insurers spend, to protect their interests. Politicians who represent places with dominant hospital systems are not eager to pick a fight with these institutions. Moreover, when an insurer denies your claim, you know it immediately. When a hospital merges and its prices go up, the harms — slower overall economic growth and job losses outside the hospital sector — are real but diffuse…

Holding that tension between the immense good that hospitals do and the economic harm their market power creates is what it will take to address the rising cost of health care.

In reaction to this editorial, the American Hospital Association Blog responded on May 6, 2026: Setting the Record Straight: Three Ways the Hospital‑blame Narrative Gets it Wrong

“Let’s start with a basic point — the entire concept of hospital “prices” is flawed. Hospitals are largely price takers, not price setters. Government programs like Medicare and Medicaid set rates administratively. But Medicare reimbursement continues to lag behind inflation — covering just 83 cents for every dollar spent by hospitals in 2023 — resulting in over $100 billion in underpayments. Needless to say, government rates fall far short of covering hospitals’ actual costs. Likewise, commercial insurers aggressively negotiate payment terms with hospitals. In many cases, these are large, vertically-integrated companies that hold significant shares in their markets. With that kind of market power, commercial insurers do not simply accept the numbers that hospitals offer and then sign on the dotted line. Thus, the notion of hospital “prices” does not reflect how those purposed “prices” are set in the real world…But here’s the reality: Over the same time frame, commercial insurance premiums have increased more than hospital prices…premiums are primarily growing due to an increased need for services: People are sicker and they need more care.”

“The essay also … appears to excuse commercial insurers’ role in deciding to raise their own premiums because they are in the “business of making money…The essay argues that policymakers must be harder on hospitals.”

“The essay also fails to ask another important question: Why are hospitals forced to raise their “prices”?…In 2025, total hospital expenses grew 7.5%, more than twice the rate of growth in hospital prices. Costs increased in every major category — workforce, drugs, medical supplies, and more. Hospital expenses also increased because of increased patient complexity; growing uncompensated care; continued government underfunding; changes in the policy landscape; and the many commercial insurer tactics like prior authorization and improper denials that the essay observes.”

My take: There are lots of reasons for high healthcare costs. There are not simple fixes nor enough incentives to make changes.

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Perito Moreno Glacier, Argentina

Big Studies Supporting Combination Advanced Therapy for Ulcerative Colitis and Crohn’s Disease

An excerpt:

Two [randomized controlled] Phase 2b trials enrolled patients with moderate-to-severe disease who had already failed one or more therapeutic classes of drugs…

One trial analyzed 693 patients with Crohn’s disease, while the other analyzed 572 patients with ulcerative colitis…The trials tested an experimental therapy that combined golimumab and guselkumab, which are already in the market…

In the Crohn’s trial, 49.2% of the most treatment-resistant patients who received a high dose of the combination therapy achieved clinical remission after 48 weeks, compared to 27.3% receiving guselkumab and 23.1% taking golimumab…And the safety profile was about the same. The results of the ulcerative colitis trial showed a similar pattern.

DUET-CD study
“In the overall population, JNJ-4804a demonstrated higher clinical remissionb rates (50.8%) and endoscopic responserates (38.1%) versus golimumab (25.4% for clinical remission, 19.8% for endoscopic response) at Week 48. The JNJ-4804 rates were also numerically higher than the rates achieved with guselkumab (42.5% for clinical remission and 33.9% for endoscopic response).”

DUET-UC study
“In the overall population, JNJ-4804a demonstrated superior clinical remissiond rates compared to golimumab, with 41.0% of JNJ-4804-treated patients achieving clinical remission at Week 48 versus golimumab (11.5%), and numerically higher rates than guselkumab (34.0%).”

“Based on results from the Phase 2b DUET studies, Johnson & Johnson will be initiating the Phase 3 DUET ENCORE-CD trial in adults with moderately to severely active CD as well as the Phase 3 DUET ENCORE-UC trial in adults with moderately to severely active UC.”

My take: In both of these phase 2b trials, the combination therapy was more effective than either guselkumab or golimumab monotherapy. The combination therapy was about 8% and 7% more effective for Crohn’s disease and Ulcerative colitis, respectively, compared to guselkumab monotherapy in terms of clinical remission.

Related blog posts:

Sunset at Kiawah Island, SC

How Does Prior Topical Steroids Affect Response to Dupilumab for Eosinophilic Esophagitis

M Chehade et al. Am J Gastroenterol 2026; 121: 649-660. Open Access! Dupilumab Efficacy in Children With Eosinophilic Esophagitis With Prior Swallowed Topical Corticosteroid Use: A Subgroup Analysis Thanks to Ben Gold for this reference.

Background: “The aim of this exploratory, post hoc subgroup analysis of EoE KIDS was to assess dupilumab efficacy and safety in patients aged 1–11 years with EoE previously treated with STCs” [swallowed topical corticosteroids]. This study further examined th EoE KIDS cohort (Chehade M, Dellon ES, Spergel JM, et al. Dupilumab for eosinophilic esophagitis in patients 1 to 11 years of age. N Engl J Med 2024;390(24):2239–51.)

Methods: The trial consisted of the following: part A, a 16-week, randomized, double-blind, placebo-controlled treatment period; part B, a 36-week, extended active treatment period in which patients knew that they received active treatment but did not know their regimen; and part C, a 108-week, open-label extension period in which all patients received higher-exposure dupilumab. Eligible patients were aged 1–11 years with a confirmed diagnosis of active EoE who were unresponsive to ≥8 weeks of PPIs.

Of 102 patients, 82 (80%) received prior STCs and 59 (58%) had prior inadequate response, intolerance, and/or contraindication (IRIC) to STCs.

Key findings:

  • At W16, higher-exposure dupilumab improved rates of histologic remission vs placebo in patients with prior STC use (60.7% vs 0.0%) and prior IRIC to STCs (60.9% vs 0.0%).
  • Responses were maintained at W52 with higher-exposure dupilumab, with improvements observed in patients who switched from placebo to higher-exposure dupilumab.
  • “Findings seemed comparable in those without prior STC use or prior IRIC, although patient numbers were small.” Only 9 patients in the treatment cohort did not haver prior STC use.

My take: It appears that dupilumab works well in those with and without prior swallowed topical corticosteroids (STCs). Though the numbers are small, the response appears more robust in those without prior STCs; perhaps, those with prior STC failure had more refractory EoE.

Some good brief YouTube EoE educational videos for families from GIKids.org (with pharmaceutical funding), links:

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Appendectomy for Refractory Ulcerative Colitis: 2026 COSTA Study

Visser E, Reijntjes M, Heuthorst L et al.The Lancet Gastroenterology & Hepatology, 2026; 11, 190-203. Appendicectomy versus switching to a JAK inhibitor in inducing remission in patients with active ulcerative colitis after biologic therapy failure (COSTA): 1-year results of a multicentre, prospective, cohort study

Last year, the ACCURE Trial (see blog post link below), showed that laparoscopic appendicectomy, in addition to standard medical therapy, significantly reduced the relapse rates for ulcerative colitis (UC) within 1 year. Most patients were treated with mesalamine.

The COSTA study examined adult patients (n=125) who were not responding to advanced therapy. Patients were offered one of three treatments: laparoscopic appendicectomy while continuing their existing advanced therapy at a stable dose; switching their advanced therapy to a JAK inhibitor; or colectomy. 116 patients were included in the modified intention-to-treat-analysis (67 received appendicectomy and 49 received JAK inhibitor (primarily tofacitinib).

Key findings:

  • 22 (32.8%) of 67 patients in the appendicectomy group were in clinical remission without therapy failure at 12 months compared with six (12.2%) of 49 patients in the JAK inhibitor group (p=0.016)
  • At 12 months, corticosteroid-free clinical remission without therapy failure was attained in 22 (32.8%) of 67 patients in the appendicectomy group compared with six (12.2%) of 49 patients in the JAK inhibitor group  (p=0.010). Clinical response in 49 (73.1%) of 67 patients compared with 26 (53.1%) of 49 patients (p=0·025), and endoscopic response in 31 (48.4%) of 64 patients compared with 11 (25.6%) of 43 patients (p=0·018)

My take (borrowed in part from the authors): “Appendicectomy as an adjunct to advanced therapy in biologic-exposed patients with active ulcerative colitis was associated with higher clinical remission rates at 12 months compared with switching to a JAK inhibitor.” We don’t know how appendectomy would influence disease course in pediatric patients. We also don’t know how this information will be incorporated into adult guidelines.

Interestingly, there have been studies (two cited below) indicating that appendectomy lowers the risk of developing inflammatory bowel disease:

Related blog post: ACCURE Trial: Appendectomy As an Adjunct Ulcerative Colitis Treatment Plus One

Kiawah Island at Sunrise

    Dr. Stacy Kahn: Clostridioides difficile 2026

    Recently, Dr. Stacy Kahn gave our group an excellent update on Clostridioides difficile. My notes below may contain errors in transcription and in omission. Along with my notes, I have included many of her slides. Dr. Kahn has been a leader on treatment and advocacy for C. difficille. In 2025, she received the Leadership Award from the Peggy Lillis Foundation recognizing her clinical, research and advocacy efforts related to C. difficile awareness and treatments.

    Key points:

    Diagnosis: C. diff is difficult to diagnose. The NAAT-based assays are highly sensitive but cannot readily distinguish active infection from colonization. ELISA toxin assays have higher specificity. However, there are many of these assays and their reliability in identifying active infection from colonization varies. In individuals with underlying diseases like IBD and IBS, this can create uncertainty about the diagnosis of C. diff.

    Presentation: Symptoms are quite variable, from asymptomatic to bloody diarrhea to fulminant colitis (uncommon in kids). Profound urgency is a common feature.

    Transmission: C. diff bacteria can survive on surfaces for 24 hrs. The spores can survive months to years. In addition, the (invisible) spores are highly resistant to heat, disinfection and antimicrobials. Thus, nursing homes and hospitals are frequent reservoirs.

    Epidemiology: C diff rates in the hospital setting have improved, likely due to antibiotic stewardship. Community rates have increased; though, precise estimates are problematic as the diagnostic testing is not straightforward.

    Costs: In 2016, the estimated annual costs due to C diff were $ 6.3 billion (Zhang S. et al. BMC Infect Dis. 2016).

    Resources/Websites:

    Severe C diff in Children: In a retrospective study of C diff in hospitalized children (2013-2019, n=17,142 children) showed that among 23,053 CDI admissions, 74 (0.3%) had a colectomy (55 in IBD patients), and 29 (0.1%) had toxic megacolon. All-cause mortality was noted in 429 (1.9%) (Reference: Edwards PT, Kahn SA, Nicholson, M et al. J Pediatr. 2023; 252:111-116.e1. Open Access! Clostridioides difficile Infection in Hospitalized Pediatric Patients: Comparisons of Epidemiology, Testing, and Treatment from 2013 to 2019).

    Testing: Recommendations include avoiding testing in those taking laxatives; however, an exception to this would be patients with motility disorders. Even combination testing cannot always distinguish between colonization and active infection. In addition, there are numerous toxin tests with variable performance.

    [From prior blog post: In a large adult study with 293 of 1416 hospitalized adults testing positive for C. diff, virtually all CDI-related complications and deaths occurred in patients with positive toxin immunoassay test results. Patients with a positive molecular test result and a negative toxin immunoassay test result had outcomes that were comparable to patients without C difficile by either method. (Overdiagnosis of Clostridium difficile with PCR Assays)]

    Treatment:

    • 1st line treatment remains vancomycin.
    • 10-day treatment course is recommended.
    • Fidaxomicin, particularly for recurrrent C. diff could be helpful and easier to administer (2/day).
    • Prophylactic treatment (low dose vancomycin) may be appropriate in high risk individuals needing to take antibiotics.
    • FMT is no longer readily available from stool banks. Donor-directed FMT may be an option after appropriate screening. Given the lack of stool banks, urgent treatment with FMT for severe cases is not available.
    • Probiotics have not been proven effective in reducing recurrence and increase the costs for families. A diet high in fruits and veggies (‘eat the rainbow‘) could help restore a more healthy microbiome.
    • Newer treatments in adults, Vowst and Rebyota, are expensive and not readily available for children. Anecdotal reports suggest they may be beneficial in pediatric patients.

    Conclusions: C diff research is difficult in pediatrics. Many of the patients who need treatment would be excluded from trials. There are very few treatment options in kids.

    Related blog posts:

    Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician. Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure. This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

    Essential Summer Safety Tips for Preventing Drowning

    I am reposting this from last year with slight modifications.

    An ICU colleague indicated that she really does not like to work on summer holiday weekends. While she is a hard worker, what she doesn’t like is seeing kids with drowning and firework injuries. All of a sudden a happy time becomes tragic. With that in mind, here are a few tips to prevent drowning.

    From Strong4Life: “Practicing water safety for kids of all ages is crucial because drowning is a leading cause of death in children from birth through the teen years. And drowning is often quick and silent.”

    Also, firearm deaths are the leading cause of death in children in the U.S. and motor vehicle accidents are second. So, firearms need to be secured and drive safely on the way to the pool, lake, river or beach.

    Related blog posts:

    C Raymond-King et al. N Engl J Med 2026;394:1958-1959. Open Access!
    Current Causes of Death among Children and Adolescents in the United States

    Legislating Directed-Donated Blood

    JW Jacobs et al. N Engl J Med 2026;394:1667-1669.
    Legislating Medicine — Directed Donation and the Politics of Patient Choice

    In a previous post (Increase in ‘Unvaccinated’ Blood Requests), the increase in requests for directed-donated blood to avoid “vaccinated” blood was discussed. This article describes pending legislation in Tennessee to make this a patient right.

    An excerpt:

    In February 2026, members of the Tennessee General Assembly introduced House Bill 2166 (HB 2166, “An Act to Amend Tennessee Code Annotated, Title 68, Chapter 32, Relative to Blood Donations”), which would require blood banks and hospitals to comply with directed-donation requests for patients scheduled for medical procedures.1 Its sponsors framed the bill as protecting patient choice by ensuring that patients have the right to select what is put into their bodies. The paradox is that the U.S. community blood supply is already among the safest in the world, the product of decades of evidence-based practice, universal donor screening, and rigorous infectious disease testing. HB 2166 does not fix a broken system. Instead, it risks undermining one that already functions safely and effectively — which is precisely why this legislation merits attention in domains beyond the blood bank. The bill exemplifies a broader pattern in which politicians seek to legislate medical practice in ways that override scientific consensus while invoking the language of autonomy and choice…

    What is emerging is not an expansion of evidence-based patient rights but a distortion of them. The patients’ rights movement of the 1970s — built around informed consent, refusal of treatment, and shared decision making — led to genuinely important protections, but it envisioned those rights operating within the framework of evidence-based medicine, not as mechanisms to compel clinicians to provide interventions that scientific organizations and medical societies have identified as harmful…HB 2166 and related bills do not just expand patient choice; they transform misinformation-driven preferences into enforceable medical policy, granting pseudoscientific fears the force of state law. The result, unfortunately, is not patient empowerment, but legislated harm delivered with the imprimatur of democratic governance.

    This dynamic extends well beyond transfusion medicine. Similar patterns are increasingly visible in vaccine policy, public health governance, and reproductive care. 

    My take: When a person decides to take additional risks (eg. riding a motorcycle, drinking raw milk, not using a seat belt), the consequences primarily impact that individual. However, it does not feel right to compel others to assist in delivering substandard care. Though, HB 2166 does not waive existing donor-eligibility and safety requirements, it could still lead to delays in care with worsened outcomes.

    Victoria Island, Argentina

    HHS Removes Experts from United States Preventive Services Task Force (USPSTF)

    AMA Statement:

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    “GLP-1 Receptor Agonists and Eating Disorders — Cause for Concern”

    A Banks. N Engl J Med 2026;394:1665-1667. GLP-1 Receptor Agonists and Eating Disorders — Cause for Concern.

    An excerpt:

    Constraining the growth of the global obesity epidemic would have clear benefits at the individual and population levels. Use of GLP-1 drugs has been linked in some patients to improved cardiovascular outcomes, a reduced risk of kidney disease, a reduced desire to drink alcohol, and potentially protective effects against neurodegenerative diseases. It is therefore easy to understand the substantial interest in investing in the development of these products and the optimism about their public health effects.

    Nonetheless, some worrisome signals have emerged…The proportion of GLP-1 receptor agonist prescriptions that were written for people without diabetes, obesity, or overweight increased from 4.5% in 2018 to 17% in 2023…1

    There is also compelling preliminary evidence suggesting that the use of these drugs could exacerbate and lead to new diagnoses of restrictive eating disorders, including anorexia nervosa…3 Lifetime prevalence of anorexia nervosa is as high as 6.3% in women and 0.3% in men,4 and the risk of death from any cause among people with anorexia nervosa is more than five times as high as that in the general population…5

    Nutrient deficiencies, electrolyte abnormalities, orthostatic hypotension, osteopenia, sarcopenia, thinning hair, and other signs of malnutrition have been observed [in users of GLP-1 agents], and the effects of long-term use are still largely unknown…

    The cumulative incidence of new eating-disorder diagnoses (most commonly anorexia nervosa) in the full study population was 1.275%…3 this proportion translates to more than 420,000 people who could develop a related eating disorder with long-term use.

    Physicians, trialists, regulators, policymakers, and drug developers are unprepared for this coming wave.

    My take: GLP-1 RAs are not for everybody; they will likely contribute to eating disorders in many patients.

    GLP-1 RAs also have been associated with a higher risk of Nonarteritic Anterior Ischemic Optic Neuropathy (aka ‘eye stroke’) in approximately in 1 in 10,000 recipients. One reference: JAMA Ophthalmology. 2026;144;(3):259-264. New-Onset Nonarteritic Anterior Ischemic Optic Neuropathy and Initiators of Semaglutide in US Veterans With Type 2 Diabetes

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    Trail to Mt Fitz Roy (Argentina)

    Beneficial Off-Target Effect: Upadacitinib Improved Eosinophilic Esophagitis (Case Report)

    N Nguyen , M Bauer. JPGN Rep. 2026;1-3.  Successful treatment of eosinophilic esophagitis with upadacitinib prescribed for atopic dermatitis. doi:10.1002/jpr3.70170

    This case report describes a 15 yo with severe atopic dermatitis and multiple atopic diseases whose eosinophilic esophagitis remained in remission after starting upadacitinib, a JAK1 inhibitor, and stopping dupilumab. JAK1 inhibitors, such as upadacitinib and abrocitinib, are approved for severe AD. 

    The discussion notes that there had been a prior case report of tofacitinib, a JAK1/JAK3 inhibitor, effectively treating refractory EoE. The authors “hypothesize that JAK inhibition of key Th1 and Th2 signaling pathways including IL-4, IL-13, and TSLP could effectively treat EoE, while also treating AD.”

    My take (borrowed from authors): “If upadacitinib is used for the treatment of AD, cessation of other therapies for EoE, particularly biologics like dupilumab, should be strongly considered.”

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