“The Broken Promises of Profit-Driven Medicine”

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N Tomes. NEJM 2025; 393: 521-524. A Gilded Age for Patients? The Broken Promises of Profit-Driven Medicine

This article (one of several in a series) describes the development of the current corporate-centered health care system over the past 100 years and the drawbacks.

An excerpt:

Between the 1920s and the 1960s, the American medical profession adopted a new doctor-controlled business model of care delivery, dependent on continual investment in new drugs, technologies, and procedures. That model created the profit opportunities that enticed corporate stakeholders to invest in health care in the 1970s and 1980s. But as the corporate presence increased, physicians lost control of their business model; the “tail” of financialization began wagging the “dog” of medical practice. That shift coincided with corporate cooptation of the language of consumerism to justify these changes as in patients’ best interests. In the process, physicians and patients lost economic autonomy over health care choices…

Insurance plans let doctors and hospitals set prices, facilitating more investment in the capital-intensive technologies equated with higher-quality care. But that dynamic also created an upward spiral of costs…These problems led to a second transformative movement: the federal government’s entry into the health insurance business, with the creation of Medicare and Medicaid, which also let doctors and hospitals set prices. This… aimed to relieve Americans of the duty of financing the medical system themselves, bringing in third parties to help. Enrollees in the new plans got more coverage but only on the terms set by those parties; uninsured people had to manage on their own. Meanwhile, the cycle of rising costs continued unabated…

Medical entrepreneurs believed that applying market discipline to health care would produce the right combination of innovation, efficiency, and cost–benefit balance to ensure better care for patients while profiting investors…

While adopting some consumer-industry practices, corporate health care players strove to avoid others, such as direct price competition. Policy efforts to rein in costs stressed the need for price transparency: consumer–patients needed to “shop” more critically for the cheapest care. In this spirit, political conservatives promoted “consumer-driven” health care. But such schemes foundered on the reality that many insurance plans gave patients little flexibility to price-shop for care…

Many powerful health care industry stakeholders still believe allowing corporate interests freer rein will produce that “golden age for patients.” The health care economy’s fragility suggests otherwise…When they [hospitals] pivoted from profitable surgeries to unprofitable Covid care, they needed massive infusions of government funding to survive.  Similarly, recent shortages of essential but low-profit drugs, including chemotherapy agents and insulin, reveal the limits of the pharmaceutical industry’s profit-oriented approach to essential drug production…

No market solution has arisen for the most critical determinant of poor health and health care outcomes in the United States: extreme income inequality. Countless studies indicate that poverty is the most important health risk factor that Americans face…little profit can be made by preventing or treating poverty-induced illnesses.

U.S. health care needs a new business model…only more collective physician and patient action will help medicine find a more equitable, sustainable model…Many people will suffer if the system collapses completely, but perhaps a more sustainable health care system can be built from the rubble.

My take: This analysis of the U.S. healthcare system, like many others, is analogous to getting the license plate of the truck that ran you over. At this time, there is little prospect of stopping the truck.

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Stone Mountain, Ga from the Cherokee Trail

New Data on the Reliability of the No-Biopsy Diagnosis in Pediatric Celiac Disease

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Chang D, Wong M, Camila Cardenas M, et al. Pediatrics. 2025;156(3):e2025070897. Positive Predictive Value of Tissue Transglutaminase IgA for Celiac Disease.

Background:For a no-biopsy celiac diagnosis, “the [ESPGHAN] criteria were revised in 2020, to specify that only a highly positive tTG IgA greater than or equal to 10× ULN and a positive EMA on a second blood sample are sufficient to diagnose celiac disease, obviating the need for HLA testing or symptoms.” NASPGHAN “has yet to adopt similar serologic criteria for diagnosing celiac disease. A clinical report in 2016 continued to recommend a confirmatory biopsy in all suspected cases of celiac disease. This recommendation cited concerns of interassay variability.”

Methods: This was a retrospective, multicenter North American cohort study of children (<18 years) with an elevated tTG IgA within 6 months of an esophagogastroduodenoscopy between January 2016 and December 2021. Biopsy-confirmed celiac disease was determined by the presence of intraepithelial lymphocytosis and villous atrophy. The primary outcomes were the PPV of an elevated tTG IgA and tTG IgA greater than or equal to 10 times the upper limit of normal (10× ULN).

The study identified 4019 children with the following characteristics: 63.3% female; 9% type 1 diabetes, and 2% Down syndrome

Key findings:

  • Histologic findings in the entire cohort were consistent with celiac disease for 3321 children (PPV = 82.6%)
  • Among the 1739/4019 (43.2%) children with tTG IgA greater than or equal
    to 10× ULN, 1651 had biopsy-confirmed celiac disease (PPV10× = 94.9%). Five percent (88/1739) of children did not have histologic findings of celiac disease, including 41/1739 (2%) with normal histology
  • EMA only marginally improved specificity as 76% of children without celiac disease and tTG IgA greater than or equal to 10× ULN had a positive EMA, albeit on the same sample. There was variations across providers, practices, and countries, which resulted in EMA not being performed in all cases or tested on the same blood sample as the tTG IgA
  • Assays performed worse in children with type 1 diabetes (PPV10× 89%) than that in those without T1DM (95.7%)
  • Of those with esophageal biopsies, 175/2980 (6%) had at least 15 eos/hpf in at least 1 esophageal biopsy
  • Of those with gastric biopsies, 912/3534 (25.8%) had histologic gastritis, including 1.4% (51/3534) with evidence of Helicobacter infection (n (49 cases of H pylori and 2 cases of H heilmannii)

My take: This study indicates that the no-biopsy diagnostic approach for celiac disease may need to be reconsidered. Though, it is likely that the no-biopsy approach would have had a higher PPV if the guidelines were actually followed (eg. separate EMA confirmatory sample). The values in this study show a much lower PPV than prior studies (96% in those without T1DM). In addition, among the 4% without celiac disease (potential celiac disease), about half of them would likely progress to celiac disease and could potentially benefit from a gluten free diet. Thus, up to 2%of patients, based on this study, would probably be harmed by being placed on a gluten free diet.

Another point to reiterate based on this study, diagnostic confirmation by a specialist prior to dietary changes is recommended. Increasingly, patients are referred after starting a gluten free diet.

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Brooklyn Botanic Gardens

Can Smartphone Use Increase the Risk of Hemorrhoids?

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There are many reasons NOT to use a phone while you are on the toilet. Now a small study indicates that smartphone use is associated with longer time on the toilet and increased rate of endoscopically-detected hemorrhoids.

An excerpt from the NBC summary:

“The longer you sit on the toilet, the worse it is for you,” said Dr. Trisha Pasricha, director of the Beth Israel Deaconess Medical Center’s Institute for Gut-Brain Research Institute in Boston. Pasricha is also an author of the study, which was published Wednesday in PLOS One…

Pasricha and colleagues surveyed 125 adults just before they were about to have a routine colonoscopy to screen for colorectal cancer. Eighty-three (66%) of the participants admitted to using their phones in the bathroom — mostly to catch up on news of the day and scroll through social media.

Gastroenterologists performing the colonoscopies looked for evidence of inflamed veins, or hemorrhoids. People who said they took their phone into the bathroom were 46% more likely to have hemorrhoids compared to the others…

The experts agreed that business on the toilet should take no longer than 5 minutes. More than 37% of study participants who used a smartphone in the bathroom stayed for longer than that, compared to 7% of people who kept their phones out of the bathroom.

My take: This study has a number of limitations; so, a definite link between smartphones and hemorrhoids has not been established. For example, there could be reverse causation. In this case, individuals who expected to be on the toilet longer may be more likely to use their smartphones rather than the smartphones making them stay longer. Nevertheless, I think multitasking on the toilet is generally not a good idea.

Brooklyn Bridge, August 2025

Is Lactated Ringer’s Better Than Normal Saline For Routine Use?

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L McIntyre et al. NEJM 2025; 393: 660-670. A Crossover Trial of Hospital-Wide Lactated Ringer’s Solution versus Normal Saline

Background: “A single-center, multiple-crossover trial involving noncritically ill patients in the emergency department found that balanced crystalloid fluids were associated with a lower incidence of major adverse kidney events at 30 days than normal saline. A systematic review of 13 randomized, controlled trials comparing balanced crystalloids with normal saline in a total of 35,884 critically ill participants showed no significant difference in mortality (17.4% with balanced crystalloids and 18.2% with saline; relative risk, 0.96; 95% confidence interval [CI], 0.91 to 1.01) or in the incidence of the use of renal replacement therapy (5.6% and 6.0%, respectively; relative risk, 0.95; 95% CI, 0.81 to 1.11) in trials with a low risk of bias.4 However, the investigators in that analysis and those in another patient-level meta-analysis involving a Bayesian approach concluded that there is a high probability that balanced crystalloids are associated with lower in-hospital mortality and a lower incidence of the use of renal replacement therapy than normal saline.5“

Methods of th “FLUID” trial: 3 hospitals used lactated ringer’s (LR) and 4 hospitals used normal saline throughout hospital setting for 12 weeks. Then after a 1-2 week washout period, the hospitals switched to the other fluid for 12 weeks.

Key finding:

Discussion: “A limitation of this trial was the inability to recruit the total of 16 hospitals as originally planned owing to the Covid-19 pandemic. Hence, the trial had less power to detect differences that were small — but important to patients — at the level of the hospital or health care system…Our findings align with those of recent meta-analyses of randomized, controlled trials that suggest a small but clinically relevant reduction in mortality with balanced crystalloids as compared with normal saline.”

My take: This study did not show a significant difference in death or readmission at 90 days. Yet, lactated ringer’s is probably just a bit better fluid for most adult patients. In the pediatric population, more studies are needed.

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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

Expert Advice for GI Manifestations of Hypermobile Ehlers-Danlos Syndrome Including Association with POTS and Mast Cell Activation Syndrome (MCAS)

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Q Aziz et al. Clinical Gastroenterology and Hepatology, Volume 23, Issue 8, 1291 – 1302. Open Access! AGA Clinical Practice Update on GI Manifestations and Autonomic or Immune Dysfunction in Hypermobile Ehlers-Danlos Syndrome: Expert Review

This review and practice update includes 16 “best practice advice” statements. Here are nine of them:

  • #1: Clinicians should be aware of the observed associations between hEDS or HSDs and POTS and/or MCAS and their overlapping gastrointestinal (GI) manifestations; while theoretical explanations exist, experimental evidence of the biological mechanisms that explain relationships is limited and evolving.
  • #2: Testing for POTS/MCAS should be targeted to patients presenting with clinical manifestations of POTS/MCAS, but universal testing for POTS/MCAS in all patients with hEDS/HSDs is not supported by the current evidence.
  • #3: Gastroenterologists seeing patients with DGBI should inquire about joint hypermobility and strongly consider incorporating the Beighton score for assessing joint hypermobility into their practice as a screening tool; if the screen is positive, gastroenterologists may consider applying 2017 diagnostic criteria to diagnose hEDS (https://www.ehlers-danlos.com/wp-content/uploads/2017/05/hEDS-Dx-Criteria-checklist-1.pdf) or offer appropriate referral to a specialist where resources are available.
  • #4: Testing for POTS through postural vital signs (eg, symptomatic increase in heart rate of 30 beats/min [40 beats/min for 12-19 yo] or more with 10 minutes of standing during an active stand or head-up tilt table test in the absence of orthostasis) and referral to specialty practices (eg, cardiology or neurology) for autonomic testing should be considered in patients with hEDS/HSDs and refractory GI symptoms who also report orthostatic intolerance after exclusion of medication side effects and appropriate lifestyle or behavioral modifications (eg, adequate hydration and physical exercise) have been attempted but is not required for all patients with hEDS/HSDs who report GI symptoms alone.
  • #5: In patients presenting to gastroenterology providers, testing for mast cell disorders including MCAS should be considered in patients with hEDS/HSDs and DGBI who also present with episodic symptoms that suggest a more generalized mast cell disorder (eg, visceral and somatic pain, pruritus, flushing, sweating, urticaria, angioedema, wheezing, tachycardia, abdominal cramping, vomiting, nausea, diarrhea, urogynecological and neurological complaints) involving 2 or more physiological systems (eg, cutaneous, GI, cardiac, respiratory, and neuropsychiatric), but current data do not support the use of these tests for routine evaluation of GI symptoms in all patients with hEDS/HSDs without clinical or laboratory evidence of a primary or secondary mast cell disorder.
  • #6: If MCAS is suspected, diagnostic testing with serum tryptase levels collected at baseline and 1–4 hours following symptom flares may be considered by the gastroenterologist; increases of 20% above baseline plus 2 ng/mL are necessary to demonstrate evidence of mast cell activation.
  • #12: Medical management of GI symptoms in hEDS/HSDs and POTS/MCAS should focus on treating the most prominent GI symptoms and abnormal GI function test results. In addition to general DGBIs and GI motility disorder treatment, management should also include treating any symptoms attributable to POTS and/or MCAS.
  • #13: Treatment of POTS may include increasing fluid and salt intake, exercise training, and use of compression garments. Special pharmacological treatments for volume expansion, heart rate control, and vasoconstriction with integrated care from multiple specialties (eg, cardiology, neurology) should be considered in patients who do not respond to conservative lifestyle measures.
  • #14: When MCAS is suspected, patients can benefit from treatment with histamine receptor antagonists and/or mast cell stabilizers, in addition to avoiding triggers such as certain foods, alcohol, strong smells, temperature changes, mechanical stimuli (eg, friction), emotional distress (eg, pollen, mold), or specific medications (eg, opioids, nonsteroidal anti-inflammatory agents, iodinated contrast).

Background: “Clinical gastroenterologists are encountering an increasing number of patients with chronic GI symptoms who also appear to experience comorbid hEDS/HSDs, POTS, and/or MCAS.15,16 Recognizing and treating GI symptoms in patients with hEDS/HSDs and comorbid POTS or MCAS present major challenges for clinicians, who often feel under equipped to address their needs.”

The article provides guidance on measuring hypermobility (Beighton Scoring System), Diagnosis/classification of mast cell activation (Table 1) and treatments for these disorders (Table 2)

My take: This is a useful reference for the overlap of DGBIs with hypermobile Ehlers-Danlos, POTS and Mast cell Activation. Nevertheless, the relationship between these disorders is unclear. In fact, there have been some studies indicating that joint mobility is not associated with an increase in functional GI disorders. Some of the association may be related to a surveillance bias.

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Impact of GLP-1 Agonists on IBD and Obesity

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P Sehgal et al. Clin Gastroenterol Hepatol 2025; 23: 1453-1454.Safety and Clinical Effectiveness of GLP1 Receptor Agonists in Inflammatory Bowel Disease Patients

Background: “The prevalence of obesity among patients with inflammatory bowel disease (IBD) is estimated at 15-40%, and continues to rise. Obesity has been associated with a more severe phenotype of IBD.”

Methods: Retrospective cohort with 244 patients. Semaglutide was the most commonly prescribed agent (54%).

Key findings:

  • GLP-1RA use led to weight loss from 102 kg to 97.6 kg at 12-24 weeks postinitiation
  • GLP-1RA was associated with a significant drop in CRP from 10.1 mg/dL to 3 mg/dL
  • In a subset of 32, fecal calprotectin values decreased from 825 mcg/kg to 235 mcg/kg (P= 0.13)

Limitations: Retrospective study with a short duration, lack of a control group for this study, and lack of endoscopic data.

My take: As with the broader population, GLP-1 RAs help with weight loss in patients with IBD. Many patients may derive health benefits from weight loss alone. This study, though with numerous limitations, indicates the potential beneficial effects on the activity of IBD based on improvements in biomarkers.

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Old Mill on the Cherokee Trail at Stone Mtn Park. Stone Mtn, GA

Pharmacologic Neuromodulation for Bloating Symptoms

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Briefy noted: EN Madva et al. Scand J Gastroenterol 2025 Aug 8:1-5. doi: 10.1080/00365521.2025.2544306. Online ahead of print. Pharmacologic neuromodulation for bloating.

This was a small retrospective study of consecutively referred patients with a DGBI (N = 77; ages 18-74, 87% female) to a tertiary neurogastroenterology clinic who were prescribed a neuromodulator for a primary complaint of bloating in 2016-2022.  Duloxetine was the most commonly prescribed neuromodulator (n = 52, 67.5%).

My take: This study shows that neuromodulators are likely beneficial for bloating symptoms. Dr. Garza () previously noted that in patients with bloating “the typical increase in excess gas during bloating symptoms is only 22 mL.” Thus, “A lot of bloating symptoms are due to increased sensitivity and ‘weird gas handling.’ The latter could include compression of diaphragm rather than elevation.”

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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.

Weight Loss Efficacy of Cagrilintide and Semaglutide

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WTGarvey et al. N Engl J Med 2025;393:635-647. Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity

This  phase 3a, 68-week, multicenter, double-blind, placebo-controlled and active-controlled trial (REDEFINE 1) examined the efficacy of the combination of Cagrilintide and Semaglutide (known as CagriSema).  Patients had a body-mass index (BMI) of 30 or higher or a BMI of 27 or higher with at least one obesity-related complication. The combination druge was delivered as a fixed-dose in a single-dose, single-use pen device. 6.1% of trial participants had BMI <30.

Percentage of patients with at least 5% weight loss
Percentage of patients with at least 20% weight loss
  • “Gastrointestinal adverse events (affecting 79.6% in the cagrilintide–semaglutide group and 39.9% in the placebo group), including nausea, vomiting, diarrhea, constipation, or abdominal pain, were mainly transient and mild-to-moderate in severity.”
  • “Although 57.4% of the participants assigned to cagrilintide–semaglutide were receiving the maximum dose at 68 weeks, 74.7% had received the maximum dose at some point after randomization…doses below the target might be highly effective for some patients and that dose reductions based on the clinical judgment…may be appropriate.”

This same issue also examined the use of this combination in patients with type 2 diabetes (REDEFINE 2). in this study with 1206 patients, “the estimated mean change in body weight from baseline to week 68 was −13.7% in the cagrilintide–semaglutide group and −3.4% in the placebo group.”

The editorial by CM Hales (“Expanding the Treat-to-Target Toolbox for Obesity and Diabetes Care”) notes that “six deaths occurred in the two trials combined, all in the cagrilintide–semaglutide groups, including one suicide in each trial. Previous studies of suicidality with GLP-1 receptor agonist treatment have not supported a causal link,6 but it continues to be of concern.”

My take (from the editorial): “A sustainable treat-to-target approach should extend to lifelong maintenance of health gains after initial weight loss. The intensity and composition of lifestyle interventions in the context of highly effective pharmacologic therapies also need further study. The pharmaceutical pipeline is promising, with potential improvements in safety (such as preservation of lean mass) and more convenience for patients (such as oral administration and monthly dosing). Greater effects on the health of Americans may be achieved not with antiobesity medications producing ever greater magnitudes of weight loss but with expanded access to safe and effective therapies for those who would most benefit.”

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How to Diagnose Celiac Disease in Patients Already Receiving a Gluten Free Diet

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Open Access: Evaluating for Celiac Disease in Patients on a Gluten-Free Diet: A Practical Approach

Algorithm -Figure 2:

Figure 3 lists the content of several common foods -some noted below

While gluten exposure increases the diagnostic yield of currently available tests, there are novel tests being developed “which may aid in the diagnosis of CeD regardless of diet, with a particular focus on immune-based assays. One such innovation involves the use of tetramer-based assays, which enable the direct detection of gluten-specific T cells in the blood. These tetramers, designed to bind to HLA-DQ2 molecules, can help identify T cells that have been activated by gluten exposure. This presents a highly specific immune marker for CeD. Even for those on a GFD, sensitivity (97%) and specificity (95%) have been impressive.”

My take: This article provides practical advice for evaluating whether celiac disease is present in those already consuming a GFD.

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And news from The Onion 8/26/25: Hummingbird Feels Like Fucking Idiot After Seeing Other Bird Gliding

Immune Dysregulation Can Mimic Celiac Disease

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A Turunen et al. JPGN Reports. 2025;6:312–315. Elevated tissue transglutaminase immunoglobulin A: Celiac disease or polytypic plasmacytosis?

Briefly noted: The authors present a case report of an adolescent girl post cardiac transplant with hypergammaglobulinemia and presumed celiac disease (CD), who had a persistently elevated anti‐tissue transglutaminase immunoglobulin A despite a gluten free diet. Ultimately, she was diagnosed with polytypic plasmacytosis from suspected immune dysregulation.

Key point:

  • This case serves as a reminder that when treating those with persistently elevated tTG IgA on a strict GFD, etiologies outside of CD need to be considered.

My take: I had a young girl several years ago who had celiac diagnosis at an outside institution. She had multiple autoimmune disorders. After not responding to treatment, she had a follow-up panendoscopy showing ongoing IELs in duodenum and villous blunting. These findings were noted in the ileum as well. On reviewing her initial biopsies, the pathologist indicated that her findings could be celiac but it was suspected to be an immune dysregulation. Subsequently, she was diagnosed with CTLA4 deficiency and had a marked response to abatacept therapy.

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