The Patient Who Was Never Sick
A man turns fifty. His insurer pays for a screening colonoscopy. He has no abdominal pain, no diarrhoea, no weight loss, no fatigue. He goes in because the schedule says it is time. The pathologist examines the biopsies and reports granulomas and chronic inflammatory changes. The gastroenterologist calls him in and tells him he has Crohn’s disease, a chronic incurable condition that will require lifelong management. He is started on adalimumab, an injected biologic costing roughly forty thousand dollars per year, with documented adverse events including serious infections, lymphoma, hepatosplenic T-cell lymphoma, and heart failure.¹ He will inject himself with this drug every two weeks for the rest of his life.
He had no complaint when he walked through the door.
This is not a hypothetical. It has a name in the gastroenterology literature: silent Crohn’s, or asymptomatic incidentally diagnosed Crohn’s. Roughly a quarter of patients with the histological findings have no symptoms at the time of diagnosis.² The treat-to-target framework now dominant in inflammatory bowel disease practice³ instructs gastroenterologists to suppress the tissue findings whether or not the patient feels ill, on the theoretical grounds that future damage might otherwise occur. The retrospective evidence in the establishment’s own journals tells a different story. Grinman and colleagues at Sheba Medical Center in Israel reviewed the records of 2,700 Crohn’s patients in their inflammatory bowel disease registry. They identified 60 patients whose Crohn’s had been discovered incidentally — found during colonoscopy or imaging done for unrelated reasons, in patients with no Crohn’s symptoms. Eighty-eight percent of these patients received no treatment after diagnosis. Of those left untreated, eighty-nine and a half percent had no flare over a median follow-up of four and a half years.⁴ The authors’ conclusion, in their own words: many asymptomatic patients with an incidental diagnosis of Crohn’s disease can probably be followed up without immediate treatment.
The practice continues regardless. A healthy person with no complaint is informed they have an incurable disease, started on a drug that costs more than most cars, and instructed to take it indefinitely. The body that was successfully managing its own affairs is now prevented from doing so.
The case this essay makes is that Crohn’s disease is a modern poisoning with a specific toxin, by a specific route, in a specific population — and that the asymptomatic-treated patient is the clearest window into what the diagnosis actually is. The body in that man’s gut was doing what bodies do when they accumulate something they cannot easily clear. Medicine saw the work and called it disease.
On 13 May 1932, three physicians at Mount Sinai Hospital in New York — Burrill Crohn, Leon Ginzburg, and Gordon Oppenheimer — presented a paper to the American Medical Association in New Orleans titled Terminal Ileitis. The published version appeared five months later in the Journal of the American Medical Association under the title Regional ileitis: a pathologic and clinical entity.⁵ The paper described fourteen patients between the ages of seventeen and fifty-two, all operated on by the Mount Sinai surgeon A. A. Berg. The lesion was characteristic: transmural inflammation of the terminal ileum, granulomas, skip lesions, fistulae. The cohort was overwhelmingly Jewish.
Earlier descriptions of similar pathology existed but were rare enough to be surgical curiosities. Morgagni had noted the picture in 1761. Antoni Leśniowski described it in Poland in 1903. Thomas Kennedy Dalziel, a Scottish surgeon, published a paper in the British Medical Journal in 1913 titled Chronic Interstitial Enteritis, describing the same condition in human patients and noting its histological resemblance to Johne’s disease — a chronic granulomatous ileitis in cattle first described by Heinrich Johne in 1895.⁶ Dalziel’s paper is not cited in Crohn’s 1932 report. The omission would shape the next ninety years of research.
From those fourteen surgical cases in 1932, the disease has expanded into a global epidemic. The 2017 Lancet systematic review by Ng and colleagues documented incidence rates above twenty per hundred thousand per year in parts of Canada and northern Europe, with prevalence exceeding 0.3% of the population in early-industrialised countries.⁷ The Global Burden of Disease 2017 IBD Collaborators estimated approximately 6.8 million people living with inflammatory bowel disease worldwide.⁸ Kaplan and Ng’s four-stage epidemiological framework places Western countries in a prevalence plateau while China, India, Brazil, and sub-Saharan Africa move rapidly through accelerating incidence — a transition the authors link explicitly to the Westernisation of diet, hygiene practices, and pharmaceutical exposure.⁹
The migration evidence makes the environmental signal unmistakable. Benchimol and colleagues documented that second-generation South Asian immigrants to the United Kingdom and East Asian immigrants to Canada acquire host-country incidence within a single generation.¹⁰ Their genes do not change in that interval. What changes is the schedule of pharmaceutical exposures, the food supply, and the injection regimen administered in childhood. The disease is acquired, not inherited.
Genetics deserves its own paragraph because the establishment has invested four decades in pursuing it. The NOD2/CARD15 gene was identified simultaneously by two groups in 2001.¹¹ Twenty-five years and over two hundred and forty susceptibility loci later, the genetic programme has produced no cure and no actionable clinical intervention.¹² The Swedish twin study of Halfvarson and colleagues found 29 monozygotic twin pairs with Crohn’s disease — only nine of them concordant for the disease, twenty discordant for life despite identical genomes. CARD15/NOD2 variants did not explain the difference; the authors concluded that the genetic variants “contribute but do not alone explain concordance of Crohn’s disease in monozygotic twins.”¹³ NOD2 variants are rare or absent in East Asian populations, where Crohn’s incidence is currently exploding. A disease that triples in a generation in Korea cannot be primarily genetic. Gene pools do not change at that rate.
What does change at that rate is what is being injected, ingested, and prescribed.
***********************
No comments:
Post a Comment