A Clinician's Case for Pattern Recognition
Medical breakthroughs don’t start in conference rooms or pharmaceutical board meetings. They start in exam rooms, with a clinician who’s paying attention, someone who sees the same thing happen often enough that it stops looking like coincidence. That’s been the engine behind my entire career.
For 38 years, I treated thousands of patients with IBS, autoimmune disease, food sensitivities, and unexplained symptoms. I did it largely by paying attention to patterns, patterns that showed up again and again, across enough patients that they were hard to dismiss as coincidence.
When my experience, my patients’ patterns, and my clinical judgment all lined up, I acted. Not on a hunch. On repetition. On outcomes. On what worked.
Evidence-based medicine has its place. It’s essential for testing drugs. But it’s not where discoveries begin. Discovery starts with observation, and observation starts with a clinician willing to trust what they see.
Here are three examples of how that works: one of the most elegant stories in medical history, a single anecdote that became a household phrase, and my own, patterns I noticed in my own practice long before the research caught up.
Evidence, and the Experience Behind It
Evidence-based medicine, or EBM, is often treated as the gold standard, because that’s what everyone was taught: if it’s not evidence-based, you can’t recommend it. But its core function is narrower than most people realize. At its heart, EBM answers a fairly specific question: does this treatment outperform placebo in a double-blind, placebo-controlled trial?
That question matters, especially for pharmaceuticals. But as I said, it’s not where discoveries begin. It’s where they get tested, confirmed or ruled out, once someone has already noticed a pattern worth studying.
Clinical experience is messier. It’s observational, human, built on intuition, not psychic intuition, but the kind that comes from repeated exposure to patterns over thousands of patient encounters. Many major medical discoveries began this way, quietly, in an exam room, long before a trial existed to confirm them.
Example One: The Pediatrician Who Saw What No One Else Saw
Willem-Karel Dicke was a Dutch pediatrician treating children with chronic diarrhea, malnutrition, abdominal pain, and failure to thrive, what was then called “Gee-Herter disease.”
He didn’t have labs. He didn’t have imaging. He didn’t have randomized trials. He had sick kids in front of him, and he had a pattern.
Every time these children ate porridge, bread, rusks, or cereal, they got worse. Take those foods away, and they improved. Bring them back, and the symptoms came roaring back with them.
Dicke didn’t know the culprit was gluten. He didn’t know the mechanism. He only knew that grain-based foods triggered relapses, and he saw it often enough that he trusted it. In 1941, he published a paper showing improvement on a diet low in wheat, rye, and oats, years before anyone could explain why.
Then World War II handed him the kind of confirmation no scientist would ever design. During the Dutch Hunger Winter of 1944 to 1945, wheat disappeared from the diet. Celiac children improved dramatically. When Allied planes dropped white bread into the Netherlands, symptoms returned within days.
The famine didn’t give Dicke the idea. It proved he was right. This is clinical intuition: pattern, then hypothesis, then confirmation.
Example Two: The Letter That Named a Syndrome
In April 1968, Dr. Robert Ho Man Kwok wrote a short letter to the *New England Journal of Medicine* describing symptoms he felt after eating at Chinese restaurants in the U.S.: numbness at the back of the neck, weakness, heart palpitations.
No study. No statistics. Just one man noticing a pattern in himself.
That letter sparked what was then called “Chinese Restaurant Syndrome,” a term the medical community has since moved away from, and MSG became the prime suspect. Media coverage exploded, and research followed, though the formal evidence has remained mixed. Most blinded studies have struggled to reproduce MSG symptoms under controlled conditions.
What hasn’t been mixed is what people report. Migraines, brain fog, sweating, chest tightness, and digestive symptoms, among others, after eating foods containing MSG.
That’s part of why you now see “No MSG” printed on menus and food labels today. People wanted to know what was in their food and whether MSG was behind what they were feeling, and that wasn’t always easy to tell, since MSG shows up under a lot of different names on ingredient lists, hydrolyzed protein, yeast extract, autolyzed yeast, among others. Enough people asked the question that restaurants and manufacturers started answering it directly.
The starting point was the same as Dicke’s: someone noticed a pattern before anyone had the evidence to explain it.
Example Three: Patterns From My Own Practice
My own work with IBS, food intolerance, and functional medicine followed a similar arc. I saw patterns long before the literature had names for them, gluten sensitivity and MSG sensitivity especially, enough that we’ve put together videos on It’s My Health that go deeper into both, if you want to see where the science and my own clinical experience stand today.
The gluten pattern
In 1989 and 1990, while writing my first IBS book, I noticed that IBS patients improved on elimination diets, symptoms returned with gluten, and autoimmune patients often improved off gluten. I noticed patients who went off gluten felt better, whether it was celiac disease, which is relatively rare, or non-celiac gluten sensitivity. Most of these patients, I now believe, were what we’d call non-celiac gluten sensitive, a term that didn’t exist yet. I didn’t have a study. I had thousands of patient outcomes.
Some of what I was seeing, I now believe, ties into what’s often called “leaky gut,” increased intestinal permeability that lets undigested proteins like gluten slip through the gut lining and trigger a wider immune and inflammatory response.
The European wheat phenomenon
I also noticed that many gluten-sensitive patients could travel to Europe and eat wheat there without symptoms. Are you one of those people? A couple of explanations seem plausible: glyphosate exposure in U.S. wheat farming, and differences between modern hybridized wheat and older European varieties.
My own MSG patient
Decades after Kwok’s letter, I saw my own version of his pattern. A patient reacted every time he ate Chinese food. MSG was still common in restaurant cooking then, though that’s less true today. The pattern was too consistent to ignore.
I was curious enough, and confident enough in the pattern, to pursue it formally. I received a grant to study whether MSG could trigger IBS symptoms in susceptible individuals. The early data pointed in the direction I expected.
I want to be honest about the limits here: the statistician I’d hired was in a car accident partway through, and while some of the data was later pulled together, the study was never completed or published. So I hold this one as a strong clinical impression, not a proven result. But it’s a good example of what clinical experience looks like when you take it seriously enough to test it.
The Bloaters: A Pattern That Deserves Its Own Conversation
Of all the patterns I saw across 38 years of practice, this one stands apart.
Do you ever get bloated immediately after you eat something, not the slow buildup over a few hours, but distention that shows up within minutes? If so, this next pattern might be familiar.
Some IBS patients would eat a meal and become distended almost immediately, not hours later, but minutes. They looked several months pregnant and were miserable. This wasn’t fermentation bloating. It was too fast. Too dramatic. Too neurologic.
The common thread? A history of fluoroquinolone antibiotic use.
Fluoroquinolones are well established as a cause of peripheral neuropathy, and there’s growing recognition of their broader neurological effects. The constellation of long-lasting symptoms some patients experience after fluoroquinolone use has come to be known as fluoroquinolone-associated disability, or FQAD.
The enteric nervous system, the gut’s own neural network, is a plausible target within that same picture. If fluoroquinolones can damage peripheral nerves, and they can, it’s worth asking whether they can affect enteric nerves too.
I collected photos from six patients. The pattern was hard to ignore.
This specific link, fluoroquinolones triggering rapid bloating through enteric nervous system dysfunction, is my own clinical hypothesis. It hasn’t been studied directly, and I present it here as a pattern I noticed rather than a settled finding. But this is exactly how Dicke’s discovery began: a clinician paying close attention to what the patients were telling him.
Why Pattern Recognition Is Medical Intuition
Medical intuition isn’t mystical. It’s repetition. Pattern recognition. Clinical memory. Real-world outcomes. It’s seeing what others miss because you’ve seen it a hundred times before.
Dicke had it. Kwok had it too, an anecdote nobody asked him to write, that turned out to be onto something real. I tried to practice it every day.
Evidence-based medicine tests discoveries. Clinical experience creates them. Both matter, but it isn’t really an either/or. Clinical experience always comes first.
And here’s the part I loved most: patients notice patterns too. They come in already connecting dots, already paying attention to what their bodies are telling them.
So here’s what I’d say to you, reading this: pay attention. Your patterns are yours. They’re valuable, and nobody else is going to find them for you.
That’s part of why It’s My Health matters to me. It’s a place where people can compare notes, share what they’ve noticed, and recognize patterns together, the same way I did for 38 years in an exam room.
Here’s the deal. Recognize your patterns. That’s what I did.
Stay curious and thrive,
Dr. G
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