The Ketogenic Cure: They Don't Teach This in Medical School

Look at this egg. Or this avocado. Or this Parmesan cheese. To most people, this is just food. But this is my medicine. Now I want to hit you with a big question: What if a ketogenic diet could cure inflammatory bowel disease? "Ketogenic diet." "Keto works so well." "Keto, keto, keto." I know that sounds dramatic. But for me, this is personal. At the end of college, before grad school and med school, I developed life-obliterating inflammatory bowel disease. "I was bleeding out my butt." 12 times per day. My muscles wasted away, my mind went foggy, and my romantic prospects went the way of the blood—down the toilet. But then on June 1st, 2019, I did something unconventional. Out of desperation, I tried a ketogenic diet, and within a week I felt like myself again. The bleeding stopped, my inflammation markers dropped to the lowest they'd ever been, and on a follow-up colonoscopy, I had no signs of disease activity. That changed everything for me. Since then, I've been on a mission, a mission to understand what happened inside my body and why this way of eating might— actually does— work for other people. Today, I want to share that journey with you, starting with the epic science. Let's dig in. Could the human ketogenic microbiome itself transfer? But what was really fascinating is what happened. Now, here's the important part. That's amazing scientifically. As a dork, I'm giddy with excitement. I hope you can see that. Through a ketogenic diet, I came back to life. But that's not even the best part. And I really get excited about starting to understand why. Now, the study I want to discuss to give you just a taste of the data, it was published in Cell. It combined experiments in both humans and mice. We're going to bounce between these, but let's start with some of the human data. So in one trial, 17 adults were enrolled in a crossover study. This means they did one diet, then another. They began on a baseline diet, a standard 50% calories from carbs diet, then switched to a ketogenic diet. Each diet was 4 weeks, and the ketogenic diet was 5% calories from carbs to get people into a state of nutritional ketosis where their body is turning fat into ketone bodies. Now, as just a really quick sidebar, the ketogenic diet used in the study for both humans and animals was not, in my opinion, optimally formulated as an anti-inflammatory ketogenic diet. It was kind of dirty keto. For more details on how to optimally formulate an anti-inflammatory ketogenic diet, Once you're done here, you can check out the tips I provide in the associated newsletter, but I don't want to get too off track. In the human trial, as expected, this "dirty keto diet" was sufficient to get participants into a state of ketosis, i.e. their ketone body levels rose. But what was really fascinating is what happened to their gut microbiome, the community of microbes, bacteria, and other microbes living in their gut. It shifted. Some species increased, others declined, and one notable drop occurred in a group of bacteria known as Bifidobacteria. That will become important later, so just put a sticky note on that. But now let's pivot to some of the mouse experiments, because when mice were placed on a ketogenic diet, they exhibited a very similar microbial shift, including this distinct drop in Bifidobacteria. And importantly, the microbiome changes in the mice corresponded with a striking shift in immune cell function, particularly among Th17 cells. Okay, what the heck are Th17 cells? These are inflammatory cells that reside in the intestines and elsewhere in the body, like in visceral fat, and they're known to drive inflammatory and metabolic diseases and contribute to inflammatory bowel disease. Now here's the important part: as the ketogenic diet reduced Bifidobacteria, it also reduced Th17 cells. Effectively, the ketogenic diet was dampening intestinal inflammation, which could help with inflammatory bowel disease, at least in theory. But was this relationship causal? Were ketones being made on the ketogenic diet actually dampening inflammation? Well, to test whether this anti-inflammatory effect was due to the ketone bodies themselves or other aspects of the diet, the researchers fed mice a standard diet but supplemented with exogenous ketones. And the results were similar to those seen with a ketogenic diet. So all this is to say, in other words, ketone bodies themselves, these molecules when found in the gut were sufficient to trigger the microbiome to shift and changes that reduced inflammation. But that's not even the best part. Now for the final, the gold standard test for causality: fecal transplants. The researchers had saved samples from the human participants. On both dietary phases: the high-carb diet, 50% carb, and the ketogenic diet, 5% carb. And then they transplanted these microbiome samples, these fecal samples, into mice that don't have their own microbiomes. This allowed them to ask the crucial question: could the human ketogenic diet, the human ketogenic microbiome itself, transfer anti-inflammatory effects? And the answer was— drum roll— yes! Yes, the mice that received the microbiota from the ketogenic phase displayed less inflammatory Th17 cell activity, less intestinal inflammation, as compared to those that received the microbiota from the high-carb phase from the same participants. The implications here are really powerful because in diseases like but not limited to inflammatory bowel diseases, ulcerative colitis and Crohn's disease, the immune system is overactive and by definition you're inflamed. But by lowering activity of inflammatory cells like Th17 cells, ketosis may help restore inflammatory tone. This allows the intestinal lining to heal like they did in me. So taken together, the results paint a striking picture: the ketogenic diet shifts the microbiome, and these microbial shifts decrease inflammatory signaling. And as an aside, the effects ripple throughout the body. For example, quoting the authors, "We detected a significant drop in Th17 cell accumulation," accumulation of these inflammatory cells, "in the visceral adipose tissue, the visceral fat, on the ketogenic diet as compared to other diets." So the end result here, the ketogenic diet caused a measurable reduction in inflammation in the intestines and across the body. And this was even transmissible between species via fecal transplant, microbiome transplant. That's amazing scientifically. As a dork, I'm giddy with excitement. I hope you can see that. But let's bring this back to what really matters. The human context, the real stakes. I can speak about them because I have lived them, literally. I was that patient, malnourished, inflamed, physically wasting away, psychologically drained, socially isolated. In every sense, I was depleted, a shell of myself. And yet, through a ketogenic diet, I came back to life. "Mmm!" And when I lived that story, the data we're talking about now, we're going through together, it didn't exist yet. But biology— and listen to me now— biology doesn't wait for peer review. It doesn't care whether a mechanism has a PubMed ID. The processes that are happening inside our body are happening regardless of whether that information has made it to the common scientific knowledge base into clinical care. So that's what I find myself wrestling with. It's what I've been wrestling with since I started and completed med school. Every time I think about clinical care, this is what I wrestle with. The tension between evidence-based care and the best possible care. Because evidence-based care, quote unquote evidence-based care, it depends on published data, randomized controlled trials, some of which are technically or practically impossible to do. And reproducibility. These are all crucial pillars of science, and I don't want to discredit that. But sometimes the best care isn't yet quote-unquote evidence-based by conventional standards. Sometimes you stumble upon it through self-experimentation, intentional or otherwise. That's what happened to me. For me, a ketogenic diet was literally life-saving. The fact that there is still no randomized controlled trial to prove than general efficacy doesn't mean the biology doesn't apply. It doesn't mean that what happened in me and is happening in others isn't real. And just to give you a flavor of others' experiences, show I'm not alone, here are some quotes from a medical case series we wrote about a ketogenic diet for inflammatory bowel disease. A 62-year-old man told us, "A ketogenic carnivore diet let me forget I had Crohn's. No drugs, no surgery. The decades I dealt with Crohn's "Like another lifetime." Or a 31-year-old woman said, "Within days, my bowel movements changed from loose to normal, and within 2 weeks I had more energy than I had in the past 10 years." Or a 30-year-old man said, "I cured my ulcerative colitis with a ketogenic diet. I want to share my story in case it can help people." We face challenges as individuals and a biomedical community because biology doesn't wait. For our human brains to catch up. It isn't paused for peer review. It's happening in real time inside real people, inside me, inside you. The question is, are we paying attention? I don't know if a ketogenic diet can cure inflammatory bowel disease in any person. I actually probably don't think it can. But I know it helped for me. And I really get excited about starting to understand why. So here's my invitation. It's the same invitation as always. Stay curious, because curiosity can literally save lives. Now for some cheese. Delicious. High protein and tons of calcium.