Sit Down Before Reading, A Memoir by Dave Bexfield
The concluding chapter of Sit Down Before Reading has been broken into five parts (1-5).
Part 2
House of Horrors
All of us have biases whether we admit them or not. I’m typically pretty openminded, but when people start crowing about things unsupported by the evidence, or worse, the science, eyebrows raise along with deep-seeded biases. And nothing, nothing, brings out my prejudices like someone waxing on—and on and on and on—about some purportedly disease-busting diet. Think someone trying to exhaustively explain the undervalued benefits of Bitcoin over lunch, only instead they are extolling the benefits of a restrictive diet while you are trying, trying, to enjoy a green-chile cheeseburger, truffle fries, and a pint of microwbrewed IPA before ordering that fresh-baked gooey chocolate-chip cookie topped with a scoop of vanilla bean ice cream for dessert. And enlightening you with news that everything you love to eat is bad, helping you to slowly dig your own grave. (Of course it’s slow, I’d say under my breath, utensils make inefficient excavators. Good thing burgers and fries are finger food.)
I always ask, sometimes aloud but usually to myself, Where’s the beef? I want research with meat on the bone, not anecdotes, before I contemplate upending my diet, particularly one that excludes said meat. I’ve railed about the weak scientific support of these diets and supplements, from op-ed submissions to The New York Times (never published, now an appendix to this memoir) to lengthy blog posts on ActiveMSers. I went so far as to dedicate part of a chapter in this memoir to this source of ongoing frustration. I even remember the internal consternation when Confidant #2 (from Chapter 11) generously—prophetically?—gifted me a book on nutrition days after I revealed my 2006 MS diagnosis to him. (Bonus fact: he even played an essential role in my Breaking Bad project, the first time we had spoken in more than a decade.)
Diets grate on me, especially those that eliminate Cheetos, and I’m not shy about expressing my distaste. But notably with these rants, I begrudgingly typically included a disclaimer. That “I don’t know” if a diet could be an unexpected bridge to a remarkable remedy. Only that if it was, one had yet to surface in the research. I would leave unsaid that I remained extremely dubious at the prospect of a diet curing disease. A level of dubiousness not dissimilar to the way most view Lyme disease.
Ohhh….
“Any grand health gains would be looked at with extreme dubiousness.” Fudge. That was what my brain told me to look for in May of 2023.
There was a reason my trial of e-stim and antibiotics had yielded bupkis. No matter how much I wanted it to work, it was not the secret combination that I had hoped it would be. Repeated trials would continue to fail. When this depressing reality settled, I wish I had had a mirror to see in real time the blood drain from my face, the waxy pallor of a man finally facing the terror that has haunted his existence while living with a chronic disease.
The cure, unbelievably, must involve … diet. My personal house of horrors. And this amateur sleuth’s nightmare scenario. Worse, I had already written a tight draft of the maybe ending to this memoir, complete with a chapter title that hinted at what was to come, “The Shocking Conclusion,” a wink toward electrical stimulation. In that draft I had warned readers that unlike many of my bold proclamations in this book, I was uneasy about this one, referencing the potential that it could be “a steaming pile of malarky.” Which now, clearly, it was. Even my paper shredder got upset with me. You could take all the disasters mentioned in this memoir, from the Deepwater Horizon to the Hindenburg, roll them into one giant cluster doobie, light it up and smoke it, and you’d have your Chapter 52, renamed Dumpster Fire. Maybe I could still do that podcast I mentioned in jest last chapter, “Hook, Line & Sucker,” with me the sucker-in-chief?
How in the hell was I going to untangle a litany of dietary modifications, much less test them? I needed a coconut miracle.
Coconut Shell Paperweight - Original coconut on which the rescue message was inscribed by Kennedy to rescue the crew of the PT-109 and delivered by natives, Biuku Gasa and Eroni Kumana, of the Solomon Islands. Photo credit: jfklibrary.org; public domain.
On the night of August 1, 1943, the PT boat commanded by Lieutenant John F. Kennedy was sunk after being hit by a Japanese destroyer in Blackett Strait, south of Kolombangara in the Solomon Islands. Four days after they had been given up as lost, Kennedy and his surviving crew were discovered by Biuku Gasa and Eroni Kumana, two indigenous Solomon Islands scouts working for the Allies. Kennedy carved the message into this coconut husk that 11 crew members were still alive and passed it along to Gasa and Kumana, who carried the message to a nearby Australian coast watcher. The chance encounter with the islanders resulted in the rescue of PT-109's crew.
I had to start somewhere. Dr. Wahls isn’t the only one who has boasted about a diet curing her disease. There’s a sizeable smattering of breathless tales on the internet about the wonders of targeted food restrictions, and three close personal friends—all with suspected Lyme—have had wild success after lengthy elimination diets. But again, these are anecdotes. Anecdotes are all but anathema to scientists. I reasoned that if there were actionable clues tucked into recent diet research, my go-to doc on YouTube, Dr. Brandon Beaber, would have posted an informed opinion about them. (Coincidentally, he even dedicated an entire video to “Why Doctors Don’t Trust Anecdotal Evidence”.)
Among his 300+ streaming videos, there’s a corner reserved for nutrition. He even dedicated an entire playlist for the dozen videos he’s created concerning Dr Wahls and her diet/recovery. But one random video, an uncategorized one from April 10, grabbed my attention with its breathless title: “Does Ozempic Prevent MS?”
Unlike standard weight-loss drugs, the new classes of these drugs—Ozempic, Wegovy, Trulicity, and the like—lowered the risk of MS by a gobsmacking amount, as much as 85% lower than expected according to an April 2024 study. Even an older drug used to treat diabetes, metformin, shocked with a 61% reduction in risk. That sounds positively nuts. “I am highly, highly skeptical of the results of this study,” said Dr. Beaber with a cocked head. “One reason: it’s just too good to be true.”
"Disproportionality analysis illustrating the association between multiple sclerosis and weight loss-inducing drugs based on the data from the FDA Adverse Event Reporting System database. The reporting odds ratio represents the odds of a certain adverse event (in this case, ‘multiple sclerosis’) occurring with the drug of interest, compared to the odds of the same adverse event occurring with all other drugs in the database. An asterisk (*) denotes the presence of an inverse association, defined when the upper limit of the 95% CI for reporting odds ratio is less than 1. GLP-1, glucagon-like peptide-1; SGLT-2, sodium-glucose cotransporter-2." Shirani A, Cross AH, Stuve O. Exploring the association between weight loss-inducing medications and multiple sclerosis: insights from the FDA adverse event reporting system database. Ther Adv Neurol Disord. 2024 Apr 1;17:17562864241241383. doi: 10.1177/17562864241241383. PMID: 38566910.
Hiding in plain sight, grand gains, extreme dubiousness. Exactly what I was looking for. Even naltrexone made the list. Although not quite as effective as the others, a low-dose version, LDN, has been used off-label in the chronic disease community for decades. If I was four and hunting for Easter eggs, this surely meant I was past “getting warmer” and into “hot-hot” close. But now for the gauntlet of truth. These drugs would have to show promise not just in MS and autoimmune disease, but across a swath of illnesses, from mental disorders and dementia to long Covid and cancers. Its success outside of weight loss would be so widespread, so shocking, that it would be called a potential miracle drug. And one more thing: scientists would have no frigging clue as to why they are so effective across such a wide and diverse range of health conditions. Except that maybe it’s because they are “anti-inflammatory.”
“Ozempic and Mounjaro have another benefit: treating inflammation,” screams a headline. “We Know Where New Weight Loss Drugs Came From, but Not Why They Work” screams another from The New York Times. Months later, the paper upped the ante. “Ozempic and other drugs like it have proven powerful at regulating blood sugar and driving weight loss,” reads the opening paragraph. “Now, scientists are exploring whether they might be just as transformative in treating a wide range of other conditions, from addiction and liver disease to a common cause of infertility.”
That explorative dive into the efficacy of these drugs on myriad health issues has been described as one that could upend medicine.
Scientists believe the drugs are about to revolutionize several fields of medicine, such as cardiology and endocrinology. Researchers are also running dozens of trials to see whether they might help with Alzheimer’s, liver disease, polycystic ovary syndrome and even skin conditions. If these trials prove successful, the drugs may extend many lives by years, save billions in medical costs and divide public health into before-and-after epochs. A researcher studying these drugs told me he felt like the scientist who first discovered antibiotics.
“’Obesity first’ doctors say they start with one medication, to treat obesity, and often find other chronic diseases, like rheumatoid arthritis, simply vanish,” reads a June 18, 2024 piece in The New York Times. Dependence on alcohol appears to significantly wane. Polycystic ovary syndrome, a leading cause of infertility, is put into retreat. Cancer defenses are buttressed while cirrhosis and liver cancer risk drop. Cardiovascular events like heart attacks and stroke have dropped so much with their use that in March the Food and Drug Administration approved these diet drugs for those at risk, and a trial in kidney disease was so successful it had to be halted. These weight-loss drugs might even cure sleep apnea, a condition that affects an estimated 936 million worldwide. That shocking study landed June 21, 2024 in the New England Journal of Medicine, leading to headlines and an aftermath that I ominously predicted: “Can You Finally Throw Away Your CPAP Machine?” accompanied by the collapse of stock in businesses that manufacture them.
“The idea that a single drug that could target so many kinds of disease might sound too good to be true,” said the June 24 edition of the NYT Morning Briefing. That includes promise in Parkinson’s, reducing cravings and addictions, slowing Alzheimer’s, lowering smoking rates, and short-circuiting depression. “These drugs, called GLP-1s (glucagon-like peptide 1 receptor agonists), mystify even the scientists who study them. When I asked researchers how it was possible that Ozempic might help with cognitive issues and nonalcoholic fatty liver disease and opioid addiction, they gave the same answer: We don’t know!”
Researchers might not know why these drugs are so effective across such a wide range of illnesses, but I know. They are all treating Lyme disease, the disease my doubters have been insisting could not possibly be the root cause of so many illnesses. A single type of parasite doing so much damage was too unbelievably horrific to be true. Now that a single type of intervention appears to work for all those same illnesses, scientists are stuck in a similar state of disbelief, only they are now cautioning that such unbelievable success is too good to be true.
It's time to start believing. (Especially after the July 5, 2024 release of a 15-year study published in JAMA that “found that the patients who received GLP-1 agonists had a significantly lower risk of developing 10 out of 13 cancers studied, including kidney, pancreatic, esophageal, ovarian, liver and colorectal cancer.”)
A Miracle Diet?
Dr. Wahls didn’t cure her MS with Ozempic. My friends didn’t buck their Lyme disease with Wegovy or Trulicity or Victoza. Neither did all those diet/lifestyle peddlers who swamp the social media feeds of those struggling with chronic illnesses.
What’s going on? Those restrictive diets and lifestyle protocols must be mimicking aspects of the newest classes of weight-loss drugs, which work, in part, by helping the body to lower blood sugar. According to the Mayo Clinic, blood sugar is measured with an A1C (or HbA1c) test, which reflect “your average blood sugar level for the past two to three months,” measuring “what percentage of hemoglobin proteins in your blood are coated with sugar (glycated).”
So that leads to the million-dollar, er, billion/trillion-dollar question. What dietary and lifestyle changes can help reduce blood sugar?
“Controlling your blood sugar often involves limiting foods such as fruits, candy, and sweetened drinks that contain obvious sugar,” say health experts. “But starches such as bread and pasta also contain a lot of sugar in the form of carbohydrates — long, complex chains of sugars.”
Carbohydrates. They dominate Western diets. It’s not just desserts, select fruits, and breads and pastas that you must be wary of. Starchy vegetables like potatoes and corn are loaded with them. Then you have your other typical sides or fillers, like rice or beans, both bursting with carbs. Cereals and sweetened yogurts are problem areas, and forget about beer and cocktails. Many of our favorite snacks—chips, crackers, pretzels, popcorn, and processed foods in general, are laden with them. Even foods you think are healthier can be carb bombs, from gluten-free baked goods and low-fat salad dressings to fruit juice and milks (cow, almond, soy, etc.).
Carbs are like the actress Olivia Colman. Everywhere. Good luck avoiding them. You can’t—they are a significant energy source (carbs, not Ms. Colman). But you can limit them. Enter most diets.
Mediterranean, gluten-free, paleo, low-fat, the Zone, vegan, DASH, Ornish, even carnivore diets. They all limit, to an extent, carbs and sugars. But there are certain diets, like Atkins, where carb reduction is the focus with few restrictions on fats and proteins. The most popular of these currently, and conveniently one of the most studied, is the ketogenic diet: a low-carb, high-fat, often protein-rich diet.
In a nutshell, keto diets severely restrict carbs, which “typically serve as the main source of energy production in the body's tissues,” capping daily consumption to 50 grams or less, about what you would find in a typical bagel. When the body is depleted of glucose, it switches to an alternate energy source: ketones, which are created by converting fat. Burning fat stores when the body enters a state of “ketosis” typically results in weight loss, hence the reason for the diet’s popularity, despite its counterintuitive components. “Diet” and “high fat” are uncommon bedfellows, causing unease among many nutritionists and dieticians.
But there is something else decidedly unusual about ketogenic diets. They weren’t originally used for weight loss.
Recall two tenets from SHARDS: history harbors hints and answers await in the anomalies. In 1915, a professor of pediatrics from Johns Hopkins University School of Medicine started studying why fasting, which triggers ketosis, helped cure his nephew of epilepsy. The answer never became clear, but in 1921 a doctor from the Mayo Clinic, Russell Wilder, M.D., proposed a “nutritional treatment for epilepsy that tricks the body into believing it is fasting”—a ketogenic diet. It worked, and wildly well. For one type of epilepsy, more than half were cured in one trial, with a remarkable 80% showing significant improvement. But as pharmaceutical solutions were developed and patients were given a choice, popping a less-effective pill had more appeal than an overly restrictive diet, and going keto gradually lost favor as a treatment option.
Revisiting this history opens a long-forgotten, hidden gateway. I didn’t know that an entire class of epilepsy is thought to be autoimmune, labeled, appropriately, autoimmune epilepsy. Again, because I’ve linked all characteristics related to autoimmunity to Lyme disease, if my theory is correct, it can mean only one thing: ketogenic diets—and by extension, forms of intermittent fasting—must help treat the bacterial infection. Which, as unlikely as it sounds, at least passes the smell test upon closer inspection. Dr. Wahls’ paleo-based diets, her most restrictive—and the one she personally follows—combines elements of ketogenesis and fasting. Other successful “disease dieters” are almost certainly restricting carbs enough to mimic aspects of ketogenic and fasting diets, whether intentional or not.
Gulp. After all that over-the-top obnoxious chatter in the last chapter about me being a potential g-word and making the GMDOAT (Greatest Medical Discovery Of All Time), it would seem the time is nigh for the measuring stick of history to finally Tonya Harding my kneecaps, my triple salchow days in jeopardy. Either that, or I’m #GeniusAF.
As with the previous gauntlets of truth, it now all comes down to whether a keto/fasting diet is the shizzle, the bomb, the GOAT of diets, treating everything from autoimmune diseases and mental disorders to long Covid and cancers. If not, all my bonkers hypotheses are mercifully capped.
Choose your method of execution: Harding or Soprano.
Genius AF
If you’ve been reading this memoir since the beginning—wading through insane story after insane story, from me landing in The New York Times and collecting $500K after winning an epic row with my health insurer to Laura and I surviving the trauma of getting locked outside our hotel room butt naked right as my Viagra kicked in—you don’t have to be Nostradamus to predict how this is going to unfold. Getting capped isn’t happening unless you count the cap Sarah the astrophysicist promised to eat in Chapter 50 if I was right. (Good thing you can find edible ones on Etsy.)
The first mentions of ketogenic and fasting diets in my inbox—“the carb reduction [diet] reduces the glucose in your body [which] may reduce MS inflammation” while fasting “reduced MS inflammation and improved some symptoms”—popped up in 2019. Former newspaper reporter Ed Tobias, a member of ActiveMSers, had sent me a preview copy of his new book, We're Not Drunk, We Have MS: A toolkit for living with multiple sclerosis. I filed that away as an interesting tidbit and quickly moved along. The diet failed to make another appearance on my radar until early April in 2024, while writing the final chapters of this memoir, when a headline in The Washington Post gave me pause: “High-fat keto diet may help people with serious mental illness”.
I remember thinking that was odd. Really odd. By that point I was sure that Lyme disease was a significant contributor to many forms of mental illness. And yet an astonishing 79% of patients with schizophrenia and bipolar disease in the Stanford trial experienced “clinically meaningful improvement” after just four months of a keto diet. That brought up a flood of questions. How could a diet possibly fight a bacterial infection? Were there any other examples of this success in clinical research? Had it even been tested in multiple sclerosis?
”Ketogenic Diet Shows Major Benefits for Multiple Sclerosis” screamed the University of Virginia announcement from 2022, an announcement I apparently missed (or, quite possibly, ignored). “Patients with relapsing-remitting multiple sclerosis who adopted a high-fat, low-carbohydrate ketogenic diet saw significant improvements in their MS – including reductions in neurologic disability, fatigue and depression and heightened overall quality of life.” The improvements were sweeping and significant. According to the published research study, participants in the 6-month trial reported a “nearly 50% decline in self-reported fatigue and depression scores” and “significant improvements were noted in Expanded Disability Status Scale scores, 6-minute walk [times] and Nine-Hole Peg Tests [for dexterity].”
These results aren’t just surprising, they best every single one of the FDA-approved MS medications on the market. It’s well known in the chronic disease community that our meds don’t improve our health, that they merely slow the progression of our illnesses. But a cheap diet trumping our expensive drugs? Before the haters can hate, it was a rather small study and “more research is needed,” so Big Pharma CEOs can breathe a sigh of relief. Like there is a group out there that has pockets deep enough to pay for a larger research study on a non-money-making diet without the financial backing of a drug company, lol. As if. Bullet dodged, all Matrix like.
For there to be any risk to established medical practices, there would have to be a boatload of at least plausible evidence to support such nonsense that the ketogenic diet and intermittent fasting may be the shizzle. There would have to be so much that it would need to fill the most famous boat in history, the Titanic, for the mere suggestion of such a hairbrained hypothesis to be taken seriously.
Of course, among the pantheon of worst mistakes in history (referenced at the start of this chapter), the unsinkable Titanic, poorly captained by one Edward Smith, sits atop most lists for a reason.
History harbors hints for what causes many disasters. In the case of the RMS Titanic, “high speeds, a fatal wrong turn, weather conditions, a dismissed iceberg warning and lack of binoculars and lifeboats all contributed to one of the worst maritime tragedies.” Haste, human error, happenstance, and hubris. And that cliché about history, that it’s destined to repeat? It’s a cliché for a reason. Like Britney Spears in 2000, oops, it looks like we did it again, only instead of putting 2,240 lives at risk, multiple billions. Oops.
“A systematic review of 70 dietary studies revealed that … fasting and calorie restriction, in particular, were associated with improvement of rheumatoid arthritis activity,” found a 2021 study. The study found similar effects in psoriatic arthritis and ankylosing spondylitis. Myriad research papers, trials, case studies, and drama-filled reports concerning these diet interventions are tucked into the corners of all autoimmune diseases, peppering research study after research study. “Intermittent fasting: A promising dietary intervention for autoimmune diseases.” “Crohn’s disease successfully treated with the paleolithic ketogenic diet.” “The ketogenic diet modifies the immune system to combat different disease conditions.”
Different diseases. It’s not just flavors of autoimmunity. Ketogenic diets have shown “promising therapeutic potential in Alzheimer’s disease, Parkinson’s disease … and migraine.” The diet currently is being “used in clinical practice for … non-neurological conditions, including heart disease, diabetes, obesity, autism, glioblastoma and cancers.” Yes, cancers, and the acclaimed Cedars-Sinai is investigating the powerful role of intermittent fasting after they noticed their patients on these diet regimens often did better.
But wait, there’s more.
“Can a low-carb, anti-inflammatory diet be the answer to long COVID woes?” wonder medical professionals. Researchers aim to find out after case studies report patients are eliminating long Covid with both the keto diet and intermittent fasting. There’s even a push to investigate the diet in mental illnesses involving diet, after cases of severe anorexia resolved after carbohydrate restriction. And like the newest weight-loss drugs, these low-carb interventions appear to dampen addictive behavior and help treat substance abuse. A January headline from NPR’s “All Things Considered” perhaps expresses it best. “Patients say keto helps with their mental illness. Science is racing to understand why.”
Enter every panicked “what’s happening?!?” meme on the internet, from Poltergeist to The Office.
How can it be remotely possible that a single class of weight-loss drugs and a single type of dietary intervention can influence so many difficult-if-not-impossible-to-treat health conditions—health conditions I’ve repeatedly tied to Lyme disease throughout this memoir? How??? HOW?!
Scientists have spitballed so many theories that they’ve become soggy from all the phlegm and sputum. It must be altering the gut microbiome. Or contributing to “specific cellular pathways in mediating neuroprotective effects.” Or it’s spurring energy supply restoration. Or it’s inducing anti-inflammatory pathways. Or it’s reducing oxidative stress. Or it’s altering epigenetic mechanisms.
Translation: they have no effing clue.
It’s none of those. Per Occam’s razor, often the simplest answer is the right one. And it couldn’t get much simpler.
